Scribd Logo
Upload

Welcome to Scribd!

  • 4K views

    Oku 10

    Uploaded by

    Melissa Villanueva
    CHAPTER 1 Patient Safety and Risk Management DOUGLAS W. LUNDY, MD STUART L. WEINSTEIN, MD. . . . . . . . . . . . . . . . 3 CHAPTER 2 Fracture Repair and Bone Grafting CHUANYONG LU, MD ERIC MEINBERG, MD RALPH MARCUCIO, PHD THEODORE MICLAU, MD . . . . . . . . . . . . . . . . 11 CHAPTER 3 Articular Cartilage and Intervertebral Disk JAMES A. MARTIN, PHD PREM S. RAMAKRISHNAN, PHD TAE-HONG LIM, PHD DANIEL THEDENS, PHD JOSEPH A. BUCKWALTER, MS, MD. . . . . . . . . . 23 CHAPTER 4 Muscle, Tendon, and Ligament LAWRENCE V. GULOTTA, MD SCOTT A. RODEO, MD. . . . . . . . . . . . . . . . . . 37 CHAPTER 5 Wound Management JAN PAUL ERTL, MD JEFFREY ANGLEN, MD, FACS . . . . . . . . . . . . . 49 CHAPTER 6 Musculoskeletal Biomechanics MICHAEL BOTTLANG, PHD DANIEL C. FITZPATRICK, MS, MD PETER AUGAT, PHD . . . . . . . . . . . . . . . . . . . . 59 CHAPTER 7 Bearing Surface Materials for Hip, Knee, and Spinal Disk Replacement JAVAD PARVIZI, MD, FRCS MICHAEL BERCIK, MD TODD ALBERT, MD . . . . . . . . . . . . . . . . . . . . 73 CHAPTER 8 Musculoskeletal Imaging KENJIROU OHASHI, MD, PHD GEORGES Y. EL-KHOURY, MD YUSUF MENDA, MD. . . . . . . . . . . . . . . . . . . . 85 CHAPTER 9 Patient-Centered Care: Communication Skills and Cultural Competence JOHN R. TONGUE, MD NORMAN Y. OTSUKA, MD . . . . . . . . . . . . . . 109 CHAPTER 10 Practice Management CRAIG R. MAHONEY, MD STEPHEN P. MAKK, MD, MBA . . . . . . . . . . . 121 CHAPTER 11 Polytrauma Care HANS-CHRISTOPH PAPE, MD, FACS PHILIPP LICHTE, MD. . . . . . . . . . . . . . . . . . . 129 CHAPTER 12 Coagulation, Thromboembolism, and Blood Management in Orthopaedic Surgery CHARLES R. CLARK, MD. . . . . . . . . . . . . . . . 137 CHAPTER 13 Work-Related Illness, Cumulative Trauma, and Compensation J. MARK MELHORN, MD, FAAOS, FAADEP, FACOEM, FACS JAMES B. TALMAGE, MD, FAADEP, FACOEM . . . . . . . . . . . . . . . . . . . . . . . 147 CHAPTER 14 Evidence-Based Orthopaedics: Levels of Evidence and Guidelines in Orthopaedic Surgery KANU OKIKE, MD, MPH MININDER S. KOCHER, MD, MPH . . . . . . . . 157 CHAPTER 15 Orthopaedic Research: Health Research Methodology BRAD A. PETRISOR, MSC, MD, FRCSC MOHIT BHANDARI, MD, MSC, FRCSC. .

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd

    Oku 10

    Uploaded by

    Melissa Villanueva
    4K views878 pages
    CHAPTER 1 Patient Safety and Risk Management DOUGLAS W. LUNDY, MD STUART L. WEINSTEIN, MD. . . . . . . . . . . . . . . . 3 CHAPTER 2 Fracture Repair and Bone Grafting CHUANYONG LU, MD ERIC MEINBERG, MD RALPH MARCUCIO, PHD THEODORE MICLAU, MD . . . . . . . . . . . . . . . . 11 CHAPTER 3 Articular Cartilage and Intervertebral Disk JAMES A. MARTIN, PHD PREM S. RAMAKRISHNAN, PHD TAE-HONG LIM, PHD DANIEL THEDENS, PHD JOSEPH A. BUCKWALTER, MS, MD. . . . . . . . . . 23 CHAPTER 4 Muscle, Tendon, and Ligament LAWRENCE V. GULOTTA, MD SCOTT A. RODEO, MD. . . . . . . . . . . . . . . . . . 37 CHAPTER 5 Wound Management JAN PAUL ERTL, MD JEFFREY ANGLEN, MD, FACS . . . . . . . . . . . . . 49 CHAPTER 6 Musculoskeletal Biomechanics MICHAEL BOTTLANG, PHD DANIEL C. FITZPATRICK, MS, MD PETER AUGAT, PHD . . . . . . . . . . . . . . . . . . . . 59 CHAPTER 7 Bearing Surface Materials for Hip, Knee, and Spinal Disk Replacement JAVAD PARVIZI, MD, FRCS MICHAEL BERCIK, MD TODD ALBERT, MD . . . . . . . . . . . . . . . . . . . . 73 CHAPTER 8 Musculoskeletal Imaging KENJIROU OHASHI, MD, PHD GEORGES Y. EL-KHOURY, MD YUSUF MENDA, MD. . . . . . . . . . . . . . . . . . . . 85 CHAPTER 9 Patient-Centered Care: Communication Skills and Cultural Competence JOHN R. TONGUE, MD NORMAN Y. OTSUKA, MD . . . . . . . . . . . . . . 109 CHAPTER 10 Practice Management CRAIG R. MAHONEY, MD STEPHEN P. MAKK, MD, MBA . . . . . . . . . . . 121 CHAPTER 11 Polytrauma Care HANS-CHRISTOPH PAPE, MD, FACS PHILIPP LICHTE, MD. . . . . . . . . . . . . . . . . . . 129 CHAPTER 12 Coagulation, Thromboembolism, and Blood Management in Orthopaedic Surgery CHARLES R. CLARK, MD. . . . . . . . . . . . . . . . 137 CHAPTER 13 Work-Related Illness, Cumulative Trauma, and Compensation J. MARK MELHORN, MD, FAAOS, FAADEP, FACOEM, FACS JAMES B. TALMAGE, MD, FAADEP, FACOEM . . . . . . . . . . . . . . . . . . . . . . . 147 CHAPTER 14 Evidence-Based Orthopaedics: Levels of Evidence and Guidelines in Orthopaedic Surgery KANU OKIKE, MD, MPH MININDER S. KOCHER, MD, MPH . . . . . . . . 157 CHAPTER 15 Orthopaedic Research: Health Research Methodology BRAD A. PETRISOR, MSC, MD, FRCSC MOHIT BHANDARI, MD, MSC, FRCSC. .

    Original Title

    OKU 10

    Copyright

    © © All Rights Reserved

    Available Formats

    PDF, TXT or read online from Scribd

    Did you find this document useful?

    Is this content inappropriate?

    CHAPTER 1 Patient Safety and Risk Management DOUGLAS W. LUNDY, MD STUART L. WEINSTEIN, MD. . . . . . . . . . . . . . . . 3 CHAPTER 2 Fracture Repair and Bone Grafting CHUANYONG LU, MD ERIC MEINBERG, MD RALPH MARCUCIO, PHD THEODORE MICLAU, MD . . . . . . . . . . . . . . . . 11 CHAPTER 3 Articular Cartilage and Intervertebral Disk JAMES A. MARTIN, PHD PREM S. RAMAKRISHNAN, PHD TAE-HONG LIM, PHD DANIEL THEDENS, PHD JOSEPH A. BUCKWALTER, MS, MD. . . . . . . . . . 23 CHAPTER 4 Muscle, Tendon, and Ligament LAWRENCE V. GULOTTA, MD SCOTT A. RODEO, MD. . . . . . . . . . . . . . . . . . 37 CHAPTER 5 Wound Management JAN PAUL ERTL, MD JEFFREY ANGLEN, MD, FACS . . . . . . . . . . . . . 49 CHAPTER 6 Musculoskeletal Biomechanics MICHAEL BOTTLANG, PHD DANIEL C. FITZPATRICK, MS, MD PETER AUGAT, PHD . . . . . . . . . . . . . . . . . . . . 59 CHAPTER 7 Bearing Surface Materials for Hip, Knee, and Spinal Disk Replacement JAVAD PARVIZI, MD, FRCS MICHAEL BERCIK, MD TODD ALBERT, MD . . . . . . . . . . . . . . . . . . . . 73 CHAPTER 8 Musculoskeletal Imaging KENJIROU OHASHI, MD, PHD GEORGES Y. EL-KHOURY, MD YUSUF MENDA, MD. . . . . . . . . . . . . . . . . . . . 85 CHAPTER 9 Patient-Centered Care: Communication Skills and Cultural Competence JOHN R. TONGUE, MD NORMAN Y. OTSUKA, MD . . . . . . . . . . . . . . 109 CHAPTER 10 Practice Management CRAIG R. MAHONEY, MD STEPHEN P. MAKK, MD, MBA . . . . . . . . . . . 121 CHAPTER 11 Polytrauma Care HANS-CHRISTOPH PAPE, MD, FACS PHILIPP LICHTE, MD. . . . . . . . . . . . . . . . . . . 129 CHAPTER 12 Coagulation, Thromboembolism, and Blood Management in Orthopaedic Surgery CHARLES R. CLARK, MD. . . . . . . . . . . . . . . . 137 CHAPTER 13 Work-Related Illness, Cumulative Trauma, and Compensation J. MARK MELHORN, MD, FAAOS, FAADEP, FACOEM, FACS JAMES B. TALMAGE, MD, FAADEP, FACOEM . . . . . . . . . . . . . . . . . . . . . . . 147 CHAPTER 14 Evidence-Based Orthopaedics: Levels of Evidence and Guidelines in Orthopaedic Surgery KANU OKIKE, MD, MPH MININDER S. KOCHER, MD, MPH . . . . . . . . 157 CHAPTER 15 Orthopaedic Research: Health Research Methodology BRAD A. PETRISOR, MSC, MD, FRCSC MOHIT BHANDARI, MD, MSC, FRCSC. .

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    4K views878 pages

    Oku 10

    Uploaded by

    Melissa Villanueva
    CHAPTER 1 Patient Safety and Risk Management DOUGLAS W. LUNDY, MD STUART L. WEINSTEIN, MD. . . . . . . . . . . . . . . . 3 CHAPTER 2 Fracture Repair and Bone Grafting CHUANYONG LU, MD ERIC MEINBERG, MD RALPH MARCUCIO, PHD THEODORE MICLAU, MD . . . . . . . . . . . . . . . . 11 CHAPTER 3 Articular Cartilage and Intervertebral Disk JAMES A. MARTIN, PHD PREM S. RAMAKRISHNAN, PHD TAE-HONG LIM, PHD DANIEL THEDENS, PHD JOSEPH A. BUCKWALTER, MS, MD. . . . . . . . . . 23 CHAPTER 4 Muscle, Tendon, and Ligament LAWRENCE V. GULOTTA, MD SCOTT A. RODEO, MD. . . . . . . . . . . . . . . . . . 37 CHAPTER 5 Wound Management JAN PAUL ERTL, MD JEFFREY ANGLEN, MD, FACS . . . . . . . . . . . . . 49 CHAPTER 6 Musculoskeletal Biomechanics MICHAEL BOTTLANG, PHD DANIEL C. FITZPATRICK, MS, MD PETER AUGAT, PHD . . . . . . . . . . . . . . . . . . . . 59 CHAPTER 7 Bearing Surface Materials for Hip, Knee, and Spinal Disk Replacement JAVAD PARVIZI, MD, FRCS MICHAEL BERCIK, MD TODD ALBERT, MD . . . . . . . . . . . . . . . . . . . . 73 CHAPTER 8 Musculoskeletal Imaging KENJIROU OHASHI, MD, PHD GEORGES Y. EL-KHOURY, MD YUSUF MENDA, MD. . . . . . . . . . . . . . . . . . . . 85 CHAPTER 9 Patient-Centered Care: Communication Skills and Cultural Competence JOHN R. TONGUE, MD NORMAN Y. OTSUKA, MD . . . . . . . . . . . . . . 109 CHAPTER 10 Practice Management CRAIG R. MAHONEY, MD STEPHEN P. MAKK, MD, MBA . . . . . . . . . . . 121 CHAPTER 11 Polytrauma Care HANS-CHRISTOPH PAPE, MD, FACS PHILIPP LICHTE, MD. . . . . . . . . . . . . . . . . . . 129 CHAPTER 12 Coagulation, Thromboembolism, and Blood Management in Orthopaedic Surgery CHARLES R. CLARK, MD. . . . . . . . . . . . . . . . 137 CHAPTER 13 Work-Related Illness, Cumulative Trauma, and Compensation J. MARK MELHORN, MD, FAAOS, FAADEP, FACOEM, FACS JAMES B. TALMAGE, MD, FAADEP, FACOEM . . . . . . . . . . . . . . . . . . . . . . . 147 CHAPTER 14 Evidence-Based Orthopaedics: Levels of Evidence and Guidelines in Orthopaedic Surgery KANU OKIKE, MD, MPH MININDER S. KOCHER, MD, MPH . . . . . . . . 157 CHAPTER 15 Orthopaedic Research: Health Research Methodology BRAD A. PETRISOR, MSC, MD, FRCSC MOHIT BHANDARI, MD, MSC, FRCSC. .

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    of 878

    Orthopaedic

    Knowledge
    Update

    OKU10_Frontmatter.indd 1

    1/11/2011 2:49:59 PM

    Orthopaedic

    Knowledge
    Update
    EDITOR:

    John M. Flynn, MD
    Associate Chief of Orthopaedics
    Childrens Hospital of Philadelphia
    Associate Professor of Orthopaedics
    University of Pennsylvania
    Philadelphia, Pennsylvania

    OKU10_Frontmatter.indd 3

    1/11/2011 2:50:05 PM

    AAOS Board of Directors, 2010-2011


    John J. Callaghan, MD
    President
    Daniel J. Berry, MD
    First Vice President
    John R. Tongue, MD
    Second Vice President
    Frederick M. Azar, MD
    Treasurer
    Joseph D. Zuckerman, MD
    Past President
    Jeffrey O. Anglen, MD
    Richard J. Barry, MD
    Kevin P. Black, MD
    M. Bradford Henley, MD, MBA
    Gregory A. Mencio, MD
    Michael L. Parks, MD
    Fred C. Redfern, MD
    David D. Teuscher, MD
    Paul Tornetta III, MD
    Daniel W. White, MD, LTC, MC
    G. Zachary Wilhoit, MS, MBA
    Karen L. Hackett, FACHE, CAE, (Ex-Officio)

    Staff
    Mark W. Wieting, Chief Education Officer
    Marilyn L. Fox, PhD, Director, Department of
    Publications

    The material presented in Orthopaedic Knowledge


    Update 10 has been made available by the American
    Academy of Orthopaedic Surgeons for educational
    purposes only. This material is not intended to present
    the only, or necessarily best, methods or procedures for
    the medical situations discussed, but rather is intended
    to represent an approach, view, statement, or opinion
    of the author(s) or producer(s), which may be helpful
    to others who face similar situations.
    Some drugs or medical devices demonstrated in Academy courses or described in Academy print or electronic
    publications have not been cleared by the Food and
    Drug Administration (FDA) or have been cleared for
    specific uses only. The FDA has stated that it is the
    responsibility of the physician to determine the FDA
    clearance status of each drug or device he or she wishes
    to use in clinical practice.
    Furthermore, any statements about commercial products are solely the opinion(s) of the author(s) and do
    not represent an Academy endorsement or evaluation
    of these products. These statements may not be used
    in advertising or for any commercial purpose.
    All rights reserved. No part of this publication may be
    reproduced, stored in a retrieval system, or transmitted,
    in any form, or by any means, electronic, mechanical,
    photocopying, recording, or otherwise, without prior
    written permission from the publisher.
    Published 2011 by the
    American Academy of Orthopaedic Surgeons
    6300 North River Road
    Rosemont, IL 60018

    Kathleen Anderson, Senior Editor

    Copyright 2011
    by the American Academy of Orthopaedic Surgeons

    Deborah Williams, Associate Senior Editor

    ISBN 978-0-89203-736-0

    Mary Steermann Bishop, Senior Manager,


    Production and Archives

    Printed in the USA

    Lisa Claxton Moore, Managing Editor

    Courtney Astle, Assistant Production Manager


    Susan Morritz Baim, Production Coordinator
    Suzanne OReilly, Graphic Designer
    Anne Raci, Database Coordinator
    Karen Danca, Permissions Coordinator
    Abram Fassler, Production Database Associate
    Charlie Baldwin, Page Production Assistant
    Hollie Benedik, Page Production Assistant
    Michelle Bruno, Publications Assistant
    Rachel Winokur, Publications Assistant

    iv

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 4

    Orthopaedic Knowledge Update 10

    1/11/2011 2:50:05 PM

    Acknowledgments
    Editorial Board, OKU 10
    John M. Flynn, MD
    Associate Chief of Orthopaedics
    Childrens Hospital of Philadelphia
    Associate Professor of Orthopaedics
    University of Pennsylvania
    Philadelphia, Pennsylvania
    Pedro Beredjiklian, MD
    Associate Professor
    Chief of Hand Surgery
    The Rothman Institute
    Jefferson Medical College
    Philadelphia, Pennsylvania
    Lisa K. Cannada, MD
    Associate Professor
    Orthopaedic Surgery
    Saint Louis University
    St. Louis, Missouri

    Kenneth J. Noonan, MD
    Associate Professor
    Pediatric Orthopaedics
    American Family Childrens Hospital
    Madison, Wisconsin
    R. Lor Randall, MD, FACS
    Professor of Orthopaedics
    Sarcoma Services
    Huntsman Cancer Institute
    Salt Lake City, Utah
    Jeffrey C. Wang, MD
    Professor, Department of Orthopaedic Surgery
    and Neurosurgery
    UCLA Spine Center
    UCLA School of Medicine
    Los Angeles, California

    John Lawrence Marsh, MD


    Professor, Carroll B. Larson Chair
    Orthopaedics and Rehabilitation
    The University of Iowa
    Iowa City, Iowa

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 5

    Orthopaedic Knowledge Update 10

    1/11/2011 2:50:05 PM

    Contributors
    JOSEPH A. ABBOUD, MD
    Clinical Assistant Professor of Orthopaedic
    Surgery
    University of Pennsylvania
    Philadelphia, Pennsylvania
    MICHAEL D. AIONA, MD
    Chief of Staff
    Shriners Hospital for Children
    Portland, Oregon
    TODD J. ALBERT, MD
    Richard H. Rothman Professor and Chair,
    Orthopaedics
    Professor of Neurosurgery
    Thomas Jefferson University Hospitals
    The Rothman Institute
    Philadelphia, Pennsylvania
    BENJAMIN A. ALMAN, MD, FRCSC
    A.J. Latner Professor and Chair of Orthopaedic
    Surgery
    Vice Chair Research, Department of
    Orthopaedic Surgery
    University of Toronto
    Head, Division of Orthopaedic Surgery
    Senior Scientist, Program in Developmental
    and Stem Cell Biology
    The Hospital for Sick Children
    Toronto, Ontario, Canada

    MICHAEL T. BENKE, MD
    Orthopaedic Surgery
    George Washington University Medical
    Faculty Associates
    Washington, DC
    MICHAEL J. BERCIK, MD
    Department of Orthopaedics
    Thomas Jefferson University
    Philadelphia, Pennsylvania
    JOSEPH BERNSTEIN, MD
    Department of Orthopedic Surgery
    University of Pennsylvania School of Medicine
    Philadelphia, Pennsylvania
    MOHIT BHANDARI, MD, MSC, FRCSC
    Assistant Professor
    Canada Research
    Department of Clinical Epidemiology and
    Biostatistics
    McMaster University
    Hamilton, Ontario, Canada

    JEFFREY ANGLEN, MD, FACS


    Professor and Chairman
    Department of Orthopaedics
    Indiana University
    Indianapolis, Indiana

    NITIN N. BHATIA, MD
    Chief, Spine Surgery
    Department of Orthopaedic Surgery
    University of California, Irvine
    Orange, California

    APRIL D. ARMSTRONG, BSC(PT), MD, MSC,


    FRCS(C)
    Associate Professor
    Milton S. Hershey Medical Center
    Penn State University
    Hershey, Pennsylvania

    N. DOUGLAS BOARDMAN III, MD


    Associate Professor of Orthopaedic Surgery
    Medical College of Virginia
    Virginia Commonwealth University
    Medical Center
    Richmond, Virginia

    PETER AUGAT, PHD


    Professor of Biomechanics
    Institute of Biomechanics
    Trauma Center Murnau
    Murnau, Germany

    MICHAEL BOTTLANG, PHD


    Director, Legacy Biomechanics Laboratory
    Legacy Clinical Research and Technology
    Center
    Portland, Oregon

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 7

    RAHUL BANERJEE, MD
    Assistant Professor
    Department of Orthopaedic Surgery
    University of Texas Southwestern
    Medical Center
    Dallas, Texas

    Orthopaedic Knowledge Update 10

    vii

    1/11/2011 2:50:05 PM

    RICHARD J. BRANSFORD, MD
    Assistant Professor
    Department of Orthopaedics and Sports
    Medicine
    Harborview Medical Center
    University of Washington
    Seattle, Washington
    JOSEPH A. BUCKWALTER, MS, MD
    Professor and Chair, Orthopaedics
    University of Iowa
    Iowa City, Iowa
    LAUREN M. BURKE, MD
    Orthopaedic Surgery
    George Washington State University Medical
    Faculty Associates
    Washington, DC
    JONATHAN E. BUZZELL, MD
    OrthoWest Orthopaedic and Sports Medicine
    Omaha, Nebraska
    MICHELLE S. CAIRD, MD
    Assistant Professor of Orthopaedic Surgery
    Department of Orthopaedic Surgery
    University of Michigan
    Ann Arbor, Michigan
    PABLO CASTAEDA, MD
    Pediatric Orthopedic Surgeon
    Shriners Hospital for Children
    Mexico City, Mexico
    JENS R. CHAPMAN, MD
    Professor and Acting Chair
    Director, Spine Services
    Hansjerg Wyss Endowed Chair
    Department of Orthopaedics and Sports
    Medicine
    Joint Professor of Neurological Surgery
    University of Washington
    Seattle, Washington
    NORMAN CHUTKAN, MD
    Professor and Chairman
    Department of Orthopaedic Surgery
    Medical College of Georgia
    Augusta, Georgia

    viii

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 8

    CHARLES R. CLARK, MD
    Dr. Michael Bonfiglio Professor of
    Orthopaedics and Rehabilitation
    Department of Orthopaedics and Rehabilitation
    University of Iowa Hospitals and Clinics
    Iowa City, Iowa
    BRETT D. CRIST, MD, FACS
    Assistant Professor
    Co-Director of Orthopaedic Trauma Service
    Orthopaedic Surgery
    University of Missouri
    Columbia, Missouri
    SCOTT D. DAFFNER, MD
    Assistant Professor
    Department of Orthopaedics
    West Virginia University School of Medicine
    Morgantown, West Virginia
    MICHAEL D. DAUBS, MD
    Assistant Professor
    Department of Orthopaedic Surgery
    University of Utah
    Salt Lake City, Utah
    MARK B. DEKUTOSKI, MD
    Associate Professor of Orthopedics
    Department of Orthopedic Surgery
    Mayo Clinic
    Rochester, Minnesota
    CRAIG J. DELLA VALLE, MD
    Associate Professor
    Director, Adult Reconstructive Fellowship
    Department of Orthopaedic Surgery
    Rush University Medical Center
    Chicago, Illinois
    DOUGLAS A. DENNIS, MD
    Adjunct Professor
    Department of Biomedical Engineering
    University of Tennessee
    Director, Rocky Mountain Musculoskeletal
    Research Laboratory
    Denver, Colorado
    MATTHEW B. DOBBS, MD
    Associate Professor
    Department of Orthopaedic Surgery
    Washington University School of Medicine
    St. Louis, Missouri

    Orthopaedic Knowledge Update 10

    1/11/2011 2:50:06 PM

    GEORGES Y. EL-KHOURY, MD
    Musculoskeletal Imaging
    Department of Radiology
    University of Iowa
    Iowa City, Iowa
    HOWARD R. EPPS, MD
    Partner, Fondren Orthopedic Group, LLC
    Texas Orthopedic Hospital
    Houston, Texas
    JAN PAUL ERTL, MD
    Assistant Professor
    Chief of Orthopaedic Surgery, Wishard Hospital
    Department of Orthopaedic Surgery
    Indiana University
    Indianapolis, Indiana
    DANIEL C. FITZPATRICK, MS, MD
    Slocum Center for Orthopedics and Sports
    Medicine
    Eugene, Oregon
    STEVEN L. FRICK, MD
    Pediatric Orthopaedic Surgeon
    Orthopaedic Residency Director
    Department of Orthopaedic Surgery
    Carolinas Medical Center/Levine Childrens
    Hospital
    Charlotte, North Carolina

    DAVID L. GLASER, MD
    Orthopaedics
    Penn Presbyterian Medical Center
    Philadelphia, Pennsylvania
    J. ERIC GORDON, MD
    Associate Professor
    Orthopaedic Surgery
    Washington University School of Medicine
    St. Louis, Missouri
    MATT GRAVES, MD
    Assistant Professor
    Division of Trauma
    Department of Orthopaedic Surgery and
    Rehabilitation
    University of Mississippi Medical Center
    Jackson, Mississippi
    LAWRENCE V. GULOTTA, MD
    Sports Medicine/Shoulder Service
    Hospital for Special Surgery
    New York, New York

    THEODORE J. GANLEY, MD
    Sports Medicine Director
    Department of Orthopaedics
    The Childrens Hospital of Philadelphia
    Philadelphia, Pennsylvania

    RANJAN GUPTA, MD
    Professor and Chair
    Orthopaedic Surgery
    University of California, Irvine
    Irvine, California

    MICHAEL J. GARDNER, MD
    Assistant Professor
    Department of Orthopaedic Surgery
    Washington University School of Medicine
    St. Louis, Missouri

    MATTHEW A. HALANSKI, MD
    Clinical Assistant Professor
    Department of Surgery and Pediatrics and
    Human Development
    Pediatric Orthopaedics
    Helen DeVos Childrens Hospital
    College of Human Medicine
    Michigan State University
    Grand Rapids, Michigan

    CHARLES L. GETZ, MD
    Assistant Professor
    Orthopaedic Surgery
    The Rothman Institute
    Thomas Jefferson Medical School
    Philadelphia, Pennsylvania

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 9

    ERIC GIZA, MD
    Assistant Professor of Orthopaedics
    Chief, Foot and Ankle Surgery
    Orthopaedics
    University of California, Davis
    Sacramento, California

    Orthopaedic Knowledge Update 10

    ix

    1/11/2011 2:50:06 PM

    DANIEL HEDEQUIST, MD
    Assistant Professor of Orthopedics
    Department of Orthopedics
    Childrens Hospital
    Harvard Medical School
    Boston, Massachusetts

    LEONID I. KATOLIK, MD, FAAOS


    Assistant Professor
    Department of Orthopaedic Surgery
    Attending Surgeon
    The Philadelphia Hand Center, PC
    Philadelphia, Pennsylvania

    SCOTT HELMERS, MD
    Staff, Orthopaedic Oncologist
    Orthopedic Surgery
    Naval Medical Center San Diego
    San Diego, California

    RAYMOND H. KIM, MD
    Adjunct Associate Professor of Bioengineering
    Department of Mechanical and Materials
    Engineering
    University of Denver
    Denver, Colorado

    JOS A. HERRERA-SOTO, MD
    Director of Orthopedic Research
    Assistant Director, Pediatric Fellowship
    Program
    Orlando Health Orthopedic Department
    Arnold Palmer Hospital
    Orlando, Florida
    WELLINGTON K. HSU, MD
    Assistant Professor
    Orthopaedic Surgery
    Northwestern University Feinberg School
    of Medicine
    Chicago, Illinois
    HENRY J. IWINSKI JR, MD
    Associate Professor of Orthopaedic Surgery
    Assistant Chief of Staff, Shriners Hospital
    University of Kentucky
    Lexington, Kentucky
    KEVIN B. JONES, MD
    Instructor
    Department of Orthopaedics
    University of Utah
    Salt Lake City, Utah
    SCOTT G. KAAR, MD
    Director of Sports Medicine and Shoulder
    Surgery
    Department of Orthopaedic Surgery
    Saint Louis University
    St. Louis, Missouri
    LEE KAPLAN, MD
    Chief, Division of Sports Medicine
    Associate Professor
    Orthopaedics
    University of Miami
    Miami, Florida

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 10

    MININDER S. KOCHER, MD, MPH


    Associate Director, Division of Sports Medicine
    Department of Orthopaedic Surgery
    Childrens Hospital Boston
    Associate Professor of Orthopaedic Surgery
    Harvard Medical School
    Boston, Massachusetts
    SCOTT H. KOZIN, MD
    Professor of Orthopaedic Surgery
    Attending Hand Surgeon
    Temple University School of Medicine
    Philadelphia, Pennsylvania
    SUMANT G. KRISHNAN, MD
    Director, Shoulder Fellowship
    Baylor University Medical Center
    Shoulder Service
    The Carrell Clinic
    Dallas, Texas
    BRIAN KWON, MD, PHD, FRCSC
    Assistant Professor
    Department of Orthopaedics
    University of British Columbia
    Vancouver, Canada
    DAWN M. LAPORTE, MD
    Associate Professor
    Department of Orthopaedic Surgery
    Johns Hopkins University School of Medicine
    Baltimore, Maryland
    ARABELLA I. LEET, MD
    Associate Professor
    Department of Orthopedics
    Johns Hopkins University
    Baltimore, Maryland

    Orthopaedic Knowledge Update 10

    1/11/2011 2:50:06 PM

    BRUCE A. LEVY, MD
    Assistant Professor
    Orthopedic Surgery and Sports Medicine
    Mayo Clinic
    Rochester, Minnesota
    PHILIPP LICHTE, MD
    Department of Orthopaedic Surgery
    University of Aachen Medical Center
    Aachen, Germany
    TAE-HONG LIM, PHD
    Professor
    Biomechanical Engineering
    University of Iowa
    Iowa City, Iowa
    FRANK A. LIPORACE, MD
    Assistant Professor
    Department of Orthopaedics, Trauma Division
    University of Medicine and Dentistry of
    New Jersey
    New Jersey Medical School
    Newark, New Jersey
    CHUANYONG LU, MD
    Assistant Researcher
    Orthopaedic Surgery
    University of California, San Francisco
    San Francisco, California
    DOUGLAS W. LUNDY, MD, FACS
    Orthopaedic Trauma Surgeon
    Chair, American Academy of Orthopaedic
    Surgeons Medical Liability Committee
    Resurgeons Orthopaedics
    Kennestone Hospital
    Atlanta, Georgia
    HUE H. LUU, MD
    Assistant Professor
    Associate Director, Molecular Oncology
    Laboratory
    Department of Surgery, Section of
    Orthopaedic Surgery
    The University of Chicago
    Chicago, Illinois

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 11

    CRAIG R. MAHONEY, MD
    Practice Management Committee, American
    Academy of Orthopaedic Surgeons
    Iowa Orthopaedic Center
    Mercy Medical Center
    Des Moines, Iowa
    STEPHEN P. MAKK, MD, MBA
    Orthopaedic Surgeon Partner
    Louisville Bone and Joint Specialists
    Louisville, Kentucky
    ARTHUR MANOLI II, MD
    Clinical Professor
    Orthopaedic Surgery
    Wayne State University
    Detroit, Michigan
    Michigan State University
    East Lansing, Michigan
    Michigan International Foot and Ankle Center
    Pontiac, Michigan
    RALPH MARCUCIO, PHD
    Assistant Professor
    Orthopaedic Surgery
    University of California, San Francisco
    San Francisco, California
    JAMES A. MARTIN, PHD
    Associate Research Professor
    Orthopaedics and Rehabilitation
    University of Iowa
    Iowa City, Iowa
    MICHAEL T. MAZUREK, MD
    Residency Program Director
    Orthopaedic Trauma
    Department of Orthopaedic Surgery
    Naval Medical Center San Diego
    San Diego, California
    JESSE A. MCCARRON, MD
    Associate Staff
    Section Head, Shoulder Section
    Department of Orthopaedics
    Cleveland Clinic
    Cleveland, Ohio

    Orthopaedic Knowledge Update 10

    xi

    1/11/2011 2:50:06 PM

    AMY L. MCINTOSH, MD
    Assistant Professor of Orthopedics
    Department of Orthopedic Surgery
    Mayo Clinic
    Rochester, Minnesota
    EDWARD J. MCPHERSON, MD, FACS
    Director
    Los Angeles Orthopaedic Institute
    Los Angeles, California
    ERIC MEINBERG, MD
    Assistant Professor
    Orthopaedic Surgery
    University of California, San Francisco
    San Francisco, California
    J. MARK MELHORN, MD
    Associate Clinical Professor
    University of Kansas School of Medicine,
    Wichita
    The Hand Center
    Wichita, Kansas
    YUSUF MENDA, MD
    Assistant Professor, Radiology
    University of Iowa
    Iowa City, Iowa

    BRIAN H. MULLIS, MD
    Chief, Orthopaedic Trauma
    Orthopaedic Surgery
    Indiana University School of Medicine
    Indianapolis, Indiana
    ANAND M. MURTHI, MD
    Assistant Professor
    Chief, Shoulder and Elbow Service
    Department of Orthopaedics
    University of Maryland School of Medicine
    Baltimore, Maryland

    THEODORE MICLAU, MD
    Professor
    Orthopaedic Surgery
    University of California, San Francisco
    San Francisco, California
    TODD MILBRANDT, MD, MS
    Assistant Professor
    Pediatric Orthopaedics
    University of Kentucky
    Lexington, Kentucky

    KENJIROU OHASHI, MD, PHD


    Musculoskeletal Imaging
    Department of Radiology
    University of Iowa
    Iowa City, Iowa

    JOSE A. MORCUENDE, MD, PHD


    Associate Professor
    Department of Orthopaedic Surgery and
    Rehabilitation
    University of Iowa
    Iowa City, Iowa

    KANU OKIKE, MD, MPH


    Department of Orthopaedic Surgery
    Massachusetts General Hospital
    Boston, Massachusetts

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 12

    THOMAS MROZ, MD
    Department of Orthopaedics
    Neurological Institute
    Cleveland Clinic
    Cleveland, Ohio

    JOSEPH R. OBRIEN, MD, MPH


    Assistant Professor of Orthopaedic Surgery and
    Neurosurgery
    Orthopaedic Surgery
    George Washington University Medical
    Faculty Associates
    Washington, DC

    SM JAVAD MORTAZAVI, MD
    Associate Professor
    Orthopedic Department
    Tehran University of Medical Sciences
    Tehran, Iran

    xii

    TAHSEEN MOZAFFAR, MD
    Associate Professor, Neurology and
    Orthopedic Surgery
    Director, University of California Irvine MDA
    ALS and Neuromuscular Center
    University of California, Irvine
    Irvine, California

    NORMAN Y. OTSUKA, MD
    Chief of Staff
    Clinical Professor, Orthopaedic Surgery
    Shriners Hospital for Children
    University of California, Los Angeles
    Los Angeles, California

    Orthopaedic Knowledge Update 10

    1/11/2011 2:50:06 PM

    HANS-CHRISTOPH PAPE, MD, FACS


    Professor
    Department of Orthopaedics
    University of Aachen Medical Center
    Aachen, Germany
    BRADFORD O. PARSONS, MD
    Assistant Professor
    Orthopaedics
    Mount Sinai
    New York, New York

    KARL E. RATHJEN, MD
    Associate Professor of Orthopaedic Surgery
    Texas Scottish Rite Hospital for Children
    Dallas, Texas

    JAVAD PARVIZI, MD, FRCS


    Professor of Orthopedic Surgery
    Orthopedic Surgery
    The Rothman Institute at Thomas Jefferson
    University
    Philadelphia, Pennsylvania

    JOHN M. RHEE, MD
    Assistant Professor
    Orthopaedic Surgery
    Emory Spine Center
    Emory University School of Medicine
    Atlanta, Georgia

    MATTHEW PEPE, MD
    Assistant Professor
    Department of Orthopaedic Surgery
    Thomas Jefferson University School of Medicine
    Philadelphia, Pennsylvania

    K. DANIEL RIEW, MD
    Mildred B. Simon Distinguished Professor
    Professor of Neurological Surgery
    Orthopaedic Surgery
    Washington University School of Medicine
    St. Louis, Missouri

    MARK D. PERRY, MD
    Professor
    Department of Orthopaedic Surgery
    University of South Alabama
    Mobile, Alabama
    CHRISTOPHER L. PETERS, MD
    Professor
    Chief of Adult Reconstruction
    Orthopaedic Department
    University of Utah
    Salt Lake City, Utah
    BRAD PETRISOR, MSC, MD, FRCSC
    Assistant Professor
    Division of Orthopaedic Surgery
    Department of Surgery
    McMaster University
    Hamilton, Canada
    PREM S. RAMAKRISHNAN, PHD
    Assistant Research Scientist
    Orthopaedics and Rehabilitation
    University of Iowa
    Iowa City, Iowa

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 13

    MATTHEW L. RAMSEY, MD
    Associate Professor of Orthopaedic Surgery
    Shoulder and Elbow Service
    Rothman Institute
    Thomas Jefferson University
    Philadelphia, Pennsylvania

    SCOTT A. RODEO, MD
    Co-Chief Sports Medicine
    Shoulder Service
    Hospital for Special Surgery
    New York, New York
    TAMARA D. ROZENTAL, MD
    Assistant Professor
    Orthopaedic Surgery
    Harvard Medical School
    Boston, Massachusetts
    HENRY CLAUDE SAGI, MD
    Director of Research and Fellowship Training
    Orthopaedic Trauma Service
    Tampa General Hospital
    Tampa, Florida
    KOICHI SAIRYO, MD, PHD
    Associate Professor
    Orthopedics
    University of Tokushima
    Tokushima, Japan

    Orthopaedic Knowledge Update 10

    xiii

    1/11/2011 2:50:06 PM

    TOSHINORI SAKAI, MD, PHD


    Assistant Professor
    Department of Orthopedics
    Institute of Health Biosciences
    The University of Tokushima Graduate School
    Tokushima, Japan
    ANTHONY SCADUTO, MD
    Charles LeRoy Lowman Professor
    University of California Los Angeles
    Department of Orthopaedic Surgery
    Los Angeles Orthopaedic Hospital
    Los Angeles, California
    KEVIN SHEA, MD
    Orthopaedic Surgeon
    St. Luke Childrens Hospital
    Boise, Idaho
    JODI SIEGEL, MD
    Assistant Professor
    University of Massachusetts
    Department of Orthopaedics
    University of Massachusetts Memorial
    Medical Center
    Worchester, Massachusetts
    RAFAEL J. SIERRA, MD
    Assistant Professor
    Consultant
    Orthopedic Surgery
    Mayo Clinic
    Rochester, Minnesota

    xiv

    VISHWAS R. TALWALKAR, MD
    Associate Professor
    Department of Orthopaedics
    University of Kentucky
    Shriners Hospital for Children
    Lexington, Kentucky
    VIRAK TAN, MD
    Associate Professor of Orthopaedics
    Department of Orthopaedics
    University of Medicine and Dentistry
    New Jersey
    New Jersey Medical School
    Newark, New Jersey
    DANIEL THEDENS, PHD
    Assistant Professor
    Radiology
    University of Iowa
    Iowa City, Iowa
    JOHN R. TONGUE, MD
    Clinical Assistant Professor
    Department of Orthopaedic Surgery
    Oregon Health Sciences University
    Portland, Oregon

    BRYAN D. SPRINGER, MD
    OrthoCarolina Hip and Knee Center
    Charlotte, North Carolina

    PAUL TORNETTA III, MD


    Professor and Vice Chairman
    Director of Orthopaedic Trauma
    Department of Orthopaedic Surgery
    Boston University Medical Center
    Boston, Massachusetts

    MICHAEL P. STEINMETZ, MD
    Assistant Professor
    Center for Spine Health
    Cleveland Clinic
    Cleveland, Ohio

    JONATHAN TUTTLE, MD
    Assistant Professor
    Department of Neurosurgery
    Medical College of Georgia
    Atlanta, Georgia

    MICHAEL J. STUART, MD
    Professor and Vice-Chairman
    Department of Orthopedic Surgery
    Mayo Clinic
    Rochester, Minnesota

    J. MICHAEL WATTENBARGER, MD
    Chief, Pediatric Orthopedics
    Carolinas Medical Center
    OrthoCarolina
    Charlotte, North Carolina

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 14

    JAMES B. TALMAGE, MD
    Occupational Health Center
    Cookeville, Tennessee

    Orthopaedic Knowledge Update 10

    1/11/2011 2:50:06 PM

    SHARON M. WEINSTEIN, MD, FAAHPM


    Professor of Anesthesiology
    Adjunct Associate Professor of Neurology and
    Internal Medicine (Oncology)
    Department of Anesthesiology
    University of Utah Huntsman Cancer Institute
    Salt Lake City, Utah

    WARREN D. YU, MD
    Associate Professor of Orthopaedic Surgery
    and Neurosurgery
    Orthopaedic Surgery
    George Washington University Medical
    Faculty Services
    Washington, DC

    STUART L. WEINSTEIN, MD
    Ignacio V. Ponseti Chair and Professor of
    Orthopaedic Surgery
    University of Iowa
    Iowa City, Iowa

    IRA ZALTZ, MD
    Department of Orthopaedic Surgery
    William Beaumont Hospital
    Royal Oak, Michigan

    BRAD J. YOO, MD
    Assistant Professor
    Department of Orthopaedics
    University of California, Davis
    Sacramento, California

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 15

    DAN A. ZLOTOLOW, MD
    Attending Physician
    Shriners Hospital of Philadelphia
    Philadelphia, Pennsylvania

    Orthopaedic Knowledge Update 10

    xv

    1/11/2011 2:50:06 PM

    Peer Reviewers
    DONALD D. ANDERSON, PHD
    Associate Professor
    Department of Orthopaedics and
    Rehabilitation
    The University of Iowa
    Iowa City, Iowa
    JEFFREY ANGLEN, MD, FACS
    Professor and Chairman
    Department of Orthopaedics
    Indiana University
    Indianapolis, Indiana
    JOSEPH S. BARR JR, MD
    Visiting Orthopaedic Surgeon
    Orthopaedic Department
    Massachusetts General Hospital
    Boston, Massachusetts
    ROBERT BARRACK, MD
    Charles F. and Joanne Knight
    Distinguished Professor
    Department of Orthopaedic Surgery
    Washington University School of Medicine
    St. Louis, Missouri
    SIGURD H. BERVEN, MD
    Associate Professor in Residence
    Department of Orthopaedic Surgery
    University of California, San Francisco
    San Francisco, California
    MATHIAS BOSTROM, MD
    Professor of Orthopaedic Surgery
    Hospital for Special Surgery
    New York, New York
    RICHARD BUCKLEY, MD, FRCSC
    Head of Orthopaedic Trauma
    Department of Surgery
    University of Calgary
    Calgary, Canada
    DENIS R. CLOHISY, MD
    Professor and Chairman
    Department of Orthopedic Surgery
    University of Minnesota
    Minneapolis, Minnesota

    xvi

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 16

    JUDD E. CUMMINGS, MD
    Assistant Professor
    Department of Orthopedic Surgery
    Indiana University School of Medicine
    Indianapolis, Indiana
    DARRYL DLIMA, MD, PHD
    Director, Musculoskeletal Research
    Orthopaedics
    Scripps Health
    La Jolla, California
    STEVEN E. FISHER, MBA
    Manager, Practice Management Group
    Electronic Media, Evaluation Programs, Course
    Operations and Practice Management
    American Academy of Orthopaedic Surgeons
    Rosemont, Illinois
    CY FRANK, MD, FRCSC
    Professor
    Department of Surgery
    University of Calgary
    Calgary, Alberta, Canada
    MURRAY J. GOODMAN, MD
    Clinical Instructor in Orthopaedic Surgery
    Salem Orthopedic Surgeons Inc.
    Harvard Medical School
    Boston, Massachusetts
    BANG H. HOANG, MD
    Assistant Professor
    Orthopaedic Surgery
    Univeristy of California, Irvine Medical Center
    Orange, California
    RAMON L. JIMENEZ, MD
    Senior Consultant
    Monterey Orthopaedic and Sports Medicine
    Institute
    Monterey, California
    WENDY LEVINSON, MD
    Sir John and Lady Eaton Professor and Chair
    Department of Medicine
    University of Toronto
    Toronto, Ontario, Canada

    Orthopaedic Knowledge Update 10

    1/11/2011 2:50:07 PM

    DOUGLAS W. MARTIN, MD, FAADEP,


    FACOEM, FAAFP
    Medical Director
    Center for Occupational Health Excellence
    St. Lukes Regional Medical Center
    Sioux City, Iowa
    ROBERT G. MARX, MD
    Professor of Orthopaedic Surgery
    Hospital for Special Surgery
    New York, New York
    TIMOTHY E. MOORE, MD
    Professor
    Radiology
    University of Nebraska Medical Center
    Omaha, Nebraska
    ROBERT NAMBA, MD
    Attending Surgeon
    Department of Orthopedics
    Kaiser Permanente
    Irvine, California
    ANDREW T. PAVIA, MD
    George and Esther Gross Presidential Professor
    Department of Pediatrics
    University of Utah
    Salt Lake City, Utah
    MICHAEL D. RIES, MD
    Professor and Chief of Arthroplasty
    Department of Orthopaedic Surgery
    University of California, San Francisco
    San Francisco, California

    DAVID D. TEUSCHER, MD
    Beaumont Bone and Joint Institute
    Beaumont, Texas
    PAUL TORNETTA III, MD
    Professor and Vice Chairman
    Director of Orthopaedic Trauma
    Department of Orthopaedic Surgery
    Boston University Medical Center
    Boston, Massachusetts
    ALEXANDER R. VACCARO, MD, PHD
    Everrett J. and Marion Gordon Professor of
    Orthopaedic Surgery
    Orthopaedic Surgery
    The Rothman Institute
    Jefferson Medical College
    Philadelphia, Pennsylvania
    DAVID VOLGAS, MD
    Associate Professor
    Department of Orthopaedic Surgery
    University of Missouri
    Columbia, Missouri
    CRAIG WALKER, MD, FACR
    Professor and Chairman
    Howard B. Hunt Centennial Chair
    Radiology Department
    University of Nebraska Medical Center
    Omaha, Nebraska
    KEVIN WARD, MD
    Chief Executive Officer
    Iowa Ortho
    Des Moines, Iowa

    EMIL H. SCHEMITSCH, MD
    Professor of Surgery
    St. Michaels Hospital
    University of Toronto
    Toronto, Ontario, Canada

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 17

    Orthopaedic Knowledge Update 10

    xvii

    1/11/2011 2:50:07 PM

    Preface
    We orthopaedic surgeons face a challenging
    conundrum: we are driven to subspecialize
    because of rapid technologic advances and
    patients seeking very specific expertise, yet we
    must remain knowledgeable across the full
    spectrum of orthopaedics in order to deliver
    optimum patient care and pass certifying and
    recertifying examinations. We have many
    ways to learn: courses, textbooks, journals,
    weekly conferencesand now Webinars
    and Web-based surgical videos. Yet with
    all these different and evolving continuing
    education options, there remains a clear
    need for a single, rigorously peer-reviewed
    compendium of our entire specialtya source
    that is comprehensive yet succinct, current yet
    founded on prior knowledge. For more than
    20 years, the Orthopaedic Knowledge Update
    series has filled this role with great success.
    The writers, section editors, and I are very
    proud to bring you OKU 10. In many ways,
    this volume builds on and improves the
    outstanding previous editions. The Principles
    of Orthopaedics and Systemic Disorders
    sections give the reader a basic science and
    medical foundation, as well as synopsis
    chapters on essential issues of our practice:
    patient safety, communication skills, evidencebased medicine, and practice management.
    The remaining sections--Upper Extremity,
    Lower Extremity, Spine, and Pediatrics-cover the injuries and conditions we treat,
    each with numerically cited references and an
    annotated reference list. One new addition:
    we have incorporated the AAOS Clinical
    Practice Guidelines wherever appropriate. In
    total, OKU 10 delivers the most up-to-date,
    concise summary of the standard of care for
    orthopaedics.

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 19

    To whom much is given, much will be


    expected: we have all benefitted from many
    great surgeon-educators who trained us, and
    many clinical and basic science researchers
    who work to answer questions and advance
    our field. In the spirit of giving back, OKU
    10 represents the culmination of an enormous
    volunteer effort of over 2 years. More than
    100 of your colleagues have given selflessly of
    their time and talent to create this outstanding
    reference. Many of us remember reading our
    OKU in training until the pages were falling
    out. OKU 10 is our chance to give back, and
    perhaps inspire a future editor, perhaps of
    OKU 15?
    During the process of creating OKU 10, one
    of our authors, Michael Mazurek, was killed
    in a tragic accident. We would like to dedicate
    this work in his memory. I would like to
    thank the incredible group of section editors
    and the members of the AAOS publications
    department, specifically, Marilyn Fox, PhD,
    director, and Lisa Claxton Moore, managing
    editor, who did the lions share of the work.
    I also want to thank my wife Mary, who
    tolerates my academic orthopaedic hobbies.
    Finally, I want to thank my children Erin,
    Colleen, John, and Kelly. Now I appreciate
    them more: they have lots of homework at
    night, and with OKU 10, so did I.
    John M. (Jack) Flynn, MD
    Editor

    Orthopaedic Knowledge Update 10

    xix

    1/11/2011 2:50:07 PM

    Table of Contents
    Section 1: Principles of Orthopaedics
    SECTION EDITOR:
    JOHN LAWRENCE MARSH, MD
    CHAPTER 1

    Patient Safety and Risk Management


    DOUGLAS W. LUNDY, MD
    STUART L. WEINSTEIN, MD. . . . . . . . . . . . . . . . 3
    CHAPTER 2

    Fracture Repair and Bone Grafting


    CHUANYONG LU, MD
    ERIC MEINBERG, MD
    RALPH MARCUCIO, PHD
    THEODORE MICLAU, MD . . . . . . . . . . . . . . . . 11
    CHAPTER 3

    Articular Cartilage and Intervertebral Disk


    JAMES A. MARTIN, PHD
    PREM S. RAMAKRISHNAN, PHD
    TAE-HONG LIM, PHD
    DANIEL THEDENS, PHD
    JOSEPH A. BUCKWALTER, MS, MD. . . . . . . . . . 23

    CHAPTER 8

    Musculoskeletal Imaging
    KENJIROU OHASHI, MD, PHD
    GEORGES Y. EL-KHOURY, MD
    YUSUF MENDA, MD . . . . . . . . . . . . . . . . . . . . 85
    CHAPTER 9

    Patient-Centered Care: Communication


    Skills and Cultural Competence
    JOHN R. TONGUE, MD
    NORMAN Y. OTSUKA, MD . . . . . . . . . . . . . . 109
    CHAPTER 10

    Practice Management
    CRAIG R. MAHONEY, MD
    STEPHEN P. MAKK, MD, MBA . . . . . . . . . . . 121
    CHAPTER 11

    Polytrauma Care
    HANS-CHRISTOPH PAPE, MD, FACS
    PHILIPP LICHTE, MD . . . . . . . . . . . . . . . . . . . 129
    CHAPTER 12

    CHAPTER 4

    Muscle, Tendon, and Ligament


    LAWRENCE V. GULOTTA, MD
    SCOTT A. RODEO, MD . . . . . . . . . . . . . . . . . . 37
    CHAPTER 5

    Wound Management
    JAN PAUL ERTL, MD
    JEFFREY ANGLEN, MD, FACS . . . . . . . . . . . . . 49
    CHAPTER 6

    Musculoskeletal Biomechanics
    MICHAEL BOTTLANG, PHD
    DANIEL C. FITZPATRICK, MS, MD
    PETER AUGAT, PHD . . . . . . . . . . . . . . . . . . . . 59
    CHAPTER 7

    Bearing Surface Materials for Hip, Knee,


    and Spinal Disk Replacement
    JAVAD PARVIZI, MD, FRCS
    MICHAEL BERCIK, MD
    TODD ALBERT, MD . . . . . . . . . . . . . . . . . . . . 73

    Coagulation, Thromboembolism, and


    Blood Management in Orthopaedic
    Surgery
    CHARLES R. CLARK, MD. . . . . . . . . . . . . . . . 137
    CHAPTER 13

    Work-Related Illness, Cumulative Trauma,


    and Compensation
    J. MARK MELHORN, MD, FAAOS,
    FAADEP, FACOEM, FACS
    JAMES B. TALMAGE, MD, FAADEP,
    FACOEM . . . . . . . . . . . . . . . . . . . . . . . 147
    CHAPTER 14

    Evidence-Based Orthopaedics: Levels of


    Evidence and Guidelines in Orthopaedic
    Surgery
    KANU OKIKE, MD, MPH
    MININDER S. KOCHER, MD, MPH . . . . . . . . 157
    CHAPTER 15

    Orthopaedic Research: Health Research


    Methodology
    BRAD A. PETRISOR, MSC, MD, FRCSC
    MOHIT BHANDARI, MD, MSC, FRCSC. . . . . 167

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 21

    Orthopaedic Knowledge Update 10

    xxi

    1/11/2011 2:50:07 PM

    Section 2: Systemic Disorders

    Section 3: Upper Extremity

    SECTION EDITOR:
    R. LOR RANDALL, MD

    SECTION EDITOR:
    PEDRO BEREDJIKLIAN, MD

    CHAPTER 16

    CHAPTER 22

    Bone Metabolism and Metabolic


    Bone Disease

    Shoulder Trauma: Bone

    HUE H. LUU, MD . . . . . . . . . . . . . . . . . . . . 181

    JOSEPH A. ABBOUD, MD
    N. DOUGLAS BOARDMAN III, MD . . . . . . . . . 271

    CHAPTER 17

    CHAPTER 23

    Musculoskeletal Oncology
    KEVIN B. JONES, MD . . . . . . . . . . . . . . . . . . 193
    CHAPTER 18

    Arthritis
    SM JAVAD MORTAZAVI, MD
    JAVAD PARVIZI, MD, FRCS . . . . . . . . . . . . . . 213
    CHAPTER 19

    Disorders of the Nervous System


    TAHSEEN MOZAFFAR, MD
    RANJAN GUPTA, MD . . . . . . . . . . . . . . . . . . 225
    CHAPTER 20

    Musculoskeletal Infection
    EDWARD J. MCPHERSON, MD, FACS
    CHRISTOPHER L. PETERS, MD . . . . . . . . . . . . 239
    CHAPTER 21

    Pain Management
    SHARON M. WEINSTEIN, MD, FAAHPM . . . 259

    Shoulder Reconstruction
    ANAND M. MURTHI, MD
    JESSE A. MCCARRON, MD . . . . . . . . . . . . . . 285
    CHAPTER 24

    Shoulder Instability and Rotator


    Cuff Tears
    CHARLES L. GETZ, MD
    JONATHAN E. BUZZELL, MD
    SUMANT G. KRISHNAN, MD . . . . . . . . . . . . . 299
    CHAPTER 25

    Shoulder and Elbow Disorders in the


    Athlete
    JOSEPH BERNSTEIN, MD
    MATTHEW PEPE, MD
    LEE KAPLAN, MD . . . . . . . . . . . . . . . . . . . . 315
    CHAPTER 26

    Elbow and Forearm Trauma


    DAVID L. GLASER, MD
    APRIL D. ARMSTRONG, MD . . . . . . . . . . . . . 325
    CHAPTER 27

    Elbow Instability and Reconstruction


    BRADFORD O. PARSONS, MD
    MATTHEW L. RAMSEY, MD . . . . . . . . . . . . . 343
    CHAPTER 28

    Hand and Wrist Trauma


    VIRAK TAN, MD
    LEONID I. KATOLIK, MD . . . . . . . . . . . . . . . . 351
    CHAPTER 29

    Hand and Wrist Reconstruction


    TAMARA D. ROZENTAL, MD
    DAWN M. LAPORTE, MD . . . . . . . . . . . . . . . 363

    xxii

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 22

    Orthopaedic Knowledge Update 10

    1/11/2011 2:50:07 PM

    Section 4: Lower Extremity

    CHAPTER 38

    SECTION EDITOR:
    LISA K. CANNADA, MD

    MATT GRAVES, MD . . . . . . . . . . . . . . . . . . . 493

    CHAPTER 30

    Fractures of the Pelvis and Acetabulum


    HENRY CLAUDE SAGI, MD
    FRANK LIPORACE, MD . . . . . . . . . . . . . . . . . 379
    CHAPTER 31

    Hip Trauma
    BRIAN H. MULLIS, MD
    JEFFREY ANGLEN, MD, FACS . . . . . . . . . . . . 399
    CHAPTER 32

    Hip and Pelvic Reconstruction and


    Arthroplasty
    RAFAEL J. SIERRA, MD
    CRAIG J. DELLA VALLE, MD . . . . . . . . . . . . . 413

    Ankle Fractures

    CHAPTER 39

    Foot Trauma
    BRAD J. YOO, MD
    ERIC GIZA, MD . . . . . . . . . . . . . . . . . . . . . . 507
    CHAPTER 40

    Foot and Ankle Reconstruction


    MARK D. PERRY, MD
    ARTHUR MANOLI II, MD . . . . . . . . . . . . . . . 523
    CHAPTER 41

    Lower Extremity Amputations


    MICHAEL T. MAZUREK, MD
    SCOTT HELMERS, MD. . . . . . . . . . . . . . . . . . 537

    Section 5: Spine
    CHAPTER 33

    Femoral Fractures
    JODI SIEGEL, MD
    PAUL TORNETTA III, MD . . . . . . . . . . . . . . . 431

    SECTION EDITOR:
    JEFFREY C. WANG, MD
    CHAPTER 42

    CHAPTER 34

    Fractures About the Knee

    Spinal Tumors
    SCOTT D. DAFFNER, MD . . . . . . . . . . . . . . . 553

    MICHAEL J. GARDNER, MD. . . . . . . . . . . . . . 443


    CHAPTER 43
    CHAPTER 35

    Soft-Tissue Injuries About the Knee


    SCOTT G. KAAR, MD
    MICHAEL J. STUART, MD
    BRUCE A. LEVY, MD . . . . . . . . . . . . . . . . . . 453

    Spinal Infections
    THOMAS E. MROZ, MD
    MICHAEL P. STEINMETZ, MD. . . . . . . . . . . . . 565
    CHAPTER 44

    Spinal Cord Injury


    CHAPTER 36

    BRIAN K. KWON, MD, PHD, FRCSC . . . . . . 573

    Knee Reconstruction and Replacement


    RAYMOND H. KIM, MD
    BRYAN D. SPRINGER, MD
    DOUGLAS A. DENNIS, MD. . . . . . . . . . . . . . . 469

    CHAPTER 45

    CHAPTER 37

    CHAPTER 46

    Tibial Shaft Fractures


    BRETT D. CRIST, MD
    RAHUL BANERJEE, MD . . . . . . . . . . . . . . . . . 479

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 23

    Adult Spinal Deformity


    MICHAEL D. DAUBS, MD . . . . . . . . . . . . . . . 585

    Lumbar Degenerative Disease


    WELLINGTON K. HSU, MD . . . . . . . . . . . . . . 599

    Orthopaedic Knowledge Update 10

    xxiii

    1/11/2011 2:50:07 PM

    CHAPTER 47

    Cervical Degenerative Disease


    JOHN M. RHEE, MD
    K. DANIEL RIEW, MD. . . . . . . . . . . . . . . . . . 611
    CHAPTER 48

    Cervical Spine Trauma


    JENS R. CHAPMAN, MD
    RICHARD J. BRANSFORD, MD . . . . . . . . . . . . 623
    CHAPTER 49

    Thoracolumbar Trauma
    NORMAL CHUTKAN, MD
    JONATHAN TUTTLE, MD. . . . . . . . . . . . . . . . 641
    CHAPTER 50

    Section 6: Pediatrics
    SECTION EDITOR:
    KENNETH J. NOONAN, MD
    CHAPTER 53

    Shoulder, Upper Arm, and Elbow Trauma:


    Pediatrics
    J. MICHAEL WATTENBARGER, MD
    STEVEN L. FRICK, MD . . . . . . . . . . . . . . . . . 675
    CHAPTER 54

    Forearm, Wrist, and Hand Trauma:


    Pediatrics
    HOWARD R. EPPS, MD
    MICHELLE S. CAIRD, MD . . . . . . . . . . . . . . . 687

    Lumbar Spondylolisthesis

    CHAPTER 55

    TOSHINORI SAKAI, MD, PHD


    KOICHI SAIRYO, MD, PHD
    NITIN N. BHATIA, MD . . . . . . . . . . . . . . . . . 651

    DAN A. ZLOTOLOW, MD
    SCOTT H. KOZIN, MD . . . . . . . . . . . . . . . . . 697

    CHAPTER 51

    CHAPTER 56

    Thoracic Disk Herniation

    Spine Trauma and Disorders: Pediatrics

    MARK B. DEKUTOSKI, MD . . . . . . . . . . . . . . 661

    ANTHONY SCADUTO, MD
    DANIEL HEDEQUIST, MD. . . . . . . . . . . . . . . . 715

    Upper Extremity Disorders: Pediatrics

    CHAPTER 52

    New Technologies in Spine Surgery


    LAUREN M. BURKE, MD, MPH
    JOSEPH R. OBRIEN, MD, MPH
    MICHAEL T. BENKE, MD
    WARREN D. YU, MD . . . . . . . . . . . . . . . . . . 665

    CHAPTER 57

    Pelvis, Hip, and Femur Trauma: Pediatrics


    AMY L. MCINTOSH, MD
    KARL E. RATHJEN, MD. . . . . . . . . . . . . . . . . 727
    CHAPTER 58

    Hip, Pelvis, and Femur Disorders:


    Pediatrics
    PABLO CASTAEDA, MD
    IRA ZALTZ, MD . . . . . . . . . . . . . . . . . . . . . . 739
    CHAPTER 59

    Knee, Leg, Ankle, and Foot Trauma:


    Pediatrics
    MATTHEW A. HALANSKI, MD
    JOS A. HERRERA-SOTO, MD . . . . . . . . . . . . 753

    xxiv

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 24

    Orthopaedic Knowledge Update 10

    1/11/2011 2:50:07 PM

    CHAPTER 60

    Lower Extremity and Foot Disorders:


    Pediatrics
    J. ERIC GORDON, MD
    MATTHEW B. DOBBS, MD . . . . . . . . . . . . . . 763
    CHAPTER 61

    Injuries and Conditions of the Pediatric


    and Adolescent Athlete
    KEVIN SHEA, MD
    THEODORE J. GANLEY, MD. . . . . . . . . . . . . . 783
    CHAPTER 62

    Skeletal Dysplasias, Connective Tissue


    Diseases, and Other Genetic Disorders
    JOSE A. MORCUENDE, MD, PHD
    BENJAMIN A. ALMAN, MD . . . . . . . . . . . . . . 797
    CHAPTER 63

    Neuromuscular Disorders in Children


    MICHAEL D. AIONA, MD
    ARABELLA I. LEET, MD. . . . . . . . . . . . . . . . . 811
    CHAPTER 64

    Pediatric Tumors and Hematologic


    Diseases
    TODD MILBRANDT, MD, MS
    HENRY J. IWINSKI JR, MD
    VISHWAS R. TALWALKAR, MD . . . . . . . . . . . . 825

    INDEX . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 837

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Frontmatter.indd 25

    Orthopaedic Knowledge Update 10

    xxv

    1/11/2011 2:50:08 PM

    Chapter 1

    Patient Safety and Risk


    Management
    Douglas W. Lundy, MD

    Stuart L. Weinstein, MD

    Overview and Joint Commission Initiatives


    Patients come to orthopaedic surgeons for evaluation
    and treatment of their musculoskeletal conditions believing that they will hold to the Hippocratic mandate
    of primum non nocere that is, first, do no harm. As
    a leader on the health care team, the orthopaedic surgeon should partner with others to ensure that the patients safety and best interests are held paramount.
    Many times, however, a more appropriate principle is
    primum succurrere that is, first, hasten to help.
    Some interventions in emergency orthopaedics may
    cause potential harm to the patient, but the physician
    should still perform certain potentially hazardous procedures to save life and limb. Nonetheless, the patients
    interests are of the utmost concern, and the risks of the
    treatment should be managed while providing timely
    and appropriate care.
    In 2009, The Joint Commission introduced its latest
    Standards Improvement Initiatives.1 Initiatives that are
    of specific interest to orthopaedic surgeons include: (1)
    Improved accuracy of patient identification this includes the use of two patient identifiers. (2) Improved
    communication between providers this includes read
    back of orders, eliminating improper abbreviations,
    and improved handoff of patients. (3) Reducing the
    risk of health careassociated infections this includes
    preventing multiple drugresistant organisms and preventing surgical site infections. (4) Reconciling medications across the continuum of care. (5) Reducing the
    risk of falls. (6) Reducing the risk of surgical fires.
    There are also three universal protocols from The
    Joint Commission that are germane to the orthopaedic
    surgeon: conducting a preprocedure verification process, marking the procedure site, and instituting a timeout.

    Dr. Lundy serves as the Chair of the Medical Liability


    Committee of the American Academy of Orthopaedic
    Surgeons. Neither Dr. Weinstein nor an immediate family member has received anything of value from or owns
    stock in a commercial company or institution related directly or indirectly to the subject of this chapter.

    2011 American Academy of Orthopaedic Surgeons

    Time-Out in the Operating Room

    1: Principles of Orthopaedics

    Patient Safety

    The purpose of the time-out is to perform a final assessment to ensure that the appropriate patient, site, procedure, position, equipment, and documentation are verified before the surgical procedure is initiated. The
    time-out is initiated by a designated member of the
    team, and this person does not necessarily need to be
    the surgeon. All members of the team must participate
    in the time-out, and all issues and questions need to be
    resolved before beginning the procedure.2 The time-out
    needs to be done in a fail-safe mode that is, no incision is made until the time-out is successfully completed. When used appropriately, the preincision timeout should eliminate wrong-site surgery in many
    instances.

    Wrong-Site Surgery
    Wrong-site surgery is a regrettable event that is of significant concern to the orthopaedic surgeon because so
    many of the procedures can be performed on either side
    of the body. Although this error appears negligent to
    the public, the inherent possibility of this happening to
    anyone at any time is clear to many conscientious orthopaedic surgeons. A retrospective closed claims study
    demonstrated that negligence cases involving wrongsite surgery resulted in an 84% rate of payment compared with a 30% rate of payment for other claims of
    medical negligence.3
    In 1998, the American Academy of Orthopaedic Surgeons (AAOS) launched the Sign Your Site program.
    Since the programs inception, preoperative marking of
    the surgical site has become an essential aspect of the orthopaedic surgeons surgical routine.3 The Joint Commission Universal Protocol2 has mandated several elements
    in preoperative site marking as outlined in Table 1.
    The AAOS has made several recommendations to orthopaedic surgeons if they find that they have started a
    procedure at the wrong site.3 The surgeon should attempt to restore the incorrectly operated site to its previous condition if at all possible. If the patients condition will allow, the surgeon should then perform the
    consented procedure at the correct site. The surgeon
    should communicate with the patient and the patients
    family (if appropriate) the occurrence of the wrong-site
    surgery and the consequences that may occur as a re-

    Orthopaedic Knowledge Update 10

    Section 1: Principles of Orthopaedics

    Table 1

    tions, and limitations as well as when and how to contact the physician in case there is a problem.

    Preoperative Site Marking According to Joint


    Commission Universal Protocol

    Communication (Handoff of Patients)

    1. The site needs to be marked specifically in regard to


    laterality (left/right), level (spine), surface (volar/dorsal),
    digit (hand/foot), and the specific lesion if there is more
    than one.
    2. The surgeon must mark the area before the patient enters
    the operating room, and the patient should be awake and
    alert if possible.

    1: Principles of Orthopaedics

    3. The person marking the site must be an individual


    licensed practitioner who is privileged by the hospital to
    perform that specific procedure. The person marking the
    patient must be involved and present during the
    procedure.
    4. The method of marking cannot be ambiguous and must
    be used throughout the hospital.
    5. The mark must be made at or near the incision site, and
    the preferred method is that the practitioner marks the
    site with his or her initials.
    6. The mark must be visible after prepping and draping.
    Stick-on markers are not sufficient.
    7. When operating on the spine, special intraoperative
    radiographic techniques are also used to ensure the
    correct site.

    sult of the error. The surgeon should proceed as the patient wishes after communicating this information. If
    the wrong-site surgical error is discovered after the procedure is completed, the surgeon should immediately
    disclose the error to the patient and the patients family
    (if appropriate) and determine an appropriate plan to
    rectify the situation.

    Safety Checklists
    Safety checklists are used throughout the patient care
    environment to improve outcomes and patient well being. When used consistently, these checklists will ensure
    that vital aspects of the patients care are not accidentally overlooked. When these checklists are used in the
    preoperative setting, there is less chance that appropriate laboratory tests, patient risk factors, and previous
    anesthetic complications will be overlooked, and it will
    be more likely that necessary special instrumentation or
    implants will be available. The surgical time-out is a
    form of checklist in that the site and side of the procedure are verified, and the presence of preoperative antibiotics and appropriate implants, radiographs, and
    documents is confirmed. Postoperative checklists can
    also be helpful, along with standardized postoperative
    orders and pathways. These documents can decrease
    the incidence of forgotten postoperative antibiotics or
    thromboembolic prophylaxis. The use of electronic
    medical records may also facilitate the use of checklists.
    Discharge checklists can ensure that the patient is given
    appropriate follow-up information, discharge prescrip4

    Orthopaedic Knowledge Update 10

    Breakdown in communication is unfortunately a significant potential cause of suboptimal patient care. Orthopaedic surgeons must ensure that appropriate information is passed and comprehended between providers
    during a transfer of care. This is especially true when
    there is an on-call physician who is temporarily covering the patient for another physician. Assumptions
    about what the other physician will do can easily lead
    to unfortunate gaps in the patients care with potential
    untoward results.
    Checkout lists for weekend call patients are effective
    in improving communication. The handoff is best done
    in person if possible. The AAOS also sponsors workshops that are effective in improving communication
    among physicians, other members of the health care
    team, and patients.

    Retained Instruments/Sponges
    Accidentally leaving sponges or instruments in a patients body cavity is a significant concern for any surgeon. Most retained items are left in the abdomen, pelvis, or vagina. According to findings based on a review
    of closed claims of a large medical liability carrier, of
    54 patients involved in this series, 69% had retained
    sponges and 31% had retained instruments.4 Sixty-nine
    percent of the patients required surgery for removal of
    the retained instrument or sponge. Risk factors for retained foreign bodies included increased body mass index, emergency surgery, and unplanned change in the
    operation. Retained surgical items may cause pain, abscess formation, organ perforation, and death.
    Retained surgical items are considered by the Centers for Medicare and Medicaid Services as a never
    event or preventable error, and this organization and
    private payers will not pay for the treatment required
    to remove a retained item or the complications arising
    from this event.

    Fires and Burns


    Fires in the operating room occur approximately 100
    times per year in the United States, resulting in approximately 20 serious patient injuries.5 The three requirements for fire (source, oxidizer, and fuel) are available
    and abundant in the operating room. Prevention of
    fires in the operating room was a focus of the Joint
    Commission in 2009 (standard NPSG.11.01.01).
    The most common sources of ignition in the operating room are the electrocautery (68% of the time) and
    the laser (13% of the time) although drills and saws
    may also be an ignition source. Electrocautery devices
    should be placed in a holster when not in use. Alcoholbased preparation solutions must be allowed to dry adequately so they will not ignite. The oxygen-rich environment of the operating room makes the setting
    especially vulnerable to fire. The surgical team should
    ensure that oxygen concentration is minimized under

    2011 American Academy of Orthopaedic Surgeons

    Chapter 1: Patient Safety and Risk Management

    the surgical drapes because this is a significant cause of


    surgical fires.6

    Device Recalls

    Risk Management

    Communicating Adverse Events


    Adverse events or disappointing outcomes may occur
    for a multitude of reasons and are not necessarily a result of error or negligence. It is the obligation of the
    treating physician to inform the patient or his or her
    family, as soon as possible, of any adverse event or unexpected findings at surgery and to discuss what may
    be perceived as a potential disappointing outcome.
    Good communication built on trust and honesty is a
    cornerstone of patient-physician relationships. Honest
    and open communication favorably affects not only patient satisfaction but health outcomes. It also often reduces the incidence of malpractice actions by mitigating
    the liability risk when patients and family members
    think that their surgeon is honest and caring and will
    not abandon them.
    If the cause of the adverse event is an error, the surgeon should immediately contact the appropriate risk
    manager or legal counsel to determine the amount of
    detail that should be provided in any discussions. Some
    information such as root cause analysis, peer review issues, results of disciplinary actions, and legal counsel
    communications are privileged and should not be part

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    Implants will occasionally be found to be defective and


    a device recall may be initiated by the manufacturer or,
    less commonly, the Food and Drug Administration
    (FDA). The orthopaedic surgeon who implanted the device should assist in completing registry and chart documentation that will ensure patient identification in
    case of recall. The orthopaedic surgeon has some responsibility for the patients safety after an implanted
    device has been recalled, and should assist in contacting
    the patients affected by a recalled device. The treating
    orthopaedic surgeon is in the unique position to further
    advance his or her role as patient advocate and help the
    patient in successfully navigating the issue of a potentially defective device. The patient should be carefully
    monitored for potential device failure and advised as to
    the potential risks and benefits of undertaking surgery
    to revise the implanted device. The AAOS strongly recommends that its members become aware of device recalls and report any information concerning defective
    devices to MedWatch under the auspices of the FDA.
    Patients may experience a significant level of anxiety
    after a device recall. In many recalls, not all of the implants may be defective, and the orthopaedic surgeon
    may be able to alleviate the patients fears and provide
    comfort. The AAOS Information Statement on implant
    device recalls states, Revision surgery, in the absence
    of evidence of clinical failure, as a preventative measure
    against possible implant device malfunction is rarely, if
    ever, recommended.7

    of patient discussions. Careful chart documentation is


    an important component when dealing with medical errors.
    Acknowledgment of what happened, and understanding and the assurance that steps will be taken so
    that the event will not occur again, and that risks of a
    similar occurrence will be minimized must be communicated as appropriate. An apology, if appropriate, that
    avoids suggestion of fault or conjecture may reduce patient anger and mistrust. Follow-up care and next steps
    must be addressed. An offer to transfer care to another
    physician may be appropriate. Comments about the
    reasons for the events should be made only after medical investigation is completed; the patient should be informed of the results of the completed investigation. It
    is best if this interaction is done in the presence of a patient liaison to not only witness the conversation but to
    help the patient and his or her family with needs or requests.8

    Responding to Patient Complaints


    Good communication skills are the key component of
    establishing the physician-patient relationship. The risk
    of receiving patient complaints can also be minimized
    by practicing patient-centered and culturally competent
    care and implementing a well-documented consent process.
    Patient complaints are based on multiple factors.
    However, several common issues underlie most patient
    complaints, and these can be categorized into four key
    areas that will help minimize risk: enhance communication; provide patient-centered culturally competent
    care; enhance the informed consent process; and explain charges and fees up front.
    Enhance Communication
    Many patients have difficulty absorbing or understanding information presented to them; therefore, informational handouts are often helpful. Patients are able to
    take the information home, discuss it, and even do
    some research (the physician may suggest some reliable Web sites such as Your Orthopaedic Connection (http://orthoinfo.aaos.org) that will facilitate better understanding of the procedure and help formulate
    questions. Patients should be able to reach the physician (or nurse or licensed provider) for questions following his or her visit via phone or email.9
    Practice Patient-Centered, Culturally Competent Care
    A patients cultural background and generational differences often affect how he or she relates to health care
    providers or processes information. In certain cultures,
    for example, questioning a physician may be considered rude or a challenge to authority. Therefore, important questions may go unanswered if the physician is
    not proactive in providing information. Enhancing cultural competency skills and developing an understanding of the predominant cultures that make up the
    patient base can help the physician avoid miscommunication.10

    Orthopaedic Knowledge Update 10

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    Enhance the Informed Consent Process


    Informed consent is a process and the formal signed
    consent form merely documents this process, which involves explaining the nature of the problem; the proposed treatment plan; the most likely or most significant risks associated with treatment; the anticipated
    benefits of treatment; and reasonable alternatives to the
    proposed treatment, including the alternative of not
    proceeding with the proposed treatment. Discussion of
    prognosis and the duration and extent of disability following treatment compared to the same factors if treatment is not performed helps the patient make good decisions with realistic expectations.
    If a procedure is recommended to a patient, the physician should distribute materials that review the basic
    procedure and address the risks and benefits of the procedure, important components of the informed consent
    process. If possible, the patient and family should be allowed time to digest the material and formulate questions. The physician should document that the patient
    was informed of the risks and benefits of the proposed
    procedure, that alternatives to the procedure were also
    offered, and that the risks and benefits of those alternatives were explained and understood. In addition, it
    should be documented that the patient had the opportunity to have his or her questions answered. The date
    on which the patient was first provided with this information always should be documented so that the length
    of time the patient was given to consider these options
    is clear on the record.11
    Explain All Charges and Fees Up Front
    A clear explanation of all financial considerations can
    help reduce complaints. All charges should be clearly
    explained to the patient, including the base charge for
    the proposed procedure and any additional charges for
    follow-up visits. In times of large deductibles and varying degrees of coverage it is always best to recommend
    that the patient check with his or her insurance company for details of coverage.
    If a physician receives a patient complaint, legal assistance, preferably from an attorney who has experience working before the state board of medicine,
    should be sought before responding to the complaint.12

    Saying Im Sorry
    Adverse events and disappointing outcomes are an unfortunate and uncomfortable aspect of an orthopaedic
    practice. Honest and open communication, including
    saying Im sorry if appropriate, favorably affects not
    only patient satisfaction but health outcomes, and often
    reduces the incidence of malpractice actions. Negligence
    claims often occur when the patient thinks he or she has
    been abandoned and that there is no other recourse.
    Communicating with the patient and family in an honest and compassionate manner as soon as possible after
    an adverse event is consistent with the principles of
    medical ethics and professionalism. However, the
    thought of saying Im sorry creates concern among
    6

    Orthopaedic Knowledge Update 10

    some that an apology will be construed as an admission


    of guilt.
    Many states have passed Im sorry laws that allow
    physicians to express compassion to patients without
    this statement being construed as an admission of guilt.
    Senate Bill 51784 (Medic Act) was introduced in 2005
    by then-Senators Clinton and Obama. One of the purposes of this act was to improve the quality of health
    care by encouraging open communication between patients and health care providers about medical error.
    Many professional liability carriers are also realizing
    the benefits of saying Im sorry and are establishing
    programs to facilitate this interaction between doctors
    and their patients.13,14

    Definition of Negligence
    Negligence as it relates to malpractice litigation implies
    that an act or omission occurred in which care provided caused injury or death to the patient and deviated
    from the accepted standards of practice in the medical
    community. There are four essential elements that must
    be present and applicable to the defendant and the injury to establish negligence: a duty was owed; a duty
    was breached; the breach caused injury; and damages
    resulted.15,16
    A Duty was Owed
    A legal duty is established whenever a provider undertakes care or treatment of a patient. It begins with the
    initiation of any service to the patient (for example,
    emergency department encounter; clinic appointment;
    telephone encounter). A patient-physician relationship
    must be proved to demonstrate that a duty was owed.
    A Duty was Breached
    A Duty was Breached A breach of duty implies failure
    of the provider to meet the standard of care for the
    time and place of the alleged injury. The standard of
    care is established by expert testimony or in obvious errors in some jurisdictions by the doctrine of res ipsa loquitor (the thing speaks for itself).
    The Breach Caused an Injury
    The claimant must demonstrate that failure to conform
    to the standard of care was a cause of the damages sustained.
    Damages Occurred
    Unless damages of some sort are sustained by the patient, there is no basis for a claim, regardless of whether
    or not the physician was negligent. Damages may be direct economic (measurable damages, such as lost earnings or medical expenses), indirect (subjective damages;
    for example, pain and suffering, loss of consortium),
    or punitive, when conduct is intentionally harmful or
    grossly negligent.

    Analyzing a Lawsuit
    The orthopaedic surgeons first notification that there is
    a pending lawsuit is often only after he or she has been

    2011 American Academy of Orthopaedic Surgeons

    Chapter 1: Patient Safety and Risk Management

    2011 American Academy of Orthopaedic Surgeons

    Settling Versus Fighting


    The opinions of the experts strongly affect the evaluation of whether the case can be won or lost at trial.
    Other parties affected by the lawsuit also contribute to
    the strategy of defense. Many attorneys name as many
    defendants as possible when filing a lawsuit to ensure
    both maximal recovery from the plaintiffs and that all
    potential parties are named within the statute of limitations. Parties may be dropped during the period of discovery if the plaintiffs attorney realizes that there is no
    benefit in maintaining the action against that individual. This strategy can also lead to conflicting theories
    and uncover facts brought to light by finger-pointing
    among multiple defendants.
    The amount of monetary damages also affects the
    decision of whether to settle or continue to defend a
    lawsuit. If the monetary damages have the potential to
    be substantial, the attorney may advise the defendant in
    consultation with the medical liability carrier to settle
    the case. If the monetary damages are small, the plaintiffs attorney may decide not to pursue the case due to
    the lack of potential recovery. A high-low arrangement
    may be agreed upon by the plaintiff and defendant
    prior to verdict. In this arrangement, both sides agree
    that the defendant will pay at least the low amount but
    will not pay more than the high amount, thereby reducing risk for both sides. These arrangements are reportable to the National Practitioners Data Bank (NPDB)
    except if the payment was at the low end, and the defendant was found to be not liable in the case.17
    The NPDB was formed by Congress in 1986 by The
    Heath Care Quality Improvement Act (Title IV 99660). Congress was concerned that the increasing occurrence of medical malpractice and the need to improve the quality of medical care have become
    nationwide problems that warrant greater efforts than
    those that can be undertaken by any individual State.
    Congress was also concerned that disreputable physicians, dentists, and other health care practitioners
    could move from state to state without disclosing their
    previous damaging or incompetent performance. The
    US Department of Health and Human Services is responsible for maintaining the NPDB.18
    The NPDB is intended to be a comprehensive alert
    system for discreet inquiries into a physicians credentials to include loss or restriction of license, membership in professional societies, malpractice payment history, and a record of clinical privileges.19 Authorized
    NPDB queriers and reporters include state licensing
    boards, medical malpractice payers (authorized only to
    report to the NPDB), hospitals and other health care
    entities, professional societies, and licensed health care
    practitioners (self-query only).20 When hospitals perform a review to credential a physician for privileges,
    the hospital makes a confidential inquiry to the NPDB.
    The information in the data bank is intended to supplement a hospitals effort, not to replace credentialing. Individual practitioners may also query the database to
    request their own record. The information in the NPDB
    is not available to the general public. In the 19-year

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    served with the summons. At that point, the orthopaedic surgeon should immediately notify his or her medical liability carrier, and the insurance company will assign an attorney to evaluate the case and defend the
    surgeon. The defendant surgeon should review the patients medical record but it should not be altered in
    any way. The attorney will request all of the medical records and schedule a meeting with the orthopaedic surgeon to discuss the specifics of the case. The defense attorney will answer the summons and the period of
    discovery is then initiated by both sides. Expert reviewers will be selected by both sides, and the medical records will be sent to them. The opinions of the experts
    are of vital importance when the defense attorney evaluates a lawsuit to determine if the case can be successfully defended and at what cost. The defendant physician may also serve as expert witness in addition to his
    or her role as a fact witness, and their active involvement in the case often improves the chance for a successful defense.
    There are many procedural and legal specifics that
    are of vital importance to the success or failure of a
    lawsuit, and these items are often beyond the knowledge of most orthopaedic surgeons. The statute of limitations is a complex doctrine that can potentially limit
    the period of time following treatment that the surgeon
    may be sued. If the alleged negligence is past the statute
    of limitations, the court may dismiss the case even
    though the defendant may have a valid complaint
    against the surgeon. Other procedural issues may also
    limit the ability of a plaintiff to sue the physician.
    Interestingly, an orthopaedic surgeon may be negligent in the care of a patient, but the case may still be
    very defendable. Even if the plaintiff can demonstrate
    that there was duty and a breach of duty, the defense
    may win the case if damages are minimal. Some cases
    are delayed by the defense knowing that the patients
    damages may be minimized over time, thus weakening
    the plaintiffs claim against the orthopaedic surgeon.
    The plaintiff may also have difficulty proving causation, that is, there may be a significant leap from the assumed breach of duty and the damages that occurred.
    The damages may have been inevitable regardless of
    the physicians breach of duty, and this makes the case
    much less attractive to effective plaintiffs attorneys.
    Other variables that an attorney assesses when evaluating a lawsuit include many intangible attributes. How
    the plaintiff and defendant present themselves during
    their depositions influences both attorneys. If they appear aloof, arrogant, or unfriendly, the attorney may be
    concerned how the jury will view the witness whether it
    is the plaintiff or the defendant. Orthopaedic practice
    within clinical practice guidelines or definitive clinical research should produce a universally successful defense or
    dismissal of the case, but unfortunately the current legal
    system does not guarantee this outcome. The doctrine of
    contributory negligence exists when the patient is partially responsible for the outcome of his or her treatment.
    In this case, damages may be decreased because of the
    patients actions, and in other instances, the patient may
    be barred from proceeding with the complaint.

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    period from September 1990 to July 2009, there were


    246,016 reports of physician medical malpractice made
    to the NPDB. The state of New York had the most reports of medical malpractice during this period
    (33,587).
    If an orthopaedic surgeon is reported to the NPDB,
    the NPDB sends a report stating such to the physician.
    A practitioner may submit a 4,000-character response
    to a report on the NPDB. This response will be included when a query is made about that practitioner to
    the NPDB. The NPDB reports licensing and privilege
    issues, but in civil legal matters, the database only reports health carerelated civil judgments taken in federal or state court only. As a result, if a physician has a
    defense verdict in a medical negligence lawsuit, there is
    no report made to the NPDB.

    Types of Liability Insurance


    Medical professionals are commonly required to maintain professional liability insurance by state regulations,
    hospital rules, and/or managed care organizations to
    offset the risk and costs of lawsuits based on medical
    malpractice. Sometimes, posting a bond may be done in
    lieu of carrying insurance. There are two basic types of
    professional liability insurance coverage; claims made
    and occurrence.21
    Claims Made
    These policies are the most common type and cover all
    claims made in the policy period, regardless of when
    the event occurred. Claims made after the policy period
    are not covered. When a claims-made policy expires or
    is cancelled, the physician no longer has coverage for
    events that have occurred but have not yet been reported. Because the policy covers only claims made
    during its term, the first few years of this type of policy
    typically has lower premiums while the policy reaches a
    steady equilibrium (maturity).
    Because medical liability claims may arise many
    years later, special policies called tail coverage (reporting endorsement coverage) can be purchased. When a
    physician ceases to maintain a claims-made policy, tail
    coverage is purchased from the carrier at the time the
    claims- made policy expires. This coverage in effect
    converts a claims-made policy into an occurrence policy. Some carriers may waive tail coverage in the event
    of death, disability, or retirement or based on years of
    coverage.
    An alternative to a reporting endorsement is prior
    acts coverage, commonly referred to as nose coverage, which is purchased from the new insurance carrier. This provides coverage for future claims on acts
    that occurred while the previous claims-made policy
    was in force. When changing claims-made policies, either a tail or a nose is required to avoid a lapse in coverage.
    Occurrence
    This type of policy covers the insured for all claims resulting from actions occurring during the period of
    8

    Orthopaedic Knowledge Update 10

    time covered by the policy, regardless of when the claim


    is made. Hence, the insured is covered for events that
    occur during the policy period, even if reported after
    the policy expires or is not renewed. The permanence
    of occurrence coverage generally makes it more expensive than claims-made coverage initially. Generally, a
    mature claims-made policy costs the same as an occurrence policy. During the early years of a claims-made
    policy, premiums may be less expensive but rates for
    occurrence policies are usually only affected by the
    market.

    Stress of a Lawsuit
    Medical negligence lawsuits can be among the most
    stressful crises that an orthopaedic surgeon will face in
    his or her professional career. Physicians often experience disbelief, anger, depression, embarrassment, and
    self-doubt after they have been served with a lawsuit.
    The stress affects not only the surgeon but also his or
    her family and close friends.
    It is important when being sued that the physician
    realize that he or she is not alone. At any particular
    time, many competent orthopaedic surgeons are defendants in a medical negligence lawsuit, and being served
    with a lawsuit does not imply that the surgeon does
    poor-quality work. There are many programs sponsored by insurance companies and medical societies to
    help physicians and their families cope with the stress
    of a lawsuit. The AAOS offers peer counseling for fellows who have been named in a medical negligence
    lawsuit.

    National Medical Liability Issues as They


    Relate to Politics, State and National
    Reform, and National Variation
    Medical malpractice will remain a point of contention
    for many years to come. Although national medical
    negligence tort reform within the next several years is
    unlikely, the AAOS continues to urge the current administration to include medical liability reform in the
    discussions on health care reform because of the effect
    of lawsuits on the expense of defensive medicine. There
    are many different options available, including noneconomic caps, health court, early tender and affirmative
    defense by practicing within clinical practice guidelines.
    Significant differences in medical liability reform exist between different states. Caps on noneconomic
    damages have been shown to effectively reduce insurance rates and limit frivolous lawsuits. States also differ
    in their approach to the statute of limitations, contributory negligence, joint and several liability, collateral
    source, and how the court deals with expert witnesses.
    The AAOS continues to urge the federal and state legislatures to pass effective and meaningful laws to protect the rights of patients to sue for damages from medical negligence while also protecting the rights of
    physicians who are named as defendants in a medical
    negligence lawsuit.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 1: Patient Safety and Risk Management

    Summary

    AAOS Information Statement: Communicating Adverse


    Outcomes. http://www.aaos.org/about/papers/advistmt/
    1028.asp.
    This AAOS information statement describes methods
    for discussing adverse outcomes with patients. Disclosure with patients in addition to risk management are
    reviewed.

    9.

    AAOS Communication Mentoring Skills Program.


    http://www3.aaos.org/education/csmp/index.cfm
    Accessed August 16, 2009.
    The Communication Skills Mentoring Program is described, including an overview of the program and locations at which the course is offered.

    10.

    White AA III, Hoffman HL: Culturally competent care


    education: overview and perspectives. J Am Acad Orthop Surg 2007;15(suppl 1):S80-S85.
    This is a report of the Harvard Medical Schools program to improve culturally appropriate medical care.
    The practices, perspectives, and experiences of this committee are portrayed.

    11.

    Holt WJ: Informed consent: A process, not a piece of


    paper http://www.aaos.org/news/bulletin/sep07/manag
    ing5.asp
    The process of informed consent is described. The process, rather than the written document, is emphasized,
    and methods to improve consent are described.

    12.

    Feinberg J: The Power of the Patient Complaint. http://


    www.aaos.org/news/aaosnow/jan08/managing8.asp.
    Four methods to decrease patient complaints are described, along with discussions on avoiding complaints
    and risk management.

    13.

    Lundy DW, Cox AR: Saying Im Sorry to Patients After an Adverse Outcome. http://www2.aaos.org/aaos/
    archives/bulletin/jun06/orm1.asp.
    The benefits of sincere apologies to patients after adverse outcomes are reviewed, along with the legal basis
    of the apology.

    14.

    Clinton HR, Obama B: Making patient safety the centerpiece of medical liability reform. N Engl J Med 2006;
    354(21):2205-2208.

    15.

    http://www.sorryworks.net/home.phtml.
    This Web site is devoted to the Sorry Works coalition,
    which advocates the process of complete disclosure to
    patients.

    Annotated References
    1.

    http://www.jointcommission.org/NR/rdonlyres/
    D619D05C-A682-47CB-874A-8DE16D21CE24/0/
    HAP_NPSG_Outline.pdf
    This Web site addresses the Standards Improvements
    Initiatives that the Joint Commission has established to
    improve the care of patients during surgery.

    2.

    http://www.jointcommission.org/NR/rdonlyres/
    31666E86-E7F4-423E-9BE8-F05BD1CB0AA8/0/
    HAP_NPSG.pdf
    This Web site further defines the national patient safety
    goals established by The Joint Commission. The tables
    presented define specifics for each of the goals.

    3.

    Information Statement AA: Wrong Site Surgery. http://


    www.aaos.org/about/papers/advistmt/1015.asp
    Wrong-site surgery is discussed, along with methods to
    avoid its occurrence. A safety checklist is included.

    4.

    Gawande AA, Studdert DM, Orav EJ, Brennan TA, Zinner MJ: Risk factors for retained instruments and
    sponges after surgery. N Engl J Med 2003;348(3):229235.

    5.

    ECRI: A clinicians guide to surgical fires: How they occur, how to prevent them, how to put them out [guidance article]. Health Devices 2003;32(1):5-24.

    6.

    http://www.jointcommission.org/SentinelEvents/
    SentinelEventAlert/sea_29.htm
    This is the Web site of The Joint Commission that describes standards to avoid surgical fires. A safety checklist is included.

    16.

    Teuscher D: Medical Legal Terms Defined: Negligence.


    http://www2.aaos.org/aaos/archives/bulletin/oct05/
    rskman3.asp.
    The definition and four elements of medical negligence
    are reviewed.

    7.

    AAOS: Information Statement: Implant Device Recalls.


    http://www.aaos.org/about/papers/advistmt/1019.asp
    This AAOS information statement discusses product recall and the implications to the orthopaedic surgeon. Patient safety and communication are emphasized.

    17.

    NPDB-HIPDB Data Bank News. http://www.npdbhipdb.hrsa.gov/pubs/newsletter/


    January_2007_Newsletter.pdf. Accessed July 22, 2010.
    Medical malpractice payment reports submitted to
    NPDB were studied.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    Patient safety and risk management are essential in the


    practice of orthopaedic surgery. As advocates for patient care, orthopaedic surgeons should endeavor to
    make the entire health care process safer so that medical errors are as infrequent as possible. Time-outs, effective handoff between providers, and safety checklists
    should reduce errors in patient care. Studies have demonstrated that sincere and timely apologies after complications improve the relationship between the patient
    and the surgeon and decrease medical negligence lawsuits. Orthopaedic surgeons are afforded significant
    protections if they are served with a medical negligence
    lawsuit, and they should be actively involved in their
    defense with their legal team. It is hoped that medical
    liability reform will expand throughout the states and
    eventually through federal legislation.

    8.

    Section 1: Principles of Orthopaedics

    18.

    http://www.npdb-hipdb.hrsa.gov/npdb.html
    The NPDB and why it was developed in addition to
    standards of confidentiality are discussed.

    20.

    Sanbar SS, ed: The Medical Malpractice Survival Handbook. Philadelphia, PA, Mosby-Elsevier, 2007.
    This text discusses issues related to the accused physician in a medical malpractice litigation.

    21.

    Teuscher D: Professional Liability Insurance: A Market


    Overview. http://www2.aaos.org/aaos/archives/bulletin/
    dec05/rskman1.asp.
    A broad overview of medical liability insurance and the
    modifications available in the market are discussed. Specifically, alternative products such as captives and risk
    retention groups are reviewed.

    1: Principles of Orthopaedics

    19.

    The Four Elements of Medical Malpractice. Yale


    New Haven Medical Center: Issues in Risk Management.
    http://info.med.yale.edu/caim/risk/malpractice/
    malpractice_2.html.
    The elements of negligence, along with the complaint,
    summons, discovery, and trial, are reviewed.

    10

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 2

    Fracture Repair and Bone Grafting


    Chuanyong Lu, MD

    Eric Meinberg, MD

    Ralph Marcucio, PhD

    Biology of Bone Repair

    Dr. Meinberg or an immediate family member is a member of a speakers bureau or has made paid presentations on behalf of AO and has received research or institutional support from AO, Brainlab, DePuy, Medtronic,
    Philips, Smith & Nephew, Stryker, Synthes, and Zimmer.
    Dr. Miclau or an immediate family member serves as a
    board member, owner, officer, or committee member of
    the American Orthopaedic Association, the Orthopaedic
    Research Society, the Orthopaedic Trauma Association,
    the San Francisco General Hospital Foundation, and The
    Foundation for Orthopaedic Trauma; serves as a paid
    consultant to or is an employee of AO, the National Institutes of Health, and the Orthopaedic Trauma Care
    Foundation, serves as an unpaid consultant to Amgen,
    has received research or institutional support from
    DePuy, the Musculoskeletal Transplant Foundation, the
    National Institutes of Health, Philips, Stryker, Synthes,
    Zimmer, the Orthopaedic Trauma Care Foundation, and
    the Orthopaedic Trauma Foundation; and has stock or
    stock options held in Johnson & Johnson, Merck, and
    Pfizer. Dr. Marcucio or an immediate family member
    owns stock or stock options in Merck; has received research or institutional support from Stryker; has received
    nonincome support (such as equipment or services),
    commercially derived honoraria, or other non-research
    related funding (such as paid travel) from Stryker and
    Plexxikon; and is a board member, owner, officer, or
    committee member for the Orthopaedic Research Society. Neither Dr. Lu nor any immediate family member
    has received anything of value from or owns stock in a
    commercial company or institution related directly or indirectly to the subject of this chapter.

    2011 American Academy of Orthopaedic Surgeons

    ily of cartilage. At this time, osteoblasts form a collar of


    bone adjacent to the fracture gap. After this initial period of stabilization, chondrocytes undergo a maturation process, the matrix becomes calcified, osteoclasts
    remove the calcified cartilage, and endothelial cells invade the cartilage. The soft callus becomes a hard callus as bone forms behind the invading vasculature.
    Once formed, the bone is remodeled until the skeletal
    injury has been completely repaired and the bone marrow cavity has been restored.

    1: Principles of Orthopaedics

    Fracture healing involves a highly integrated sequence


    of events through which bone is restored to its preinjured condition. The events that occur during healing
    have been classically divided into four phases: inflammation, soft callus, hard callus, and remodeling (Figure
    1). Initially, during the inflammatory stage, a hematoma forms in response to the trauma, and the inflammatory cells in the hematoma dbride the wound and
    may help recruit cells that facilitate repair. As skeletal
    progenitor cells are recruited and begin to differentiate
    into osteoblasts and chondrocytes, the hematoma is
    slowly transformed into a soft callus composed primar-

    Theodore Miclau, MD

    The Inflammatory Phase


    Inflammation plays a key role in the initiation of fracture repair. During the inflammatory stage of repair,
    numerous lymphocytic cells, including macrophages,
    neutrophils, and degranulating platelets, infiltrate the
    fracture site and release cytokines, which include
    platelet-derived growth factor (PDGF), tumor necrosis
    factor (TGF-), interleukins 1, 6, 10, and 12 (IL-1,
    IL-6, IL-10, and IL-12), and tumor necrosis factor
    (TNF-).1-3 Some of these cytokines are detected at the
    fracture site as early as 24 hours postinjury and are important for the expansion of the inflammatory response
    by acting on a variety of cells in the bone marrow, periosteum, and fracture hematoma.2
    Inflammatory molecules may directly regulate bone
    healing. In the absence of TNF-, both endochondral
    and intramembranous ossification are delayed during
    repair, suggesting that this molecule plays an important
    role in the induction of osteochondro-progenitor recruitment and differentiation.4,5 The inactivation of
    cyclooxygenase-2 (COX-2), the enzyme required for
    the production of prostaglandins, a metabolite of
    arachidonic acid metabolism, has been shown to delay
    mesenchymal cell differentiation into the osteoblastic
    lineage during fracture healing via the repression of
    runx-2 and osterix, two important transcription factors
    for osteoblast differentiation.6 In addition, suppression
    of the inflammatory response through the administration of nonsteroidal anti-inflammatory drugs (NSAIDs)
    has been shown to impede fracture repair by inhibiting
    COX enzymes.7 Recently, leukotrienes, another metabolite of arachidonic acid, have been implicated in the
    repair process. Treatment of animals with either montelukast sodium or zileuton, which either block signaling or inhibit production of leukotrienes, respectively,
    stimulates chondrocyte proliferation during fracture
    healing in animal models.8

    Orthopaedic Knowledge Update 10

    11

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 1

    The process of tibia fracture healing in adult mice. Tibia fractures were not stabilized. Fracture tissues were fixed,
    decalcified, and processed for paraffin sectioning. Safranin O/Fast Green staining (A,F,K,P,Q,U,V) and trichrome
    staining (C,H,M,R,S,W,X) were used to stain cartilage red and bone blue, respectively. Transcripts of collagen type II
    (B,G,L, a marker of chondrocytes), collagen type X (L, a marker of hypertrophic chondrocytes), and osteocalcin (OC)
    (D,I,N, a marker of osteoblasts) were detected by in situ hybridization and pseudocolored red, yellow, and green,
    respectively. Macrophages were stained brown via immunohistochemistry using the F4/80 antibody (E). Immunohistochemistry using anti-PECAM (J,O, platelet/endothelial cell adhesion molecule, also CD31) antibody was performed to see blood vessels in fracture calluses. Blood vessels were stained black. Osteoclasts were stained red by
    tartrate-resistant acid phosphatase (T,Y). A, At 3 days after fracture, no cartilage or (B) Col II/Col X transcripts were
    detected. C, No bone or (D) OC was present. E, A large amount of macrophages were present near the fracture
    site. F, At 5 days after fracture, immature cartilage (G) expressing Col II but not Col X was observed in the area of
    periosteal reaction. H, A small amount of new bone and (I) OC expression was apparent in the area of perisoteal
    reaction (J), which is highly vascularized. K, At 7 days after fracture, cartilage is beginning to mature, and Col X
    transcripts (yellow) were apparent (L). M, More new bone and OC expression (N) was seen at the fracture site. O,
    Vascular invastion was observed around hypertrophic cartilage. P and Q, At day 14, a large amount of cartilage
    and bone (R and S) were formed. T, Multiple tartrate-resistant acid phosphatase positive osteoclasts were located
    at the front of endochondral ossification. U and V, At 21 days after fracture, cartilage has been largely replaced by
    bone. W and X, Fractures have healed by bony bridging. Y, Osteoclasts located on the surface of trabecular bone
    are responsible for remodeling the callus tissues. Scale bar: A-D, G-I, L-O, Q, S, V, and X, 250 m; E, T, and Y, 60
    m; F, K, P, U, R, and W, 1 mm).

    The Soft Callus Phase


    Following injury, mesenchymal cells aggregate and
    form condensations at the site of the fracture in response to growth factors and cytokines that are present. During this early stage of repair, stem cells differentiate into chondrocytes or osteoblasts depending on
    the mechanical environment. In general, mechanical instability favors chondrocyte differentiation and endo12

    Orthopaedic Knowledge Update 10

    chondral ossification, whereas mechanical stabilization


    favors osteoblast differentiation and intramembranous
    ossification.9 During endochondral ossification, cells
    condense and differentiate into chondrocytes. Production of cartilage provides stabilization of the fracture
    site, and bone eventually forms to replace the cartilage
    template. In contrast, during intramembranous ossification, mesenchymal cells condense and osteoblasts dif-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 2: Fracture Repair and Bone Grafting

    ferentiate in these condensations in conjunction with


    invading endothelial cells that establish a blood supply.
    Clinically, the primary mode of healing is via endochondral ossification, but intramembranous ossification occurs simultaneously to varying degrees, depending on the extent of mechanical stability.

    comorbidities, cannot be altered, whereas others can be


    treated or manipulated to improve the rate of union
    and eventual outcome. Optimization of these different
    factors, including patient-specific factors and medications, may prove useful in achieving bone union.

    Patient Factors
    The Hard Callus Phase and Remodeling

    Source of Stem Cells During Fracture Repair


    There are multiple sources of stem cells during fracture
    healing, which include the periosteum and endosteum,
    the bone marrow, the adjacent muscles, and the circulatory system. Recent evidence suggests that the major
    source of cells that form the cartilage and bone during
    fracture repair are derived from the periosteum and endosteum, with a potential contribution from the bone
    marrow.13 Although bone marrowderived mesenchymal stem cells may be an adequate source of cells for
    tissue engineering, the role of endogenous mesenchymal
    stem cells in fracture healing appears to be minimal.

    Factors Affecting Bone Healing


    A variety of factors must be considered when clinically
    treating a patient with a fracture or nonunion. Some of
    these factors, such as the severity of injury or patient

    2011 American Academy of Orthopaedic Surgeons

    There are a variety of known patient-related variables


    that affect fracture healing. Often, multiple comorbidities are found in a single patient and may act synergistically to decrease the union rate and ultimate clinical
    outcome. Additionally, as the population ages, individuals are living longer and have more medical problems,
    which present further challenges to the treating physician.
    Nutritional deficiencies, especially abnormalities in
    vitamin D and calcium, have long been associated with
    impaired fracture healing. Patients with unexplained
    nonunions who have undergone thorough endocrinologic assessment have been found to have associated
    metabolic or endocrine abnormalities that have not
    been previously diagnosed. In one study, 84% of patients referred for management of a nonunion were
    found to have a metabolic abnormality, and 68% were
    found to have a vitamin D deficiency.14 Animal studies
    have also demonstrated the impact of protein malnutrition on fracture healing and enhancement of fracture
    union by means of a high-protein anabolic diet.15 To
    date, the impact of protein supplementation on fracture
    and wound healing has been poorly studied in humans.
    Gastric bypass surgery, used increasingly for the
    management of morbid obesity, has profound effects on
    bone metabolism. The Roux-en-Y procedure, the most
    commonly performed bariatric procedure, bypasses the
    duodenum, the primary site for calcium absorption.
    This results in calcium and vitamin D deficiency, upregulation of parathyroid hormone, and increased calcium
    resorption. These patients require calcium and vitamin
    D supplementation. Unlike those who undergo the
    Roux-en-Y procedure, patients who have a gastric
    banding procedure do not develop secondary hyperparathyroidism because the small intestine is not bypassed.16
    Smoking has been long associated with delayed fracture union and increased risk of non-union. Nicotine
    inhibits tissue differentiation and the angiogenic response in early stages of fracture healing,17 and interferes with osteoblast function.18 In one study, grade I
    open tibial shaft fractures took 69% longer to heal in
    smokers than in nonsmokers.19 A significantly higher
    rate of nonunion in Ilizarov reconstruction has also
    been reported.20 Whenever practical, patients should be
    counseled to stop smoking to improve fracture healing.
    Diabetes mellitus, in addition to its many associated
    complications and comorbidities such as neuropathy
    and peripheral vascular disease, is known to affect fracture healing. Lower extremity fractures in patients with
    diabetes have been shown to take approximately 1.6
    times as long to heal than in control subjects who do
    not have diabetes,21 whereas an ankle fracture in pa-

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    During the healing process, the soft callus is slowly


    transformed into a hard callus via the process of endochondral ossification. Chondrocytes in the fracture callus produce a cartilaginous matrix and undergo a maturation process that eventually leads to their terminal
    differentiation into hypertrophic chondrocytes. The
    process of terminal differentiation is complex and involves the interplay of several signaling molecules and
    pathways, including Indian hedgehog (Ihh), parathyroid hormonerelated peptide (PTHrP), fibroblast
    growth factors (FGFs), and bone morphogenetic proteins (BMPs). During development, these molecules
    pattern the growth plate in the developing endochondral skeleton and coordinate the timing and location of
    chondrocyte proliferation, maturation, hypertrophy,
    and terminal differentiation.10 These molecules and
    pathways all are candidates for stimulating repair after
    injury.
    Throughout the process of chondrocyte maturation,
    the chondrocytes begin to express collagen type X
    (col10), release proteases (such as mmp13) that degrade the extracellular matrix,11 and express angiogenic
    factors such as vascular endothelial growth factor
    (VEGF).12 Eventually the cartilage becomes calcified at
    the junction of the maturing chondrocytes and the
    newly formed bone. The chondrocytes then undergo
    apoptosis, the extracellular matrix is degraded, and
    new blood vessels invade the interface. The newly
    formed woven bone then undergoes remodeling
    through organized osteoblast and osteoclast activity,
    eventually forming bone that is indistinguishable from
    the adjacent skeletal tissues.

    13

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    tients with Charcot arthropathy can take up to 3


    months longer to heal than in those patients with protective sensation. This is thought to be caused by decreased cellularity of the fracture callus, delayed endochondral ossification, and decreased strength of the
    callus.22 In animal studies, this pathway can be reversed
    with normalization of blood glucose with insulin,23 suggesting the importance of careful glycemic control in
    clinical practice.
    Because of the success of antiretroviral drugs, HIV can
    now be considered a chronic disease with a long-term
    asymptomatic phase. Patients with HIV have been noted
    to have a higher prevalence of osteopenia, osteonecrosis,
    and fragility fractures, as well as delayed bone and
    wound healing.24 Many factors, including antiretroviral
    medications, intraosseous circulation, and derangement
    in cytokines such as TNF- have been implicated. Patients also tend to have poorer nutrition and a reduced
    body mass index, further complicating bone healing.

    Medications
    The use of bisphosphonates in treatment is increasing
    as osteoporotic fractures are being recognized as a major public health problem. Although bisphosphonate
    treatment significantly decreases the incidence of osteoporotic fractures in the spine and hip, long-term bisphosphonate use may be associated with some side effects. Bisphosphonates inhibit the ostoclastic resorption
    of bone, therefore slowing remodeling and, possibly,
    bone healing.25 Recent radiographic studies have demonstrated a longer time to union in surgically treated
    wrist fractures26 and an increased rate of nonunion in
    humerus fractures.27 It has been suggested that while
    healing time is increased, ultimate bone density and callus strength is improved. Long-term bisphosphonate
    use may be associated with higher risk of atypical subtrochanteric and femoral shaft fractures.28,29 However,
    due to the low incidence of these atypical fractures,
    larger scale clinical studies are needed to further establish a causal relationship.30
    Systemic long-term administration of corticosteroids
    inhibits fracture healing and callus strength in animal
    models.31 Increased complications have been reported in
    clinical studies, including a 6.5% higher rate of nonunion of intertrochanteric hip fractures compared to that
    of control models.32 In addition to steroids, NSAIDs have
    been associated with prolonged healing time due to their
    antiprostaglandin action. Animal data suggest that
    COX-2 selective NSAIDs have a similar negative dosedependent effect on bone healing and should be avoided
    in the early stages of postfracture care.33

    Enhancement of Fracture Healing


    Many physical and biologic methods have been developed to enhance fracture healing. Some are widely used
    clinically, such as bone grafting and the placement of
    BMPs, whereas others are still in their early stages of
    development.
    14

    Orthopaedic Knowledge Update 10

    Bone Grafting
    Autogenous Bone Grafts
    Autogenous bone grafting continues to be the gold
    standard for treating osseous defects and stimulating
    new bone formation. Autogenous bone grafts have osteoinductive and osteoconductive properties, and can
    provide osteogenic cells, which are important for early
    bone formation. Autogenous cortical bone grafts can
    provide mechanical support with limited capability to
    supply osteoblasts. Most of the osteocytes in a cortical
    bone graft will die after grafting, and the nonviable
    bone will be slowly replaced by creeping substitution.
    Creeping substitution is a slow process that may take
    years to complete, and in many instances may never be
    fully accomplished. Autogenous bone grafts can be harvested from the anterior or posterior iliac crests, or local metaphyseal regions during a procedure. Harvesting
    of autogenous bone grafts is associated with a significant risk of complications, such as persistent pain at
    the surgical site; the amount of bone graft that can be
    harvested is limited. Therefore, efforts have been made
    to develop different bone graft substitutes.
    Allografts
    Allografts are harvested from donor cadaver tissue,
    thereby avoiding the complications associated with autograft harvesting. Allograft bone is available as cancellous, cancellous/cortical morcellized chips, or structural
    cortical grafts. Allografts have both osteoconductive
    and osteoinductive properties, but their osteoinductive
    capacity is limited in comparison with that of autografts. In addition, allografts do not provide viable
    osteogenic cells; therefore, their ability to form bone is
    not as good as that of autografts. Regular processing of
    allografts includes physical dbridement of soft tissue, a
    wash with ethanol to remove blood and live cells, and
    gamma irradiation to sterilize the bone tissues. Processing, especially gamma irradiation, has a significant influence on the performance of allografts. High doses of
    irradiation, which may help kill bacteria and viruses,
    impair the biomechanical properties of allografts by
    causing splitting of polypeptide chains or radiolysis of
    water molecules. Irradiation may also affect the osteoconductive and osteoinductive capacities of allografts
    in a dose-dependent manner.34
    Demineralized bone matrix (DBM) is a special form
    of allograft. It is prepared by acid extraction of allograft bone. DBM retains bone collagenous and noncollagenous proteins, including BMPs, and has both osteoinductive and osteoconductive properties. Because
    of demineralization, DBM has better osteoinductive capacity than regular allografts. In some reports, comparable capacity for bone formation has been observed
    between DBM and autogenous bone graft 35, suggesting
    DBM may be a suitable alternative and supplement to
    autogenous bone graft. There are several commercially
    available DBM products that are used clinically to improve spinal fusion, graft fracture nonunions, and fill
    bone defects. However, the efficacy of DBM varies due
    to different processing methods.36 The age of the donor

    2011 American Academy of Orthopaedic Surgeons

    Chapter 2: Fracture Repair and Bone Grafting

    Synthetic Bone Substitutes


    Synthetic bone substitutes were developed as an alternative to autografts and allografts. Their compositions
    include calcium sulfate, calcium phosphate, tricalcium
    phosphate, and bioglass. They are available in different
    forms, including powder, pellet, or putty, and can be
    used as implant coating or bone defect filler. Synthetic
    bone substitutes are osteoconductive, but not osteoinductive. Several clinical studies (level I evidence) have
    shown that using calcium phosphatebased bone substitutes may allow for bone defect filling, early rehabilitation, and prevention of articular subsidence in distal
    radius and tibial plateau fractures.38-40 Level II evidence
    suggests that calcium sulfate is a safe and effective bone
    substitute.41 The current trend is to develop different
    tissue engineering approaches and make composites
    from synthetic bone substitutes with collagen, DBM,
    growth factors, bone marrow cells, or mesenchymal
    stem cells to improve their osteogenic potential.

    Platelet-Rich Plasma
    Platelets play an important role in the inflammatory response after bone injury. Activated platelets release
    many growth factors, including PDGF, TGF-, and
    VEGF. The effectiveness of platelet-rich plasma (PRP)
    in fracture healing has been tested in both animal experiments and clinical trials. In a rat diabetic fracture
    model, PRP improves cellular proliferation and chondrogenesis during early fracture healing and increases
    the mechanical strength of callus during late fracture
    healing.42 The effect of PRP on fracture healing is associated with altered expression of TGF-1 and BMP-2.43
    Clinically, the efficacy of PRP on fracture healing has
    not been fully confirmed. The findings of a systemic literature search showed that there is no strong evidence
    supporting the routine use of PRP in either acute or delayed fracture healing.44 Further high-quality, randomized, and prospective clinical trials are required to determine whether PRP is beneficial in the treatment of
    fracture nonunions.

    Bone Marrow Aspirate


    Bone marrow aspirate has been used to enhance bone
    repair for more than two decades. Many clinical studies

    2011 American Academy of Orthopaedic Surgeons

    have shown its safety and efficacy in treating fracture


    nonunions and bone defects.45,46 It is well established
    that bone marrow contains mesenchymal stem cells,
    which can be expanded in culture and can differentiate
    into osteoblasts, chondrocytes, and other connective
    tissue cells in vitro under appropriate conditions. Bone
    marrow is also the source of circulating endothelial
    progenitors that can contribute to adult vasculogenesis.
    Therefore, some of the effects of bone marrow aspirate
    on fracture healing could be due to the local application of osteochondrogenic cells and/or endothelial progenitor cells during bone healing. However, there is not
    enough evidence showing these cells can actually differentiate into osteoblasts, chondrocytes, or endothelial
    cells, and further investigation is required to determine
    the exact role of these transplanted cells in fracture
    healing.

    1: Principles of Orthopaedics

    is not a factor that significantly affects the efficacy of


    DBM.37
    Because allografts are harvested from donors, safety
    issues such as disease transmission are of major concern. Although harvesting techniques and thorough
    sterilization are important, strict donor screening is essential for reducing the risk of disease transmission.
    The American Association of Tissue Banks (AATB) has
    adopted a protocol for strict screening of tissues, and
    its program of accreditation has put many tissue banks
    under its oversight, which helps improve the safety of
    bone allografts. As a result, it is believed that the actual
    magnitude of viral transmission from allografts is very
    low, with estimates of less than 1 in 1 million procedures.

    Bone Morphogenetic Proteins


    BMPs were first discovered in 1965 by Urist; at least 20
    different BMPs have been found thus far. All of these
    BMPs, except BMP-1, belong to the group of TGF-
    superfamily growth factors. BMP-1 is a metalloprotease that acts on procollagen I, II, and III. Among all
    the BMPs, BMP-2 and BMP-7 have been extensively
    studied for their capacity to induce bone in a variety of
    conditions. BMPs are capable of recruiting stem cells
    from distant sites and inducing osteoblast and chondrocyte differentiation, leading to ectopic bone formation.
    Recent studies have shown that BMPs are involved in
    angiogenesis, the process of new blood vessel formation
    and vascular repair. BMP-7 is capable of inducing new
    blood vessel formation in chick chorioallantoic membranes,47 and BMP-2, which acts in a manner similar to
    that of BMP-7, can increase vascularization of tumors.48 The US Food and Drug Administration (FDA)
    has approved the clinical use of rhBMP-2, marketed as
    Infuse Bone Graft, in acute open fractures of the tibia
    and spinal fusion surgery, and recombinant human
    BMP-7 (rhBMP-7), or osteogenic protein-1 (OP-1), as
    an alternative to autograft in recalcitrant long bone
    nonunions and in compromised patients requiring revision posterolateral lumbar spinal fusion under a Humanitarian Device Exemption (HDE). Level I clinical
    evidence demonstrates that rhBMP-2 improves the repair of open tibia fractures.49 Prospective case series
    studies have shown that rhBMP-7 is effective in treating tibial and femoral nonunions. 50,51

    Vascular Endothelial Growth Factor


    Blood supply is crucial for normal fracture healing.
    Lack of perfusion is often associated with delayed
    union or nonunion. Investigators have suggested that
    stimulating vascular repair may represent a novel
    method to stimulate bone healing. Vascular repair after
    bone injury occurs largely through a process called angiogenesis, which is the sprouting of new blood vessels
    from preexisting ones. During fracture healing, angiogenesis is orchestrated by a variety of factors including
    VEGF, FGFs, and matrix metalloproteinases (MMPs).

    Orthopaedic Knowledge Update 10

    15

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    Among these factors, VEGF is currently recognized as


    the most potent angiogenic factor, and it plays an important role during both skeletal development and
    adult bone regeneration.52 In fracture calluses, VEGF is
    expressed by hypertrophic chondrocytes and may be released from cartilage matrix by matrix degradation mediated by MMP-9.12 VEGF acts on endothelial cells and
    induces vascular invasion of the hypertrophic cartilage.
    The ability of VEGF to enhance bone regeneration has
    been explored in several animal models. VEGF delivered as a protein or through genetic approaches can
    promote healing of femoral fractures in mice,53 radius
    segmental defects in rabbits,53,54 and bone drilling defects in rats.55 VEGF and BMPs may have synergistic
    effects on bone regeneration.56 Recently, another
    unique approach has been developed to enhance angiogenesis during fracture healing by regulating hypoxia
    inducible factor-1 (HIF-1), which is a master regulator of VEGF expression. Inhibiting HIF prolyl hydorxylase, an enzyme that deactivates HIF-1, can stabilize
    HIF/VEGF production, increase angiogenesis, and improve fracture healing.57

    Fibroblast Growth Factors


    FGFs are involved in bone development and fracture
    healing. The expression patterns of FGFs and their receptors during bone repair have been well documented.58 In animal bone repair models, both acidic
    FGF and basic FGF (bFGF) stimulate cartilage formation, leading to larger fracture calluses.59 bFGF may
    also increase the number of osteoclasts and accelerate
    remodeling of fracture calluses.60 The effects of bFGF
    on bone formation are dose dependent. There is evidence showing that bFGF stimulates osteogenesis at
    lower doses but inhibits bone formation at high
    doses.61 Clinical trials are required to establish the effectiveness of FGFs on fracture healing or repair of
    bone defects in patients.

    Parathyroid Hormone
    Parathyroid hormone (PTH) is secreted by the parathyroid glands and its normal function is to increase the
    calcium levels of the blood by indirectly stimulating
    bone resorption, increasing renal reabsorption of calcium, and increasing intestinal calcium absorption.
    Low-dose, intermittent administration of PTH has anabolic effects on bone metabolism, whereas continuous
    administration of high doses leads to catabolic effects.
    PTH (1-34), the 1-34 amino acid segment of recombinant human PTH, is the active form of PTH. The commercially available PTH (1-34), teriparatide, is an
    FDA-approved drug for postmenopausal osteoporosis
    and osteoporosis associated with sustained systemic
    glucocorticoid therapy. It can increase the bone mineral
    density in the lumbar spine and femoral neck in patients with osteoporosis, and reduce fracture risk.62 Recent experimental studies have shown that PTH (1-34)
    is effective for enhancing fracture healing in animals.63
    PTH (1-34) treatment stimulates early bone and cartilage formation, increases callus formation, accelerates
    16

    Orthopaedic Knowledge Update 10

    callus remodeling, and improves the biomechanical


    properties of callus tissue. Further mechanistic analyses
    show that systemic administration of PTH (1-34) upregulates the expression of Osx and Runx2 in bone
    marrowderived mesenchymal stem cells and promotes
    osteoblast differentiation.64 These data suggest that
    PTH (1-34) is a promising treatment of fracture nonunion. However, to date there is no published clinical
    study on the efficacy of PTH (1-34) on fracture healing.

    Wnt
    Wnts are a family of extracellular cellcell signaling
    molecules that regulate embryogenesis and tissue homeostasis in adults. It has been recently documented
    that Wnt signaling plays an important role in fracture
    healing. In the adult skeleton, Wnt signaling proteins
    are expressed by osteocytes, in the endosteum and bone
    marrow.65 After bone injury, Wnt signaling is upregulated and inhibition of the Wnt pathway leads to a delay in bone regeneration.65,66 Mutation of a Wnt coreceptor, Lrp5, results in constitutive Wnt activation. In
    mice that lack Lrp5, proliferation of skeletal progenitor
    cells at the site of bone injury is increased, but bone repair is delayed.65 Further research has shown that Wnt
    signaling inhibits undifferentiated mesenchymal cells
    but may have positive effects on cells that have committed to the osteoblast lineage.66 These research findings
    suggest that the Wnt signaling pathway is a potential
    target to enhance fracture healing. Indeed, lithium
    treatment, which activates the Wnt pathway, is found
    to accelerate bone formation and increase bone mass in
    mice.67 However, lithium treatment should be avoided
    during the early stage of fracture healing because activated Wnt signaling has a negative effect on undifferentiated mesenchymal cells.68

    Ultrasound/Electrical Stimulation
    Biophysical treatments such as electrical stimulation,
    ultrasound, extracorporeal shock wave therapy
    (ESWT), and vibration can improve fracture healing.
    Electrical stimuli create low levels of electric currents in
    tissue, leading to lowered tissue Po2, increased expression of factors such as TGF- and BMPs, improved
    neovascularization, and enhanced osteogenesis. Four
    methods have been developed to deliver electric stimuli
    to the fracture site: direct current, capacitively coupled
    electric fields, pulsed electromagnetic fields, and combined magnetic fields.69 These methods have been promoted as useful treatments of established nonunions
    and failed spinal fusion. Low-intensity pulsed ultrasound (LIPUS), as a physical method to enhance bone
    repair, has gained popularity recently. The exact mechanisms through which LIPUS improves fracture healing
    have not been well determined but could include altered gene expression, increased blood supply, and the
    creation of a gradient of mechanical strain. Both experimental and clinical studies have shown that LIPUS is
    effective in treating delayed union and nonunions,
    achieving healing rates at about 80%. It appears that
    LIPUS may work better on delayed fracture healing

    2011 American Academy of Orthopaedic Surgeons

    Chapter 2: Fracture Repair and Bone Grafting

    than nonunions and is also effective on septic fracture


    nonunions.70 There are reports showing that ESWT can
    be used to treat delayed fracture healing and nonunions, however, its efficacy needs to be better determined. Currently, ESWT is still considered an experimental clinical procedure.71 Additionally, providing
    cyclic mechanical loadings to the fracture site using
    low-magnitude high-frequency vibration may also stimulate bone formation.72

    Summary

    Annotated References
    1.

    Barnes GL, Kostenuik PJ, Gerstenfeld LC, Einhorn TA:


    Growth factor regulation of fracture repair. J Bone
    Miner Res 1999;14(11):1805-1815.

    2.

    Einhorn TA, Majeska RJ, Rush EB, Levine PM, Horowitz MC: The expression of cytokine activity by fracture
    callus. J Bone Miner Res 1995;10(8):1272-1281.

    3.

    Rundle CH, Wang H, Yu H, et al: Microarray analysis


    of gene expression during the inflammation and endochondral bone formation stages of rat femur fracture repair. Bone 2006;38(4):521-529.

    4.

    Gerstenfeld LC, Cho TJ, Kon T, et al: Impaired fracture


    healing in the absence of TNF-alpha signaling: The role
    of TNF-alpha in endochondral cartilage resorption.
    J Bone Miner Res 2003;18(9):1584-1592.

    5.

    Gerstenfeld LC, Cho TJ, Kon T, et al: Impaired intramembranous bone formation during bone repair in
    the absence of tumor necrosis factor-alpha signaling.
    Cells Tissues Organs 2001;169(3):285-294.

    6.

    Zhang X, Schwarz EM, Young DA, Puzas JE, Rosier


    RN, OKeefe RJ: Cyclooxygenase-2 regulates mesenchymal cell differentiation into the osteoblast lineage and is
    critically involved in bone repair. J Clin Invest 2002;
    109(11):1405-1415.

    7.

    Gerstenfeld LC, Thiede M, Seibert K, et al: Differential


    inhibition of fracture healing by non-selective and
    cyclooxygenase-2
    selective
    non-steroidal
    antiinflammatory drugs. J Orthop Res 2003;21(4):670-675.

    8.

    Wixted JJ, Fanning PJ, Gaur T, et al: Enhanced fracture


    repair by leukotriene antagonism is characterized by increased chondrocyte proliferation and early bone formation: A novel role of the cysteinyl LT-1 receptor.

    2011 American Academy of Orthopaedic Surgeons

    9.

    Thompson Z, Miclau T, Hu D, Helms JA: A model for


    intramembranous ossification during fracture healing.
    J Orthop Res 2002;20(5):1091-1098.

    10.

    Kronenberg HM: PTHrP and skeletal development. Ann


    N Y Acad Sci 2006;1068:1-13.

    11.

    Behonick DJ, Xing Z, Lieu S, et al: Role of matrix metalloproteinase 13 in both endochondral and intramembranous ossification during skeletal regeneration. PLoS
    One 2007;2(11):e1150.
    Matrix metalloproteinase 13 (MMP-13) is expressed by
    hypertrophic chondrocytes and osteoblasts in fracture
    calluses. MMP-13 mutant mice exhibit delayed cartilage
    resorption and delayed callus remodeling.

    12.

    Colnot C, Thompson Z, Miclau T, Werb Z, Helms JA:


    Altered fracture repair in the absence of MMP9. Development 2003;130(17):4123-4133.

    13.

    Colnot C, Huang S, Helms J: Analyzing the cellular


    contribution of bone marrow to fracture healing using
    bone marrow transplantation in mice. Biochem Biophys
    Res Commun 2006;350(3):557-561.

    14.

    Brinker MR, OConnor DP, Monla YT, Earthman TP:


    Metabolic and endocrine abnormalities in patients with
    nonunions. J Orthop Trauma 2007;21(8):557-570.
    In a selected cohort of patients with unexplained nonunions, 31 of the 37 patients were found with metabolic
    abnormalities including vitamin D deficiency. Level of
    evidence: III.

    15.

    Hughes MS, Kazmier P, Burd TA, et al: Enhanced fracture and soft-tissue healing by means of anabolic dietary
    supplementation. J Bone Joint Surg Am 2006;88(11):
    2386-2394.

    16.

    Wang A, Powell A: The effects of obesity surgery on


    bone metabolism: What orthopedic surgeons need to
    know. Am J Orthop (Belle Mead NJ) 2009;38(2):77-79.
    This article reviews the effects of obesity surgery, including the Roux-en-Y procedure and gastric banding, on
    endocrine and bone metabolism.

    17.

    Daftari TK, Whitesides TE, Heller JG, et al: Nicotine on


    the revascularization of bone graft: An experimental
    study in rabbits. Spine (Phila Pa 1976) 1994;19:904911.

    18.

    Rothem DE, Rothem L, Soudry M, Dahan A, Eliakim


    R: Nicotine modulates bone metabolism-associated gene
    expression in osteoblast cells. J Bone Miner Metab
    2009;27(5):555-561.
    Nicotine affects cultured osteoblast cells in a biphasic

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    Major advancements have been achieved in the field of


    bone repair during the last several decades. Further discoveries in stem cell biology, molecular biology, biomaterials, and tissue engineering will continue to improve
    understanding of cellular and molecular factors. It is
    expected that orthopaedic surgeons will have more options available to stimulate and enhance bone repair.

    J Cell Physiol 2009;221(1):31-39.


    Mice treated with Singulair (montelukast sodium), a
    cysteinyl leukotriene type 1 receptor antagonist, or zileuton, a 5-lipoxygenase enzyme inhibitor, exhibit increased bone and cartilage formation during early fracture healing.

    17

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    manner. High levels of nicotine inhibit cell proliferation


    and downregulate gene expression of osteoclacin, type I
    collagen, and alkaline phosphatase. Low levels of nicotine have opposite effects.
    19.

    Schmitz MA, Finnegan M, Natarajan R, Champine J:


    Effect of smoking on tibial shaft fracture healing. Clin
    Orthop Relat Res 1999;365:184-200.

    20.

    McKee MD, DiPasquale DJ, Wild LM, Stephen DJ,


    Kreder HJ, Schemitsch EH: The effect of smoking on
    clinical outcome and complication rates following
    Ilizarov reconstruction. J Orthop Trauma 2003;17(10):
    663-667.

    21.

    Loder RT: The influence of diabetes mellitus on the


    healing of closed fractures. Clin Orthop Relat Res
    1988;232:210-216.

    22.

    Macey LR, Kana SM, Jingushi S, Terek RM, Borretos J,


    Bolander ME: Defects of early fracture-healing in experimental diabetes. J Bone Joint Surg Am 1989;71(5):722733.

    23.

    Kayal RA, Alblowi J, McKenzie E, et al: Diabetes causes


    the accelerated loss of cartilage during fracture repair
    which is reversed by insulin treatment. Bone 2009;
    44(2):357-363.
    In a mouse fracture model, diabetes increases chondrocyte apoptosis and osteoclastogenesis, leading to cartilage loss and less callus formation. These effects of diabetes can be reversed by insulin.

    24.

    Richardson J, Hill AM, Johnston CJ, et al: Fracture


    healing in HIV-positive populations. J Bone Joint Surg
    Br 2008;90(8):988-994.
    The authors reviewed the current evidence for an association between HIV infection and poor fracture healing.

    25.

    Li C, Mori S, Li J, et al: Long-term effect of incadronate


    disodium (YM-175) on fracture healing of femoral shaft
    in growing rats. J Bone Miner Res 2001;16(3):429-436.

    26.

    Rozental TD, Vazquez MA, Chacko AT, Ayogu N,


    Bouxsein ML: Comparison of radiographic fracture
    healing in the distal radius for patients on and off bisphosphonate therapy. J Hand Surg Am 2009;34(4):595602.
    Bisphosphonate use is associated with longer times to
    radiographic union of distal radius fractures. However,
    the differences in healing times are small and not considered clinically significant. The authors concluded that
    bisphosphonate therapy can be continued after fracture.
    Level of evidence: III.

    27.

    18

    Solomon DH, Hochberg MC, Mogun H, Schneeweiss S:


    The relation between bisphosphonate use and nonunion of fractures of the humerus in older adults. Osteoporos Int 2009;20(6):895-901.
    In a cohort of older adults with humerus fractures, bisphosphonate use was associated with an approximate

    Orthopaedic Knowledge Update 10

    doubling of the risk of nonunion. Clinical evidence level


    III.
    28.

    Lenart BA, Neviaser AS, Lyman S, et al: Association of


    low-energy femoral fractures with prolonged bisphosphonate use: A case control study. Osteoporos Int 2009;
    20(8):1353-1362.
    In this matched casecontrol study, the authors found
    that prolonged bisphosphonate use is associated with
    low-energy subtrochanteric/shaft fractures in postmenopausal women who have no obvious secondary causes
    of bone loss. Furthermore, bisphosphonate use of
    greater than 5 years was associated with a characteristic
    fracture of the femur, defined as a simple transverse or
    oblique fracture with cortical thickening and beaking of
    the cortex in the subtrochanteric/shaft region. This fracture is an atypical fracture for osteoporotic women.
    Level of evidence: III.

    29.

    Kwek EB, Goh SK, Koh JS, Png MA, Howe TS: An
    emerging pattern of subtrochanteric stress fractures: A
    long-term complication of alendronate therapy? Injury
    2008; 39(2):224-231.
    In this study, the authors analyzed low-energy subtrochanteric insufficiency fractures in 17 patients who have
    been on alendronate therapy for an average of 4.8 years.
    The authors identified a characteristic fracture configuration suggestive of an insufficiency stress fracture. This
    consisted of (1) cortical thickening in the lateral side of
    the subtrochanteric region, (2) a transverse fracture, and
    (3) a medial cortical spike. In addition, 9 (53%) patients
    had bilateral findings of stress reactions or fractures.
    Level of evidence: III.

    30.

    Black DM, Kelly MP, Genant HK, et al; Fracture Intervention Trial Steering Committee; HORIZON Pivotal
    Fracture Trial Steering Committee: Bisphosphonates
    and fractures of the subtrochanteric or diaphyseal femur. N Engl J Med 2010;362(19):1761-1771.
    The authors reviewed 284 records for hip or femur fractures among 14,195 women in three large, randomized
    bisphosphonate trials: the Fracture Intervention Trial
    (FIT), the FIT Long-Term Extension (FLEX) trial, and
    the Health Outcomes and Reduced Incidence with Zoledronic Acid Once Yearly (HORIZON) Pivotal Fracture
    Trial (PFT). The authors concluded that the occurrence
    of fracture of the subtrochanteric or diaphyseal femur
    was very rare, even among women who had been
    treated with bisphosphonates for as long as 10 years.
    There was no significant increase in risk associated with
    bisphosphonate use, but the study was underpowered
    for definitive conclusions. Level of evidence: I.

    31.

    Waters RV, Gamradt SC, Asnis P, et al: Systemic corticosteroids inhibit bone healing in a rabbit ulnar osteotomy model. Acta Orthop Scand 2000;71(3):316-321.

    32.

    Bogoch ER, Ouellette G, Hastings DE: Intertrochanteric


    fractures of the femur in rheumatoid arthritis patients.
    Clin Orthop Relat Res 1993;294:181-186.

    33.

    Dimmen S, Nordsletten L, Madsen JE: Parecoxib and


    indomethacin delay early fracture healing: A study in
    rats. Clin Orthop Relat Res 2009;467(8):1992-1999.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 2: Fracture Repair and Bone Grafting

    Rats with tibia fractures that were treated with parecoxib or indomethacin for 7 days after injury exhibited
    decreased bone mineral density and biomechanical
    properties of fracture callus for 2 to 3 weeks.
    34.

    Nguyen H, Morgan DA, Forwood MR: Sterilization of


    allograft bone: Effects of gamma irradiation on allograft
    biology and biomechanics. Cell Tissue Bank 2007;8(2):
    93-105.
    This article reviews the effects of gamma irradiation on
    the biologic and mechanical properties of allograft
    bone.
    Drosos GJ, Kazakos KI, Kouzoumpasis P, Verettas DA:
    Safety and efficacy of commercially available demineralised bone matrix preparations: A critical review of
    clinical studies. Injury 2007;38(suppl 4):S13-S21.
    The authors present a critical overview of the current
    clinical applications of DBM.

    36.

    Peterson B, Whang PG, Iglesias R, Wang JC, Lieberman


    JR: Osteoinductivity of commercially available demineralized bone matrix. Preparations in a spine fusion
    model. J Bone Joint Surg Am 2004;86(10):2243-2250.

    37.

    Traianedes K, Russell JL, Edwards JT, Stubbs HA, Shanahan IR, Knaack D: Donor age and gender effects on
    osteoinductivity of demineralized bone matrix.
    J Biomed Mater Res B Appl Biomater 2004;70(1):2129.

    38.

    Russell TA, Leighton RK; Alpha-BSM Tibial Plateau


    Fracture Study Group: Comparison of autogenous bone
    graft and endothermic calcium phosphate cement for
    defect augmentation in tibial plateau fractures: A multicenter, prospective, randomized study. J Bone Joint Surg
    Am. 2008;90(10):2057-2061.
    The authors enrolled 120 acute, closed, unstable tibial
    plateau fractures. Subarticular defects were filled with
    either calcium phosphate cement or autogenous bone
    graft. The cement did not improve the union rates and
    the time to union. However, the bioresorbable calcium
    phosphate cement used in this study appears to be a better choice, at least in terms of the prevention of subsidence, than autogenous iliac bone graft for the treatment of subarticular defects associated with unstable
    tibial plateau fractures. Level of evidence: I.

    39.

    Cassidy C, Jupiter JB, Cohen M, et al: Norian SRS cement compared with conventional fixation in distal radial fractures: A randomized study. J Bone Joint Surg
    Am 2003;85(11):2127-2137.

    40.

    Johal HS, Buckley RE, Le IL, Leighton RK: A prospective randomized controlled trial of a bioresorbable calcium phosphate paste (alpha-BSM) in treatment of displaced intra-articular calcaneal fractures. J Trauma
    2009;67(4):875-882.
    The authors prospectively randomized 47 patients with
    52 closed displaced intra-articular calcaneal fractures
    necessitating operative fixation to receive ORIF alone (n
    = 28) or ORIF plus alpha-BSM (n = 24). The results
    confirmed the safety of alpha-BSMand the alpha-BSM
    treated fractures better retained Bhlers angle at 6

    2011 American Academy of Orthopaedic Surgeons

    41.

    Kelly CM, Wilkins RM, Gitelis S, Hartjen C, Watson


    JT, Kim PT: The use of a surgical grade calcium sulfate
    as a bone graft substitute: Results of a multicenter trial.
    Clin Orthop Relat Res 2001;(382):42-50.

    42.

    Gandhi A, Doumas C, Dumas C, OConnor JP, Parsons


    JR, Lin SS: The effects of local platelet rich plasma delivery on diabetic fracture healing. Bone 2006;38(4):
    540-546.

    43.

    Simman R, Hoffmann A, Bohinc RJ, Peterson WC, Russ


    AJ: Role of platelet-rich plasma in acceleration of bone
    fracture healing. Ann Plast Surg 2008;61(3):337-344.
    In a rat femur fracture model, PRP enhances bone formation, which is associated with changes of TGF-1
    and BMP-2 expression.

    44.

    Griffin XL, Smith CM, Costa ML: The clinical use of


    platelet-rich plasma in the promotion of bone healing: A
    systematic review. Injury 2009;40(2):158-162.
    This systemic literature review found limited clinical
    studies and no solid evidence for the efficacy of PRP in
    acute or delayed fracture healing.

    45.

    Goel A, Sangwan SS, Siwach RC, Ali AM: Percutaneous


    bone marrow grafting for the treatment of tibial nonunion. Injury 2005;36(1):203-206.

    46.

    Lokiec F, Ezra E, Khermosh O, Wientroub S: Simple


    bone cysts treated by percutaneous autologous marrow
    grafting: A preliminary report. J Bone Joint Surg Br
    1996;78(6):934-937.

    47.

    Ramoshebi LN, Ripamonti U: Osteogenic protein-1, a


    bone morphogenetic protein, induces angiogenesis in
    the chick chorioallantoic membrane and synergizes with
    basic fibroblast growth factor and transforming growth
    factor-beta1. Anat Rec 2000;259(1):97-107.

    48.

    Raida M, Clement JH, Leek RD, et al: Bone morphogenetic protein 2 (BMP-2) and induction of tumor angiogenesis. J Cancer Res Clin Oncol 2005;131(11):741750.

    49.

    Govender S, Csimma C, Genant HK, et al: Recombinant human bone morphogenetic protein-2 for treatment of open tibial fractures: A prospective, controlled,
    randomized study of four hundred and fifty patients.
    J Bone Joint Surg Am 2002;84(12):2123-2134.

    50.

    Kanakaris NK, Calori GM, Verdonk R, et al: Application of BMP-7 to tibial non-unions: A 3-year multicenter experience. Injury 2008;39(suppl 2):S83-S90.
    The authors treated 68 patients with tibial nonunion
    with BMP-7. Nonunion healing was verified in 61 patients (89.7%) in a median period of 6.5 months. Level
    of evidence: III.

    51.

    Kanakaris NK, Lasanianos N, Calori GM, et al: Application of bone morphogenetic proteins to femoral nonunions: A 4-year multicentre experience. Injury 2009;40

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    35.

    months and 1 year after surgery. Level of evidence: I.

    19

    Section 1: Principles of Orthopaedics

    formation in a sheep model. J Biomed Mater Res B


    Appl Biomater 2008;85(1):87-92.
    In a sheep bone defect model, the addition of 200 mg of
    bFGF to tricalcium phosphate (TCP) cement decreased
    bone ingrowth into the cement.

    (suppl 3):S54-S61.
    The authors treated 30 femoral nonunions with BMP-7.
    Nonunion healing was verified in 26 of 30 cases in a
    median period of 6 months. Level of evidence: III.
    52.

    1: Principles of Orthopaedics

    53.

    62.

    Neer RM, Arnaud CD, Zanchetta JR, et al: Effect of


    parathyroid hormone (1-34) on fractures and bone mineral density in postmenopausal women with osteoporosis. N Engl J Med 2001;344(19):1434-1441.

    63.

    Cipriano CA, Issack PS, Shindle L, Werner CM, Helfet


    DL, Lane JM: Recent advances toward the clinical application of PTH (1-34) in fracture healing. HSS J 2009;
    5(2):149-153.
    This paper summarizes the experimental evidence that
    suggests PTH (1-34) accelerates callus formation and remodeling, and improves the biomechanical properties of
    the fracture callus.

    64.

    Kaback LA, Soung do Y, Naik A, et al: Teriparatide


    (1-34 human PTH) regulation of osterix during fracture
    repair. J Cell Biochem 2008;105(1):219-226.
    In a mouse model, teriparatide treatment increases osterix expression and improves fracture healing. Bone
    marrowderived mesenchymal stem cells isolated from
    teriparatide-treated mice exhibit accelerated osteoblast
    maturation.

    65.

    Shen X, Wan C, Ramaswamy G, et al: Prolyl hydroxylase inhibitors increase neoangiogenesis and callus formation following femur fracture in mice. J Orthop Res
    2009;27(10):1298-1305.
    In a mouse fracture model, prolyl hydroxylase inhibitors
    activate HIF-1, increase VEGF expression, increase tissue vascularity, and lead to more bone formation.

    Kim JB, Leucht P, Lam K, et al: Bone regeneration is


    regulated by wnt signaling. J Bone Miner Res 2007;
    22(12):1913-1923.
    The authors found that Wnt signaling is activated during fracture healing. Inhibition of Wnt signaling prevents the differentiation of osteogenic progenitor cells
    and reduces bone regeneration.

    66.

    Schmid GJ, Kobayashi C, Sandell LJ, Ornitz DM: Fibroblast growth factor expression during skeletal fracture
    healing in mice. Dev Dyn 2009;238(3):766-774.
    The authors quantitatively evaluated the temporal expression patterns of FGFs and their receptors up to 14
    days after fracture in a mouse model.

    Chen Y, Whetstone HC, Lin AC, et al: Beta-catenin signaling plays a disparate role in different phases of fracture repair: Implications for therapy to improve bone
    healing. PLoS Med 2007;4(7):e249.
    Beta-catenin signaling is regulated by Wnt ligands. Absence of -catenin inhibits fracture healing and activation enhances bone repair.

    67.

    Clment-Lacroix P, Ai M, Morvan F, et al: Lrp5independent activation of Wnt signaling by lithium


    chloride increases bone formation and bone mass in
    mice. Proc Natl Acad Sci U S A 2005;102(48):1740617411.

    Street J, Bao M, deGuzman L, et al: Vascular endothelial growth factor stimulates bone repair by promoting
    angiogenesis and bone turnover. Proc Natl Acad Sci U S
    A 2002;99(15):9656-9661.

    54.

    Eckardt H, Ding M, Lind M, Hansen ES, Christensen


    KS, Hvid I: Recombinant human vascular endothelial
    growth factor enhances bone healing in an experimental
    nonunion model. J Bone Joint Surg Br 2005;87(10):
    1434-1438.

    55.

    Tarkka T, Sipola A, Jms T, et al: Adenoviral VEGF-A


    gene transfer induces angiogenesis and promotes bone
    formation in healing osseous tissues. J Gene Med 2003;
    5(7):560-566.

    56.

    Kempen DH, Lu L, Heijink A, et al: Effect of local sequential VEGF and BMP-2 delivery on ectopic and orthotopic bone regeneration. Biomaterials 2009;30(14):
    2816-2825.
    Implanted ectopically, VEGF increases tissue vascularity
    and BMP-2 induces bone formation in rats. A combination of VEGF and BMP-2 significantly enhances ectopic
    bone formation compared to BMP-2 alone.

    57.

    58.

    59.

    60.

    61.

    20

    Carvalho RS, Einhorn TA, Lehmann W, et al: The role


    of angiogenesis in a murine tibial model of distraction
    osteogenesis. Bone 2004;34(5):849-861.

    Nakajima F, Ogasawara A, Goto K, et al: Spatial and


    temporal gene expression in chondrogenesis during fracture healing and the effects of basic fibroblast growth
    factor. J Orthop Res 2001;19(5):935-944.
    Nakamura T, Hara Y, Tagawa M, et al: Recombinant
    human basic fibroblast growth factor accelerates fracture healing by enhancing callus remodeling in experimental dog tibial fracture. J Bone Miner Res 1998;
    13(6):942-949.
    Maus U, Andereya S, Ohnsorge JA, Gravius S, Siebert
    CH, Niedhart C: A bFGF/TCP-composite inhibits bone

    Orthopaedic Knowledge Update 10

    68. Chen Y, Alman BA: Wnt pathway, an essential role in


    bone regeneration. J Cell Biochem 2009;106(3):353362.
    This comprehensive paper reviews the role of Wnt pathway in bone regeneration.
    69.

    Karamitros AE, Kalentzos VN, Soucacos PN: Electric


    stimulation and hyperbaric oxygen therapy in the treatment of nonunions. Injury 2006;37(suppl 1):S63-S73.

    70.

    Romano CL, Romano D, Logoluso N: Low-intensity

    2011 American Academy of Orthopaedic Surgeons

    Chapter 2: Fracture Repair and Bone Grafting

    pulsed ultrasound for the treatment of bone delayed


    union or nonunion: A review. Ultrasound Med Biol
    2009;35(4):529-536.
    This article summarizes the effects of LIPUS on fracture
    healing, including an updated review of the basic science, animal studies, and clinical trials of LIPUS.
    71.

    Birnbaum K, Wirtz DC, Siebert CH, Heller KD: Use of


    extracorporeal shock-wave therapy (ESWT) in the treatment of non-unions: A review of the literature. Arch

    Orthop Trauma Surg 2002;122(6):324-330.


    72.

    Leung KS, Shi HF, Cheung WH, et al: Low-magnitude


    high-frequency vibration accelerates callus formation,
    mineralization, and fracture healing in rats. J Orthop
    Res 2009;27(4):458-465.
    In a rat model, low-magnitude high-frequency vibration
    improves fracture healing through increased callus formation and accelerated remodeling.

    1: Principles of Orthopaedics

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    21

    Chapter 3

    Articular Cartilage and


    Intervertebral Disk
    James A. Martin, PhD
    Daniel Thedens, PhD

    Prem S. Ramakrishnan, PhD

    Tae-Hong Lim, PhD

    Joseph A. Buckwalter, MS, MD

    Structure and Function


    Articular cartilage is structurally well suited to support
    joint function: it provides a nearly frictionless interface
    between joint surfaces and protects underlying bones
    by redistributing loads. By bulk chemical analysis cartilage consists mainly of water (more than 70% of wet
    mass), proteoglycan (15% of wet mass), and collagen
    (15% of wet mass). More than 80% of the proteoglycan present is in the form of high-molecular-weight
    (more than 3.5 x 106 Da) aggregates of hyaluronic acidlinked aggrecan, a 250-kDa protein that is heavily
    populated with polyanionic sulfated glycosaminoglycans (keratan and chondroitin sulfate). In the matrix,
    aggrecan entrapment within a collagen fibril network
    results in densely packed negative charges, which are
    available to interact with water via hydrogen bonding.
    Electrostatic repulsion and a strong tendency to retain
    bound water enable cartilage to resist deformation under compression and to redistribute stresses by hydrostatic pressurization of the matrix.
    Histologic analysis reveals depth-dependent variation in cartilage matrix structure; four distinct zones
    (superficial, transitional, radial, calcified) can be distinguished based on differences in cell morphology, matrix
    composition, and collagen fibril orientation. These
    depth-dependent variations result in marked anisotropy
    and, as a result, chondrocytes experience different
    stresses depending on their location in the depth of the
    matrix. The superficial zone is relatively low in proteoglycan content compared with the deeper zones and, in

    Dr. Buckwalter or an immediate family members serves


    as a paid consultant for or is an employee of ISTO and
    Carbylan Bioscience and is a board member, owner, officer, or committee member of the American Orthopaedic
    Association. None of the following authors nor any immediate family member has received anything of value
    from or owns stock in a commercial company or institution related directly or indirectly to the subject of this
    chapter: Dr. Martin, Dr. Ramakrishnan, and Dr. Thedens.

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    Articular Cartilage

    contrast to deeper zones where collagen fibrils run perpendicular or orthogonal to the surface, the collagen
    network runs parallel to the surface. Thus, this zone is
    specialized to resist tensile stresses. Superficial zone
    chondrocytes are also somewhat distinct from cells in
    other zones: they are comparatively flat in shape and
    less rigid due to the absence of vimentin filaments,
    which enhance the stiffness of the cytoskeleton. These
    features appear to be an adaptation to the relatively
    higher strains experienced by these cells compared with
    cells lodged in the deeper zones where proteoglycan is
    more abundant. Superficial chondrocytes also secrete a
    specialized glycoprotein called lubricin (also known as
    superficial zone protein, or PRG4), which coats cartilage surfaces and lowers surface friction. Intra-articular
    injection of recombinant lubricin prevented cartilage
    degeneration in a rat meniscal tear model of osteoarthritis (OA), indicating that friction plays a role in cartilage degeneration in OA.1
    The cartilage extracellular matrix (ECM) is thinly
    populated by chondrocytes, cells of mesenchymal lineage that are adapted for life in the demanding environment of the articular surface. Despite their low tissue
    density, articular chondrocytes exert a profound influence on cartilage matrix stability. Chondrocyte depletion is associated with aging and OA, and the prevention of chondrocyte death blocks matrix degeneration
    after cartilage injury. Chondrocytes maintain the ECM
    by actively synthesizing its components, but also contribute to matrix degradation by synthesizing matrix
    proteases. Disturbance in the balance between biosynthetic and degradative activities destabilizes the ECM
    and is a hallmark of OA.
    Cartilage is avascular and nourished only by way of
    synovial fluid at its surface and through subchondral
    bone at its base. Intratissue oxygen saturation is predictably low (2% to 10%), but chondrocytes tolerate
    such mild hypoxic conditions, relying for the most part
    on glycolysis for adenosine triphosphate (ATP) production. Presumably, in normal cartilage ATP is generated
    in sufficient quantity to meet demands for
    maintenance-level biosynthesis of proteoglycans and
    collagens. However, very low oxygen levels (less than
    1%) inhibit glycolytic activity via negative feedback by

    Orthopaedic Knowledge Update 10

    23

    Section 1: Principles of Orthopaedics

    reduced intermediates such as nicotinamide adenine dinucleotide (NADH) and nicotinamide adenine dinucleotide phosphate (NADPH), which accumulate in the
    absence of oxidants.2 Recent studies support earlier
    findings that moderate to severe intra-articular hypoxia
    accompanies arthritis and joint inflammation. In addition to interfering with ATP production, such severely
    hypoxic conditions induce chondrocytes to express vascular endothelial growth factor (VEGF), which promotes blood vessel invasion of the tidemark, a classic
    pathologic feature of OA.3

    1: Principles of Orthopaedics

    Influence of Mechanical Stresses on


    Matrix Composition and Cellularity
    In addition to lacking blood vessels, cartilage is deprived of the neural input that drives adaptation of
    bone and muscle to prevailing loading conditions. Yet,
    numerous examples of loading effects on cartilage
    would seem to indicate an intrinsic capacity for load
    adaptation. These observations have focused attention
    on chondrocyte mechanoresponses, which appear to
    mediate many of the effects of loading on cartilage. A
    wealth of in vitro studies indicate that chondrocytes are
    sensitive to frequency, rate, and magnitude of loading.
    In general, physiologic cyclic stress (1 to 5 MPa) applied at moderate frequencies (0.1 to 1 Hz) and rates
    (less than 1,000 MPa/s) stimulate matrix synthesis and
    inhibit chondrolytic activity, whereas excessive stress
    amplitudes (more than 5 MPa), static loading (less than
    0.01 Hz), or stress rates in excess of 1,000 MPa/s suppress matrix synthesis and promote chondrolytic activity. The transduction of mechanical signals resulting in
    changes in gene expression has long been known to involve integrins and the cytoskeleton. However, more recent findings suggest that primary cilia may act as a
    mechanosensory organ in chondrocytes and osteoblasts. These studies show that intracellular calcium
    flux, a primary effect of mechanical strain, is mediated
    by single cilia that protrude into the pericellular matrix
    and are connected to stretch-activated channels in the
    cell membrane.4 The hypothesis that cilia play a role in
    cartilage homeostasis is supported by data from transgenic mice lacking functional cilia; signs of abnormal
    cartilage development and degeneration were apparent.5
    Evidence of load adaptation in cartilage was revealed by a study in which the effects of moderate running exercise (1 hour per day 5 days per week for 15
    weeks) on the stifle joints of beagle dogs were determined. The authors found that running was associated
    with significant gains in cartilage thickness and increased proteoglycan content in femoral condyles and
    patellae.6 However, later studies showed that more
    strenuous long-distance running (up to 40 km per day
    for 40 weeks) resulted in cartilage thinning and proteoglycan loss,7 indicating that load tolerance and adaptive
    capabilities of canine cartilage are limited. The relevance of the canine models to humans is uncertain.
    There were no substantial differences in knee MRIs between elite athletes and nonathletes, suggesting that the
    24

    Orthopaedic Knowledge Update 10

    capacity for human cartilage to add mass in response to


    increased loading is more limited than in dogs.8 However, another study showed substantial (14%) patellar
    cartilage thickening in weight lifters and bobsled sprinters compared to nonathletic control subjects.9 It remains to be seen whether human cartilage shows
    changes in matrix composition similar to those observed in the dog model. In a 2008 study, long-distance
    running effects in the human knee were tracked by serial radiography of patients over two decades (mean
    age = 58 years). Multivariate analysis revealed that runners (n = 45) showed no substantial increase in
    Kellgren-Lawrence scores compared to control subjects
    (n = 53), indicating that running was not associated
    with increased risk of OA.10
    Habitual strenuous loading is clearly harmful to cartilage, but some form of mechanical stimulation is required for cartilage health. Atrophy in response to unloading is well documented in both animals and
    humans. Joint immobilization models consistently
    show cartilage thinning, softening, and proteoglycan
    loss. Recent work in a rat model revealed increases in
    chondrocyte apoptosis, and increased hypoxia inducible factor-, VEGF, matrix metalloproteinase-8
    (MMP-8), and MMP-13 expression.11 This finding suggests that hypoxia may play a role in immobilization
    effects. MRI studies of human knees have shown progressive cartilage thinning within 2 years of spinal cord
    injury,5 indicating atrophy similar to that observed in
    joint immobilization models. The ability of cartilage to
    return to a trophic state when loading is resumed is
    also well established. Data from immobilization models
    have shown varying degrees of recovery of normal cartilage thickness, stiffness, and proteoglycan (PG) content. However, in most cases, extended immobilization
    results in permanent deficits of up to 25% in PG content and mechanical properties. The risk of such permanent effects on cartilage in patients with extended
    partial weight bearing is unclear due to uncertainties
    regarding the time course for immobilization-induced
    atrophy in humans; however, a study of patients recovering from ankle fracture showed significant losses of
    patellar cartilage thickness (-3%) and tibial cartilage
    thickness (-6%) after only 7 weeks of reduced loading.12
    Aging and Arthritis
    The age-dependent incidence of OA supports the notion that age-related changes in articular cartilage are
    pathogenic. However, the connection of aging to OA
    remains unclear. Distinguishing normal age-related
    changes in cartilage, which do not progress to OA,
    from early changes that reliably progress to OA is still
    controversial. Therefore, longitudinal MRI studies may
    prove useful. In one example, MRI examination of patients with knee OA symptoms showed significant reductions in cartilage thickness over 1 year, indicating
    disease progression.13 Presumably, similar studies in
    age-matched patients without symptomatic OA would
    show less progressive thinning. This coupled with an

    2011 American Academy of Orthopaedic Surgeons

    Chapter 3: Articular Cartilage and Intervertebral Disk

    2011 American Academy of Orthopaedic Surgeons

    cal CpG islands in the ADAMTS-4 gene promoter.18


    Loss of DNA methylation in a patient with developmental dysplasia of the hip was associated with increased expression of MMP-13, MMP-9, and MMP-3,
    all of which contribute to ECM degradation.17 The
    availability of drugs targeting methylation and histone
    modification for cancer therapy has stirred discussion
    of their use in the treatment of OA.
    Cell senescence, a phenomenon underlying many degenerative diseases, also occurs in articular cartilage. Senescence is defined as permanent growth arrest, but the
    term is also often used in connection with profound alterations in gene expression. Senescent cells can be longlived, which might not be problematic except that they
    are not entirely quiescent and show abnormalities in matrix metabolism that actively disrupt tissue function.19
    Chronic oxidative damage has been shown to induce senescence in human chondrocytes and senescent cells accumulate in articular cartilage with aging. Chondrocytes
    generate oxidants in response to mechanical stress, suggesting a connection between mechanical factors, oxidative damage, and senescence.20 Thus, it appears that aging changes might be slowed by avoiding stresses that
    result in deleterious oxidant release.
    In most of the studies described above it is implicitly
    assumed that aging affects all cells in cartilage in the
    same way. However, it is increasingly apparent that cartilage harbors progenitor cells, which are distinct from
    normal chondrocytes in that they are highly migratory,
    pluripotent, and clonogenic. Progenitor cells have been
    identified in late-stage osteoarthritic cartilage, and may
    participate in the repair of damaged matrix.21 Thus,
    age-related declines in this subpopulation could have a
    disproportionate effect on matrix stability.22

    1: Principles of Orthopaedics

    initial examination using MRI methods that are sensitive to cartilage matrix composition (delayed
    gadolinium-enhanced MRI of cartilage [dGEMRIC],
    T2, or T1) could help to distinguish initial conditions
    that predispose patients to OA from those that do not.
    Except in connection with injury, cell division is rare
    in mature articular cartilage, suggesting that most chondrocytes present at skeletal maturity are likely to remain
    in place for decades. Although their numbers remain relatively stable for most of adult life in normal cartilage,
    early OA is marked by increased apoptosis and, at later
    stages, by hypocellularity.14 Preventing apoptosis using
    caspase inhibitors ameliorates the development of OA in
    animal models and holds great promise for the treatment
    of some forms of OA in humans.
    Although most chondrocytes may be long-lived, several in vitro tests document age-related declines in their
    performance, especially after the fourth decade of life
    when the risk of OA increases sharply.15 Losses in overall biosynthetic activity, particularly under growth factor stimulation, could contribute to the risk of OA by
    undermining matrix maintenance and repair. However,
    a pathogenic role for these relatively subtle cellular
    changes remains to be proved. Indeed, it is possible that
    age-related loss of matrix biosynthesis activity constitutes a successful metabolic adaptation to decreasing
    nutrition or other environmental changes, and that its
    association with OA is coincidental.
    More obviously pertinent to OA are age-related
    changes in chondrocyte phenotype that lead to increased expression of catabolic cytokines and matrix
    proteases. Recent work suggests that dysregulation of
    the Wnt/-catenin pathway, which regulates multiple
    genes involved in cartilage development, is strongly associated with OA. Wnt-induced signaling protein 1
    (WISP-1) was found to upregulate matrix protease expression in chondrocytes.16 Inactivating mutations in
    the gene encoding frizzled-related protein-3, a key negative regulator of the Wnt pathway, were found to predispose patients to OA. Moreover, transgenic mice
    overexpressing -catenin, a key positive regulator of
    the Wnt pathway, develop osteoarthritic changes. Interestingly, -catenin activation is regulated by mechanical
    stresses in chondrocytes, suggesting a role for the Wnt
    pathway in integrin-mediated mechanoresponses.
    The cause of age-related changes in the Wnt pathway or other alterations in phenotype is uncertain.
    Some evidence suggests that the age-dependent accumulation of epigenetic changes alters the pattern of
    chondrocyte gene expression.17 This involves altered activity of DNA methyltransferases and/or histone
    acetylases/deacetylases, which inappropriately silences
    or activates gene expression by modifying cis-acting sequences that control gene transcription. For example,
    the expression of the aggrecanase encoding gene a disintegrin and metalloproteinase with thrombospondin
    motif-4 (ADAMTS-4) in normal and osteoarthritic cartilage was analyzed, and the enzyme was found to be
    upregulated in superficial zone chondrocytes in OA.
    Further analysis revealed that increased expression in
    OA was related to loss of cytosine methylation at criti-

    Injury and Repair


    Biologic Responses to Mechanical Injury
    Physical injury to articular cartilage surfaces can occur
    under a variety of circumstances, including articular
    fracture, ACL rupture, or simple sprains. High loading
    rates (>1,000 MPa/s) and high peak stress amplitudes
    (>20 MPa) initiate focal damage that can spread to involve even larger areas of the joint surface, leading to
    posttraumatic OA. Biologic responses act to repair or
    limit the damage inflicted by injurious stress, but progressive degeneration is a common sequela to injury,
    particularly in middle-aged and elderly patients. At the
    high loading rates characteristic of impact injuries,
    overall cartilage strain and water loss are minimal.
    However, local strains in the superficial zone during
    impact injuries can exceed 40%, and matrix fissuring
    and chondrocyte death are evident postimpact. These
    changes have been shown to lead to the development of
    OA in a rabbit model of single blunt-impact injury.23
    Strategies to Promote Healing or Regeneration
    Superficial zone chondrocyte death is strongly associated with physical injury to articular cartilage. Most of
    the available evidence indicates that the resulting devitalization of the cartilage matrix is permanent and de-

    Orthopaedic Knowledge Update 10

    25

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 1

    The effects of blunt impact injury on oxidant production and viability in osteochondral explants are shown. A, The
    confocal micrograph shows the surface of an explant stained with calcein AM for live cells (green) and dihydroethidium for superoxide production (red) 30 minutes after blunt impact with a 5-mm-diameter platen (size and placement indicated by the white circle). Note the heavy oxidant production near the periphery of the impacted site. B,
    Chondrocyte viability determined by confocal microscopy at 48 hours postimpact in the absence of treatment (No
    Tx) or when treated immediately with NAC, rotenone, P-188, or Z-VAD-fmk. Con indicates results for nonimpacted cartilage. Asterisks indicate significant improvement of viability over untreated control. Note also that viability in the group treated with rotenone, the mitochondrial electron transport inhibitor, was significantly greater
    than in the group treated with Z-VAD-fmk, a pan caspase inhibitor. (Data courtesy of the Iowa Orthopaedic Biology Laboratory.)

    stabilizing; thus, injury-induced cell death is among the


    earliest pathogenic events in posttraumatic OA. Preventing cell death in the immediate aftermath of injury
    has become a major target of therapy for posttraumatic
    OA as it has for stroke and heart attack. Interestingly,
    neuronal death after stroke and chondrocyte death after cartilage injury both appear to involve oxidative
    damage associated with free radical release.
    Both apoptosis and necrosis have been observed at
    sites of high-energy impact injury. Impact-induced
    chondrocyte apoptosis is a caspase-dependent process.
    Caspase inhibitors reduce the severity of OA in vivo.
    Caspase inhibitors and the surfactant P-188 were also
    shown to prevent nearly 50% of the chondrocyte death
    that occurred in human ankle cartilage subjected to a
    single impact.24 P-188 is thought to prevent necrosis by
    restoring cell membrane integrity, which is compromised by injury. In addition, BMP-7 applied intraarticularly within 3 weeks after an experimental impact
    injury in the sheep stifle joint prevented apoptosis and
    ameliorated progressive degenerative changes in the
    cartilage matrix.25
    Evidence of mitochondrial involvement in injuryinduced apoptosis comes from a cartilage explant injury model, in which it was shown that a wave of calcium was released from the endoplasmic reticulum
    following blunt impact injury. An increase in calcium
    level induced permeability transition pore (PTP) formation in the inner mitochondrial membrane. The resulting depolarization was associated with cytochrome C
    release, Bcl-2 degradation, and caspase-dependent
    26

    Orthopaedic Knowledge Update 10

    apoptosis.26 Chondrocyte apoptosis was inhibited by


    blocking the increase in cytoplasmic calcium or by
    blocking PTP formation. These results show the central
    role of calcium in chondrocyte responses to mechanical
    trauma and provide evidence that mitochondriadependent apoptosis is a significant consequence of the
    disruption of calcium homeostasis.
    Recent work in a bovine explant model showed that
    impact-induced chondrocyte death was significantly reduced by treatment with the intermediate free-radical
    scavenger N-acetyl cysteine (NAC),20 and similar effects
    have been shown using a superoxide dismutase (SOD)
    mimetic. NAC applied within 2 hours of impact spared
    more than 75% of cells that would have otherwise died
    within 72 hours of injury. Moreover, impact-related decline in PG content 7 days after injury was blocked by
    early postimpact NAC treatment. Additional studies established that superoxide radicals are released from mitochondria in response to impact injury; blocking mitochondrial electron transport at complex I using
    rotenone ablated superoxide release had chondrocytesparing effects similar to those of NAC (Figure 1).
    These studies demonstrate the central role of oxidative stress and mitochondrial dysfunction in acute
    chondrocyte death induced by articular injury. It is
    known that cell death under these conditions is preventable and that preserving cellularity improves tissue
    function and short-term matrix stability. However, the
    ability of such acute cytotherapies to prevent OA is not
    yet clear. Relieving contact stresses in injured joints via
    distraction offers considerable promise. This strategy,

    2011 American Academy of Orthopaedic Surgeons

    Chapter 3: Articular Cartilage and Intervertebral Disk

    which involves external fixation and separation joint


    surfaces, has been applied to patients with OA of the
    ankle. In one study conducted 30 months after frame
    removal, 21 patients (91%) experienced significant improvement; only 2 of these patients had arthrodesis.27
    The mechanisms of distraction effects on articular cartilage repair and stability are still largely unknown.

    Noninvasive Assessment of Cartilage Health

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    Novel MRI-Based Approaches


    The exquisite soft-tissue contrast of MRI and the multiplicity of contrast mechanisms available in a single examination have established MRI as the method of
    choice for imaging articular cartilage. A typical MRI
    protocol will acquire proton density, T1, T2, and fatsuppressed images, which give a comprehensive picture
    of the morphologic changes associated with injury and
    subsequent degenerative processes. Ultimately, however,
    it is the biomechanical properties of cartilage that determine its functional state. Biomechanical properties of
    cartilage may in turn be assessed based on related biochemical composition of the ECM, especially in terms of
    PG and collagen content, the primary components responsible for the mechanical strength of healthy cartilage. Thus, the development of a noninvasive and quantitative assessment of cartilage PG content would greatly
    enhance the evaluation of acute injury and treatment efficacy in the clinical setting. MRI is presently the only
    imaging modality capable of generating this information,
    with four distinct techniques available to generate PGsensitive images for interpretation and quantification.
    These include sodium (23Na) imaging, T2 mapping,
    dGEMRIC, and T1 imaging. Sodium nuclear magnetic
    resonance spectroscopy has long been applied to investigate PG depletion in cartilage. The basis for this
    method is that PG loss yields a reduction of fixed charge
    density and a loss of sodium ions (as well as a change in
    sodium relaxation parameters). These changes can be
    seen and quantified from sodium-based MRI as well and
    present a very direct correlation to PG loss. However, sodium MRI requires specialized hardware, and has relatively poor resolution and signal-to-noise ratio, and is
    unlikely to translate to standard clinical imagers. At the
    other end of the spectrum, T2-based MRI is a widely
    used and mature technique, and T2-weighted images are
    routinely acquired as part of musculoskeletal MRI protocols. Quantification of T2 relaxation times is also a
    readily available technique on most clinical scanners.
    Several studies have shown significant changes in T2 relaxation times in areas of cartilage degeneration, and
    these changes may be seen in subjects with OA in the absence of volume and thickness changes, suggesting sensitivity to biochemical changes in early OA. These
    changes in T2 relaxation time are relatively small, and
    may result from multiple mechanisms such as PG loss,
    water content, and collagen concentration and orientation. Thus, although T2 changes in cartilage are seen in
    degenerative processes and may often be diagnostically
    valuable, it can be unclear which of these mechanisms is
    the predominant cause, potentially limiting the sensitivity and specificity to PG loss.

    The dGEMRIC protocol is currently the most widely


    used of the methods for in vivo characterization of PG
    loss.28 The principle of dGEMRIC is based on the fact
    that glycosaminoglycans (GAGs), which are linked to
    core proteins to form PGs, are negatively charged. If a
    negatively charged MRI contrast agent such as Gd(DPTA)2 is introduced, the distribution of this agent
    will be in inverse proportion to the GAG concentration. Further, the Gd(DPTA)2 concentration can be
    measured through measurement of T1 relaxation time
    through standard imaging and processing techniques,
    yielding a marker of GAG concentration and PG loss.
    Numerous in vivo and in vitro studies suggest dGEMRIC is the most specific for GAG concentrations
    among the described methods, demonstrating direct
    correlations between dGEMRIC measurements and
    GAG and even mechanical properties. This specificity
    comes at a cost of high complexity in implementing the
    examination. Subjects receive an intravenous injection
    of contrast agent, followed by a period of mild exercise
    to distribute the agent. Imaging then takes place 1 to 2
    hours after injection. In many cases, a precontrast examination is also desirable for robust measurement of
    relaxation changes. Thus, while dGEMRIC shows
    strong abilities for accurate measurements of PG depletion, the rigors of the examination may prevent its use
    in clinical settings. T1 MRI represents a promising
    middle ground between T2 mapping and dGEMRIC.
    T1 MRI is a completely noninvasive method for quantifying cartilage PG content without the need for special hardware, contrast agents, exercise, or extended
    timing considerations29 while generating information
    very similar to dGEMRIC.
    The relaxation processes measured with T1 depend
    primarily on the exchange of protons between water
    and macromolecules, but are also influenced by interactions caused by collagen fibril orientation. The T1
    technique generates images with a standard spin-echobased pulse sequence attached to the beginning with a
    group of magnetization preparation pulses to set up
    varying amounts of T1 contrast, and can therefore be
    implemented on any clinical scanner. The image analysis required to quantify T1 is very similar to that required for T2 measurements. The close ties between PG
    content and cartilage function make T1 MRI a much
    more direct and valuable indicator of cartilage health
    and treatment efficacy than purely anatomic imaging.
    Because of the dependence on proton exchange between water and PGs, quantifying PG depletion associated with early OA development with T1 is a more
    discriminatory cartilage assessment than T2 sequences.29 Thus, T1 MRI pulse sequences may be able
    to detect cartilage compromise occurring after catastrophic ACL ruptures. Although this dependence
    may not be as exclusively based on PG content as
    dGEMRIC, both in vitro and in vivo studies suggest
    that the relationship is sufficiently strong and sensitive
    that it may be preferred in many cases because of the
    considerably simpler logistical requirements. The development and validation of T1 MRI as an objective and
    quantitative measurement standard of cartilage condi27

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 2

    The biomechanics of an intact intervertebral disk


    are shown. The biomechanical functions of the
    intervertebral disk are directly related to the
    ECM components. Aggrecans present in the nucleus pulposus are highly hydrophilic, imbibing
    water and establishing an internal hydrostatic
    pressure in the intervertebral disk. This hydrostatic pressure (swelling pressure) is generated
    by the resistance provided by the anulus fibrosus and end plates to fluid transport. The swelling pressure in the nucleus pulposus also provides resistance to compressive forces. In
    addition to facilitating the maintenance of the
    swelling pressure, collagen fibrils run at an angle of about 60 (alternating between adjacent
    lamellae), ensuring tension of the anulus fibrosus structures during rotational movements. The
    composite nature of the end plates provides resilience and prevents fractures in the motion
    segment during load transmission.

    tion may dramatically improve the assessment and understanding of acute injury, diagnosis, and treatment.
    The appearance of techniques for robust and noninvasive assessments of cartilage composition, structure,
    and function would be invaluable for all phases of the
    disease process in OA. Such information may yield detection of early OA markers before morphologic
    changes or physical symptoms occur. It could also direct treatment options and assess recovery in later
    stages of OA development. Further study is needed to
    validate these noninvasive techniques as clinical tools.
    Biomarkers
    Numerous biomarkers related to cartilage matrix metabolism have been tested for their power to predict the
    progression of primary arthritis. The crosslinked
    C-telopeptide of type II collagen (CTX-II) generated in
    articular cartilage by noncollagenase proteinases is a reliable urinary marker of cartilage degeneration in primary OA. Collagen type II neoepitopes resulting from
    collagenase activity (Col2-3/4 long, Col2-3/4 short)
    have also been extensively used as degenerative markers as has the aggrecan neoepitope (VDIPEN) generated
    by MMPs. Markers of cartilage matrix biosynthesis in28

    Orthopaedic Knowledge Update 10

    clude the C-terminal propeptide of type II collagen (PIICP) and chondroitin sulfate epitopes of aggrecan (for
    example, 3B3). In addition to cartilage matrix markers,
    urinary glucosyl galactosyl pyridinoline (Glc-Gal-PYD)
    levels have been used to assess synovial degeneration,
    which is evident in OA.30
    In general, the cartilage biomarker studies show that
    the levels of individual markers do not predict OA consistently, perhaps due in part to the influence of factors
    including age, sex, and body mass index. However,
    combinations of markers appear to give better results.31
    One study found that levels of CTX-II in urine correlated with multiple indices of joint degeneration in patients with hip or knee OA. High CTX-II levels and low
    collagen propeptide levels (PIINP) were found to be related to the rate of progression of knee OA. However,
    the ratio between CTX and PIINP was more strongly
    predictive of arthritis breakdown than either marker
    alone. Based on these findings, it is suggested that the
    calculated ratio represents disturbances in the equilibrium between collagen degradation and synthesis in osteoarthritic cartilage. The ratio of COL2-3/4 short to
    COL2-3/4C long was also shown to be more predictive
    of OA progression than the individual markers.32 Urinary levels of the synovium-specific carbohydrate
    marker Glc-Gal-PYD also effectively predicted OA progression and correlated with pain and other symptoms
    better than cartilage matrix markers.33

    Intervertebral Disk

    Structure and Function


    The intervertebral disk is a fibrocartilaginous structure
    that resides between adjacent vertebral bodies of the
    spine collectively called a motion segment (Figure 2).
    The three principal regions of the intervertebral disk,
    the nucleus pulposus, anulus fibrosus, and the end
    plates, form this specialized structure that maintains an
    optimal biomechanical environment in the spine. The
    nucleus pulposus, the central element of the intervertebral disk, has a fluidic matrix primarily composed of
    aggrecan and type II collagen. The cells that reside in
    the nucleus pulposus are originally derived from the
    notochord and may contain large vacuoles and prominent cytoskeletal elements in situ. Based on their biosynthetic profile and response to mechanical stimuli,
    nucleus pulposus cells are distinct from other cell populations in the intervertebral disk. The anulus fibrosus
    is composed of concentric lamellae of collagen type I fibers that circumferentially confine the fluidic nucleus
    pulposus. Cells of the anulus fibrosus have an ellipsoidal morphology, reside within lamellae of the anulus fibrosus, and produce both type I and type II collagen.
    Cells within the innermost annular regions are more
    rounded and sparsely distributed. By early adulthood in
    the human, however, the nucleus pulposus becomes
    populated by chondrocyte-like cells that may migrate
    from the adjacent end plate or inner regions of the anulus fibrosus. The vertebral bodies are separated from

    2011 American Academy of Orthopaedic Surgeons

    Chapter 3: Articular Cartilage and Intervertebral Disk

    Development and Maturation


    The development of the spinal column begins at the
    embryonic stage with the nucleus pulposus derived
    from the central notochord (endoderm) with the rest of
    the structure (vertebral bodies, cartilage, and anulus fibrosus) from the surrounding mesenchyme (mesoderm). In the embryonic disk, there is a distinct structural and compositional demarcation between the fluidlike nucleus pulposus (rich in notochordal cells and PG)
    and the fibrous anulus fibrosus (fibroblast-like cells and
    collagen). Above and below the newly forming embryonic disks, the notochord disappears and is replaced by
    mesenchymal cells, giving rise to the bone and cartilaginous end plates of the vertebrae. Changes in the composition of the embryonic disk begin right after birth.
    In the nucleus pulposus, notochordal cells are slowly
    replaced by chondrocyte-like cells. Complete replacement of notochordal cells occurs by 10 years after
    birth, leading to compositional changes and making the
    nucleus pulposus resemble the inner anulus fibrosus.
    Concurrently, the vertebral end plates decrease in thickness and diameter due to endochondral ossification. In
    a mature intervertebral disk, cell density is significantly
    low compared to its earlier stages of development, providing the rationale of decreased repair capability of a
    mature disk. Lack of vascularization and immune compromise limits removal of cell remnants and cellular organelles. A recent study showed that nucleus pulposus
    cells are capable of phagocytosis34 and this event may
    be important in maintaining tissue structure and func-

    2011 American Academy of Orthopaedic Surgeons

    tion during major cell loss. Although a mature disk is


    inhabited by cells of similar origin (mesenchymal), they
    express very distinct phenotypes depending on their location and matrix composition.

    Normal Aging Compared With Degeneration


    Aging causes progressive changes in disk matrix composition that resemble those of other aging collagenous
    tissues such as the articular cartilage. One of the earliest age-related phenomena is the fragmentation of the
    PGs in the nucleus. There is also a concurrent increase
    in collagen content (especially type I) rendering the nucleus pulposus more fibrous. Fragmented PGs degrade
    further and leach out of the nucleus pulposus, decreasing its capacity to imbibe water. The decrease in fluid
    retention results in inadequate hydrostatic pressure, a
    major biomechanical deficit. Because of limited repair
    capability, low cell density, and decreased matrix turnover, the intervertebral disk fails to recover, leading to
    further biologic and structural deterioration. In addition, increased crosslinking among collagen fibers and
    nonenzymatic glycation further inhibits matrix turnover. With exception to localized proliferation after injury, cell density and cellular function decrease with
    age, resulting in reduced matrix turnover. Phenotypic
    changes in cell populations are observed with changes
    in matrix composition and local stress distribution. The
    loss of hydrostatic pressure in the nucleus pulposus results in the anulus fibrosus sharing most of the compressive loads. These changes transform the intervertebral disk from a structure that is strong, hydrated, and
    flexible to one that is very stiff, desiccated, and weak.
    At this juncture, normal biomechanical forces become excessive, and lead to structural damage such as
    delamination and tears of the anulus fibrosus, disk prolapse, herniation, and end plate fractures. Narrowing
    of the disk space and radial bulging also occur because
    of loss of fluid pressure and end plate fractures. Agerelated changes peak and signs of discogenic pain are
    observed as early as the third decade of life.
    Degeneration and aging have similar biochemical
    and structural changes. However, the distinction can be
    made by the magnitude and mechanisms that lead to
    the changes in the intervertebral disk. Age-related
    changes that involve structural disruptions are fewer
    and smaller, whereas degenerative changes exhibit major structural disruptions. Aging is an inevitable process
    that starts soon after birth and changes are unrelated to
    pain in the disk, whereas degeneration is correlated to
    discogenic pain. Age-related changes also are common
    to all disks of the spine, whereas macroscopic degenerative changes occur only at levels L4-S1. Although agerelated changes render the disk susceptible to further
    degenerative changes, intervertebral disk degeneration
    can be defined as a condition of structural failure and
    irreversible loss of biomechanical function through
    physical and biologic mechanisms. A degenerated disk
    can have accelerated and advanced signs of aging along
    with a possibility of pain generation. Hence, multiple
    factors may, in combination, incrementally predispose
    the intervertebral disk to degenerative disk disease.

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    the nucleus pulposis superiorly and inferiorly by cartilagenous end plates.


    A normal adult intervertebral disk consists of a large
    amount of ECM and very few viable cells (approximately 1% of total disk volume). Despite very low
    numbers, the resident cells are necessary for maintaining disk health, producing matrix components, and
    controlling matrix turnover by regulating the activation
    and production of extracellular and intracellular proteases. Inactive forms of growth factors such as basic fibroblast growth factor (bFGF), transforming growth
    factor-beta (TGF-), and insulin-like growth factor
    (IGF) are normally bound by cartilage intermediate
    layer protein to the ECM. When chondrocytes secrete
    MMPs, matrix is degraded to make room for newly
    synthesized matrix products. Matrix-bound growth
    factors are released during this event that in turn stimulate the resident cells to produce more matrix, and inhibit the production of MMPs. The other factors that
    play important roles in maintaining tissue turnover are
    tissue inhibitors of metalloproteinases (TIMPs),
    interleukin-1 (IL-1), interferon (IFN), and tumor necrosis factor- (TNF-).
    Due to its lack of vascularity, the intervertebral disk is
    deficient in nutrient supply and exchange of metabolic
    waste products. This deficit in solute transport manifests
    itself in the form of steep gradients in oxygen tension and
    glucose and lactic acid concentrations, which play roles
    in maintaining the phenotype of disk cells.

    29

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    Nutritional Deficiency
    As mentioned previously, the intervertebral disk is avascular with blood vessels restricted to the outer anulus
    fibrosus. Most metabolite transport occurs through diffusion across end plates. Aging causes decreased metabolite transport, whereas degenerative changes and end
    plate disruption increase solute transport affecting intervertebral disk homeostasis. The porosity of the end
    plate is significantly reduced due to calcification. Periannular solute transport is minimal and occurs through
    microtubes, with diffusivity decreasing from the inner
    anulus fibrosus to its outer rims. Low oxygen tension
    in the center of a disk leads to anaerobic metabolism,
    resulting in a high concentration of lactic acid and low
    pH. In vitro experiments show that a chronic lack of
    oxygen causes nucleus pulposus cells to become quiescent, whereas a chronic lack of glucose can cause cell
    death.35 Interestingly, mature nucleus pulposus cells are
    more tolerant to hypoxia when compared to notochordal cells, indicating that end plate porosity plays a
    role in regulating the phenotype of nucleus pulposus
    cells. Deficiencies in metabolite transport appear to
    limit both the density and metabolic activity of disk
    cells. As a result, disks have only a limited ability to recover from any metabolic or mechanical injury. Computational models developed to study solute transport
    in normal and degenerated disks suggest that aging,
    end plate calcification/disruption, and mechanical loads
    influence solute concentrations, affecting cell viability
    and activity.36
    Nutritional deficiencies are a by-product of aging
    and it is unclear if improving metabolite transport
    would save the intervertebral disk from degenerative
    changes. However, there is evidence to suggest that accelerated degenerative signs may occur due to pathologic and/or environmental factors (for example, diabetes and smoking, respectively) that can affect vascular
    health and in turn render the metabolic status out of
    balance before natural aging could take its course.
    Tools for early detection and intervention may be beneficial to slow the process of degeneration.
    Soluble Factors
    The process of degeneration is manifested by a chronic
    imbalance in matrix turnover, with increased expression of catabolic cytokines and decreased anabolic activity. The stromelysin family of enzymes (MMPs) and
    ADAMTS collection are involved in matrix catabolism
    during intervertebral disk degeneration. MMPs-1,-3,
    -7, -9, -10, and -13 have been shown to be involved
    in degenerative activities in various studies. The
    ADAMTS family is composed of aggrecans that have
    been shown to be highly active in degenerated disks. In
    particular, ADAMTS-1, -4, -5, -15 are upregulated in
    degenerated intervertebral disks whereas endogenous
    TIMP-3 expression is low, affecting matrix homeostasis. TNF- and IL-1 and are proinflammatory cytokines that have been studied extensively in the context of their regulation of MMPs. TNF- has also been
    shown to induce sensory nerve in growth in the in30

    Orthopaedic Knowledge Update 10

    tervertebral disk, indicating their possible role in pain


    induction in degenerative disks. Upregulation of the
    IL-1 system is shown to induce MMPs,37 ADAMTS,
    and proteinase-activated receptor-2 (PAR-2).38 Cytokines also suppress synthesis of matrix components such
    as collagen type II, which is largely replaced with collagen type I in the nucleus pulposus. Cytokines mediate
    catabolic responses to advanced glycation end products
    via the advanced glycation and end products receptor
    (RAGE) complex.39 Furthermore, angiogenesis, neuronogenesis and apoptosis of intervertebral disk cells depend to some extent on cytokines. The receptor antagonist of IL-1 system (IL-1Ra), which inhibits IL-1
    signaling, is not upregulated in degenerated disks. Gene
    expression profiling of degenerated human disks suggests that TNF- may be an early response mediator of
    degeneration, whereas IL-1 may be the key mediator
    that sustains the upregulation of matrix-degrading molecules.37
    Recently, the presence of nerve growth factor, brainderived neurotrophic factor (and associated receptors)
    and the pain-associated neuropeptide substance P were
    identified in human nucleus pulposus tissue along with
    upregulation of IL-1, suggesting that proinflammatory
    cytokines can stimulate nociception and initiate pain response via nerve ingrowth. Although implicated in regulating cell proliferation, apoptosis, and senescence, elevated expression of stress proteins such as Hsp-27 and
    Hsp-72 in degenerated disks suggests their possible role
    in the degenerative catabolic process.40 Local expression
    of Fas ligand (FasL) was found to be decreased in degenerated human nucleus pulposus, supporting the hypothesis that FasL may be involved in inhibiting pathologic neovasularization.41 Increased expression of
    connective tissue growth factor in degenerated disks is
    associated with angiogenesis in intervertebral disk degeneration.42 Angiogenesis may also be driven by overproduction of hypoxia inducible factor-1 , which is coexpressed with VEGF in the nucleus pulposus.43 Caveolin-1
    has been shown to be increased in the nucleus pulposus
    of degenerated disks but not in aged normal disks, indicating its role in degenerative rather than age-induced
    changes in the nucleus pulposus.44 In the same study, a
    positive correlation with the expression of cyclindependent kinase inhibitor p16INK4a shows that
    caveolin-1 may be linked to the senescent phenotype in
    the intervertebral disk caused by a phenomenon known
    as stress-induced premature senescence. These findings
    also support the senescence-related increased SA-Gal
    expression in degenerated disk.45 The pathogenic role of
    reactive oxygen species and reactive nitrogen species in
    OA suggests they may also play a role in intervertebral
    disk degeneration. The presence of nitrosylation products in the degenerated nucleus pulposus and stimulation
    of IL expression (-1, -6, and -8) by peroxynitrite supports this hypothesis.46 Moreover, mechanically induced
    reactive oxygen species production is a phenomenon described in articular cartilage, and could also contribute
    to stress-induced premature senescence in cells of the intervertebral disk.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 3: Articular Cartilage and Intervertebral Disk

    It is unclear what initiates the imbalance in cytokine


    profiles in intervertebral disk, but there is evidence to
    suggest the involvement of mechanical loading and genetic factors.

    Mechanical Influences
    Computational models and in vitro biomechanical studies have previously shown that the incidence of disk degeneration and discogenic pain may be directly related
    to increased mechanical demands of the lumbar spine.
    There is increasing evidence that mechanical loads regulate solute transport and there is a physiologic range of
    micromechanical stimuli that may promote maximum
    biosynthesis, maintain cellular phenotype and cellmediated repair.49 Excessive spinal loading caused by environmental factors (such as heavy lifting and increased
    body weight), significant traumatic injury, annular injury, and scoliosis50 can lead to the development of the
    radiologic and biochemical features of degeneration.
    Once initiated, degeneration is expected to alter the local mechanical environment51 furthering degeneration,
    via further mechanical overload, structural damage, vascularization, and altered cell and matrix biology.52 Concerted efforts are under way to understand the role of
    mechanical stimuli on intervertebral disk biology at the
    cellular level. Recently, in vivo and in vitro studies have
    re-emphasized existing hypotheses that dynamic loading
    is more tissue-friendly than static loading.49,52 There is

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    Genetic Influences
    Heritable factors are linked to the risk for intervertebral disk degeneration. Based largely on studies of
    twins, the variance in genetic predisposition to disk degeneration has been estimated at 29% to 74%. These
    studies strongly implicate polymorphisms of vitamin D
    receptor and collagen IX to increased risk for degeneration. Other candidate degeneration-linked genes include collagen type I, IL-6, aggrecan, MMP-3, thrombospondin, TIMP-1 and cyclo-oxygenase (COX-2),
    cartilage intermediate layer protein, and IL-1 family
    members. In a recent study that involved 588 subjects,
    aggrecan, collagen types (COL-9A1, -9A2, -1A1, -3A1
    and -11A1), and ILs (IL-1A,-18R1, and -18RAP) were
    found to be associated with cardinal signs of degeneration such as disk bulging and desiccation. Significant
    correlation between genetic influence and range of motion (in particular, flexion) was observed in patients
    with degeneration with an attributable variance of
    64%.47 Asporin, also known as periodontal ligamentassociated protein 1, is a member of the family of small
    leucine-rich PG family. It is identified as a susceptibility
    gene in OA and was also found to be locally expressed
    in the outer anulus of degenerated disks among Asian
    and caucasian subjects.48
    Although genetic factors associated with degeneration are significant, their mechanistic effect on the degenerative cascade in the intervertebral disk is still
    largely unknown. Functional analysis of genetic polymorphisms in the context of molecular pathology intervertebral disk degeneration warrants investigation.

    also current evidence that the effect of degradative enzymes can be inhibited by mechanical stimulation,53 providing new insights to the subject of forestalling degeneration. Disk cells are responsive to mechanical loads
    depending on the type, magnitude, duration, and also anatomic zone of origin.
    Although cellular responses to mechanical stimuli
    are documented, little is known of the mechanisms that
    regulate these cellular changes, nor is much known regarding the precise mechanical stimuli experienced by
    cells during loading. Advances in the field of computational biomechanics and intervertebral disk biology
    may provide new insights into intervertebral disk
    mechanobiology. Guidelines for tissue engineering and
    regeneration, better management of low back health,
    and prevention of intervertebral disk degeneration are a
    few goals that are currently envisioned.

    Summary
    Several recent developments inspire renewed confidence
    that cartilage degeneration in OA may be subject to interventions that delay or even reverse its progression.
    This optimism is based on a more comprehensive understanding of the molecular and biomechanical mechanisms driving degeneration, which provide a wealth of
    potential targets for pharmacologic intervention. In
    that regard, BMP-7, Wnt pathway modulators, antioxidants, and caspase inhibitors all show considerable
    promise as disease modulators. Moreover, the further
    development of strategies such as joint distraction
    aimed at modifying mechanical conditions in vivo can
    only be enhanced by recent advances in understanding
    the mechanobiology of cartilage. The ability to quantify the effects of such treatments in vivo using MRI
    and molecular biomarkers provides an enormous opportunity to further accelerate progress in treatment development.
    The intervertebral disk is a highly specialized tissue
    with a heterogeneous structure and composition. The
    cells residing inside the intervertebral disk are influenced by their microenvironments and exhibit unique
    phenotypes depending on their regional location. Based
    on studies to date, the cause of intervertebral disk degeneration is multifactorial. However, it is also evident
    that there may be a salient factor(s) that may outweigh
    the others during the initiation and progression of the
    disease. Genetic inheritance may increase predisposition to intervertebral disk degeneration. However, disk
    degeneration does not occur until the fourth decade of
    life and affects only the lower lumbar spine, indicating
    that environmental factors may play a greater role and
    genetic predisposition may only be an additive risk factor. Nutritional deficit is one of earliest changes that
    occurs in the intervertebral disk during maturation,
    with the nucleus pulposus being the most affected.
    However, aging changes may be the primary cause of
    nutritional changes and the cells seem to adapt to the
    environments accordingly by altering their phenotype.
    Numerous molecular factors have been shown to be al-

    Orthopaedic Knowledge Update 10

    31

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    tered in degeneration. Although of potential therapeutic value, all soluble factors identified to date are also
    involved in adaptive remodeling and growth. Also, cytokines and growth factor imbalance are only effects of
    a cause and not necessarily the underlying factor of
    degeneration. Current understanding suggests that the
    mechanical influence on intervertebral disk degeneration may have a greater bearing on initiation and progress of disk degeneration. Animal studies have shown
    that cell-mediated changes always occur following
    structural failure due to mechanical trauma. Hence,
    mechanically induced structural damage may outweigh
    all other factors in initiating an irreversible cellmediated cascade leading to further degradation. Aging, genetic inheritance, nutritional deficit, and soluble
    factors may only predispose the disk to degeneration by
    weakening the structure. The role of reactive oxygen
    species in intervertebral disk degeneration has not received much attention in intervertebral disk biology. As
    in the articular cartilage, intervertebral disk may undergo similar age- and trauma-related increases in oxidative stress, weakening the tissues metabolic system
    and inducing premature senescence and even cell death.
    There is immense therapeutic value in understanding
    the role of pro-oxidants in intervertebral disk degeneration and further studies are warranted. Advances in
    the field of intervertebral disk mechanobiology may
    also provide new insights in to disk pathology, facilitating development of novel interventions to prevent the
    initiation or forestall the progression of this debilitating
    disease.

    4.

    Whitfield JF: The solitary (primary) ciliuma mechanosensory toggle switch in bone and cartilage cells. Cell
    Signal 2008;20(6):1019-1024.
    Articular chondrocytes sense and respond to the strains
    imposed on cartilage via nonmotile single cilia protruding into the pericellular matrix, which act as switches
    that trigger calcium release upon cartilage compression.
    Calcium release in turn activates intracellular signaling
    that results in altered gene expression, which helps cartilage to adapt to changing mechanical conditions.
    Moreover, the chondrocyte cilium with its Indian
    hedgehog-activated Smo receptor is a key player along
    with PTHrP in endochondral bone formation.

    5.

    Kaushik AP, Martin JA, Zhang Q, Sheffield VC, Morcuende JA: Cartilage abnormalities associated with defects of chondrocytic primary cilia in Bardet-Biedl syndrome mutant mice. J Orthop Res 2009;27(8):10931099.
    Wild-type mice and mice bearing mutations in the ciliary proteins Bbs1, Bbs2, and Bbs6 were evaluated with
    respect to histologic and biochemical differences in
    chondrocytes from articular cartilage and xiphoid processes. The fraction of ciliated chondrocytes in cultures
    from mutant mice was significantly lower than in the
    wild-type cultures (P < 0.05). Bbs mutant mice showed
    significantly thinner articular cartilage (P < 0.05) and
    lower PG content (P < 0.05) than wild-type mice.

    6.

    Kiviranta I, Tammi M, Jurvelin J, Smnen AM,


    Helminen HJ: Moderate running exercise augments glycosaminoglycans and thickness of articular cartilage in
    the knee joint of young beagle dogs. J Orthop Res 1988;
    6(2):188-195.

    7.

    Arokoski J, Kiviranta I, Jurvelin J, Tammi M, Helminen


    HJ: Long-distance running causes site-dependent decrease of cartilage glycosaminoglycan content in the
    knee joints of beagle dogs. Arthritis Rheum 1993;
    36(10):1451-1459.

    8.

    Eckstein F, Guermazi A, Roemer FW: Quantitative MR


    imaging of cartilage and trabecular bone in osteoarthritis. Radiol Clin North Am 2009;47(4):655-673.
    Cartilage measurements at 1.5 or 3 Tesla are technically
    accurate, reproducible, and sensitive to change. The authors suggest that MRI of articular tissues represents a
    potent tool in experimental, epidemiologic, and pharmacologic intervention studies.

    9.

    Gratzke C, Hudelmaier M, Hitzl W, Glaser C, Eckstein


    F: Knee cartilage morphologic characteristics and muscle status of professional weight lifters and sprinters: A
    magnetic resonance imaging study. Am J Sports Med
    2007;35(8):1346-1353.
    Fourteen professional athletes (seven weight lifters and
    seven bobsled sprinters) were examined and compared
    with 14 nonathletic volunteers who had never performed strength training. Cartilage morphology was assessed with MRI. Patellar cartilage was 14% thicker in
    athletes than in nonathletes, but there were no significant differences in thickness in other areas of the knee.

    10.

    Chakravarty EF, Hubert HB, Lingala VB, Zatarain E,


    Fries JF: Long distance running and knee osteoarthritis:

    Annotated References
    1.

    2.

    3.

    32

    Flannery CR, Zollner R, Corcoran C, et al: Prevention


    of cartilage degeneration in a rat model of osteoarthritis
    by intraarticular treatment with recombinant lubricin.
    Arthritis Rheum 2009;60(3):840-847.
    A recombinant form of lubricin (LUB1) was delivered
    intra-articularly one to three times per week for 4 weeks
    after induction of OA in a rat meniscal tear model.
    Compared to saline controls LUB1 treatment significantly reduced cartilage degeneration and structural
    damage.
    Lee RB, Urban JP: Functional replacement of oxygen by
    other oxidants in articular cartilage. Arthritis Rheum
    2002;46(12):3190-3200.
    Murata M, Yudoh K, Masuko K: The potential role of
    vascular endothelial growth factor (VEGF) in cartilage:
    How the angiogenic factor could be involved in the
    pathogenesis of osteoarthritis? Osteoarthritis Cartilage
    2008;16(3):279-286.
    Hypoxia inducible factor-1 expression induced by hypoxia in inflamed arthritic joints activates VEGF expression by chondrocytes, leading to neovascularization of
    cartilage. VEGF is also thought to promote the expression of catabolic factors that contribute to cartilage degeneration. This suggests that hypoxia and VEGF contribute significantly to the pathogenesis of OA.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 3: Articular Cartilage and Intervertebral Disk

    A prospective study. Am J Prev Med 2008;35(2):133138.


    The knees of 45 long-distance runners and 53 control
    subjects with a mean age of 58 years in 1984 were imaged by serial radiography through 2002. Radiographic
    scores showed little initial OA (6.7% of runners and 0
    control subjects) and by the end of the study runners did
    not have more prevalent OA than did control subjects
    (P = 0.25). In contrast, higher initial body mass index
    and initial radiographic damage were associated with
    worse radiographic OA at the final assessment.
    11.

    12.

    Hinterwimmer S, Krammer M, Krtz M, et al: Cartilage


    atrophy in the knees of patients after seven weeks of
    partial load bearing. Arthritis Rheum 2004;50(8):25162520.

    13.

    Eckstein F, Maschek S, Wirth W, et al; OAI Investigator


    Group: One year change of knee cartilage morphology
    in the first release of participants from the Osteoarthritis Initiative progression subcohort: Association with
    sex, body mass index, symptoms and radiographic osteoarthritis status. Ann Rheum Dis 2009;68(5):674679.
    3T MRI was used to study articular cartilage thinning
    over 1 year in 79 women and 77 men (mean age 60.9
    years) with symptomatic and radiographic knee OA.
    The greatest rate of cartilage loss (1.9% per year) was
    observed in the weight-bearing medial femoral condyle.
    There was a trend toward higher thinning rates in obese
    participants, but this was not statistically significant.

    14.

    15.

    Del Carlo M Jr, Loeser RF: Cell death in osteoarthritis.


    Curr Rheumatol Rep 2008;10(1):37-42.
    Preclinical studies suggest that caspase inhibition, which
    prevents chondrocyte apoptosis, might slow OA progression. Because of the potential for unwanted systemic
    side effects from such agents, caspase treatments will
    likely need to be delivered intra-articularly. Additional
    interventions will be needed to reverse catabolicanabolic imbalance in surviving cells.
    Aigner T, Haag J, Martin J, Buckwalter J: Osteoarthritis: Aging of matrix and cellsgoing for a remedy. Curr
    Drug Targets 2007;8(2):325-331.
    Aging is the foremost risk factor for OA. This might be
    attributed to mechanical wear and tear, or the accumu-

    2011 American Academy of Orthopaedic Surgeons

    16.

    Blom AB, Brockbank SM, van Lent PL, et al: Involvement of the Wnt signaling pathway in experimental and
    human osteoarthritis: Prominent role of Wnt-induced
    signaling protein 1. Arthritis Rheum 2009;60(2):501512.
    Wnt-induced signaling protein 1 (WISP-1) expression
    was strongly increased in the synovium and cartilage of
    mice with experimental OA. Wnt-16 and Wnt-2B were
    also markedly upregulated during the course of disease.
    Interestingly, increased WISP-1 expression was also
    found in human OA cartilage and synovium. Stimulation of macrophages and chondrocytes with recombinant WISP-1 resulted in IL-1independent induction of
    several MMPs and aggrecanase and overexpression of
    WISP-1 in murine knee joints induced cartilage damage.

    17.

    da Silva MA, Yamada N, Clarke NM, Roach HI: Cellular and epigenetic features of a young healthy and a
    young osteoarthritic cartilage compared with aged control and OA cartilage. J Orthop Res 2009;27(5):593601.
    Epigenetic features were characterized in hip articular
    cartilage from patients with primary age-related OA and
    from a 23-year-old patient with secondary OA due to
    developmental hip dysplasia. MMP-3, MMP-9, MMP13, and ADAMTS-4 were immunolocalized and the
    methylation status of specific promoter CpG sites was
    determined. Both primary and secondary OA were characterized by loss of aggrecan, formation of clones, and
    abnormal expression of the proteases that correlated
    with epigenetic DNA demethylation.

    18.

    Cheung KS, Hashimoto K, Yamada N, Roach HI: Expression of ADAMTS-4 by chondrocytes in the surface
    zone of human osteoarthritic cartilage is regulated by
    epigenetic DNA de-methylation. Rheumatol Int 2009;
    29(5):525-534.
    ADAMTS-4, one of the major aggrecanases involved in
    OA, was nearly absent in control cartilage, but was expressed by numerous chondrocytes in OA cartilage and
    increased with disease severity. DNA methylation was
    lost at specific CpG sites in the ADAMTS-4 promoter in
    OA chondrocytes, suggesting that ADAMTS-4 is epigenetically regulated and plays a role in aggrecan degradation in human OA.

    19.

    Loeser RF: Aging and osteoarthritis: The role of chondrocyte senescence and aging changes in the cartilage
    matrix. Osteoarthritis Cartilage 2009;17(8):971-979.
    Articular chondrocytes exhibit an age-related decline in
    proliferative and synthetic capacity while maintaining
    the ability to produce proinflammatory mediators and
    matrix degrading enzymes. These findings are characteristic of the senescent secretory phenotype and are most
    likely a consequence of extrinsic stress-induced senescence driven by oxidative stress rather than intrinsic
    replicative senescence.

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    Sakamoto J, Origuchi T, Okita M, et al:


    Immobilization-induced cartilage degeneration mediated through expression of hypoxia-inducible factor1alpha, vascular endothelial growth factor, and
    chondromodulin-I. Connect Tissue Res 2009;50(1):3745.
    Immobilization effects on cartilage morphology and on
    the expression of hypoxia inducible factor-1, VEGF, and
    the antiangiogenic factor, chondromodulin-I (ChM-1),
    were studied in ankle joints of 12-week-old rats. Significant thinning of the articular cartilage was noted in immobilized joints and vascular channels were found between calcified cartilage and subchondral bone. Hypoxia
    inducible factor-1 and VEGF expression increased and
    ChM-1 expression declined with immobilization.

    lation of time-related modifications of the matrix, or the


    loss of viable cells over time. However, recent findings
    support the hypothesis that stressful conditions might
    promote chondrocyte senescence, which might be of
    particular importance for the progression of OA. Senescence might someday be targeted for therapeutic intervention.

    33

    Section 1: Principles of Orthopaedics

    20.

    1: Principles of Orthopaedics

    21.

    22.

    23.

    24.

    Martin JA, McCabe D, Walter M, Buckwalter JA,


    McKinley TO: N-acetylcysteine inhibits post-impact
    chondrocyte death in osteochondral explants. J Bone
    Joint Surg Am 2009;91(8):1890-1897.
    Bovine osteochondral explants subjected to a single impact load and treated thereafter with N-acetylcysteine,
    or a pan-caspase inhibitor, or P-188 surfactant.
    N-acetylcysteine doubled the number of viable chondrocytes assayed 48 hours after impact, and this effect was
    significantly greater than that caspase inhibitor or
    P-188. Moreover, N-acetylcysteine treatment significantly improved PG content at the impact sites at both 6
    and 14 days after injury.
    Khan IM, Williams R, Archer CW: One flew over the
    progenitors nest: Migratory cells find a home in osteoarthritic cartilage. Cell Stem Cell 2009;4(4):282-284.
    In this preview, the authors cite Miosge and colleagues
    (Koelling et al, 2009) who reported that migratory progenitor cells occupy degenerating OA tissue but that this
    population is not present in healthy cartilage. Better understanding of this system will enable the manipulation
    of chondrogenic progenitor cells to fully commit to the
    chondrogenic phenotype and drive the process of repair
    and regeneration.
    Mimeault M, Batra SK: Aging of tissue-resident adult
    stem/progenitor cells and their pathological consequences. Panminerva Med 2009;51(2):57-79.
    The fascinating discovery of tissue-resident adult stem/
    progenitor cells in recent years led to an explosion of interest in the development of novel stem cellbased therapies for improving the regenerative capacity of these
    endogenous immature cells or transplanted cells for the
    repair of damaged and diseased tissues. This review discusses therapeutic strategies for treating premature aging and age-related disorders including hematopoietic
    and immune disorders, heart failure and cardiovascular
    diseases, neurodegenerative, muscular, and gastrointestinal diseases, atherosclerosis, and aggressive and lethal
    cancers.
    Borrelli J Jr, Silva MJ, Zaegel MA, Franz C, Sandell LJ:
    Single high-energy impact load causes posttraumatic
    OA in young rabbits via a decrease in cellular metabolism. J Orthop Res 2009;27(3):347-352.
    A single high-energy impact blow to the medial femoral
    condyles of young rabbits resulted in histologic signs of
    articular cartilage degeneration (chondrocyte and PG
    depletion) at 3 and 6 months postinjury. In situ hybridization revealed that type II collagen and BMP-2 mRNA
    declined at injury sites at 3 months, suggesting impactrelated impairment of anabolic activity.
    Pascual Garrido C, Hakimiyan AA, Rappoport L,
    Oegema TR, Wimmer MA, Chubinskaya S: Antiapoptotic treatments prevent cartilage degradation after
    acute trauma to human ankle cartilage. Osteoarthritis
    Cartilage 2009;17(9):1244-1251.
    Histologic analysis showed that a single impact delivered to human ankle cartilage resulted in chondrocyte
    death, cartilage degeneration, and spread of apoptosis
    to areas around the impact site. Inhibitors of caspases-3
    and -9 reduced death in the impact site only at early

    34

    Orthopaedic Knowledge Update 10

    time points, but were ineffective in the area around the


    site, whereas P-188 prevented cell death in both the impact site and adjacent cartilage.
    25.

    Hurtig M, Chubinskaya S, Dickey J, Rueger D: BMP-7


    protects against progression of cartilage degeneration
    after impact injury. J Orthop Res 2009;27(5):602-611.
    Impact injuries in sheep stifle joints were treated by two
    intra-articular injections of BMP-7 (OP-1) at varying
    times after injury and effects were evaluated after at
    least 97 days postinjury. Treatment within the first 21
    days significantly reduced OA progression, but delaying
    treatment until 90 days was ineffective. Chondroprotective effects were thought to be due to enhanced chondrocyte survival.

    26.

    Huser CA, Davies ME: Calcium signaling leads to mitochondrial depolarization in impact-induced chondrocyte
    death in equine articular cartilage explants. Arthritis
    Rheum 2007;56(7):2322-2334.
    Transient mitochondrial depolarization was observed in
    equine cartilage explants subjected to impact. This leads
    to activation of caspase-9 and apoptosis. Blocking intracellular calcium release from the endoplasmic reticulum,
    or blocking activation of calcium-dependent kinase or
    calcium-dependent proteases, inhibited both depolarization and apoptosis.

    27.

    Tellisi N, Fragomen AT, Kleinman D, OMalley MJ,


    Rozbruch SR: Joint preservation of the osteoarthritic
    ankle using distraction arthroplasty. Foot Ankle Int
    2009;30(4):318-325.
    This is a retrospective review of 25 patients who underwent ankle distraction from 1999 to 2006. SF-36 scores
    showed modest improvement in all components. Only
    two of the patients in the study underwent fusion after
    ankle distraction. Total ankle motion was maintained in
    all patients, with improvement in the functional arc of
    motion in five patients who started with mild equinus
    contractures.

    28.

    Burstein D: Tracking longitudinal changes in knee degeneration and repair. J Bone Joint Surg Am 2009;
    91(suppl 1):51-53.
    MRI parameters, T2-weighted, T1rho-weighted, and
    dGEMRIC, enable clinicians to see OA as a regional
    and responsive (reversible) disease and may lead to new
    paradigms for developing and applying lifestyle, medical, and surgical therapeutic interventions.

    29.

    Regatte RR, Akella SV, Lonner JH, Kneeland JB, Reddy


    R: T1rho relaxation mapping in human osteoarthritis
    (OA) cartilage: Comparison of T1rho with T2. J Magn
    Reson Imaging 2006;23(4):547-553.

    30.

    Gineyts E, Garnero P, Delmas PD: Urinary excretion of


    glucosyl-galactosyl pyridinoline: A specific biochemical
    marker of synovium degradation. Rheumatology (Oxford) 2001;40(3):315-323.

    31.

    Garnero P, Aronstein WS, Cohen SB, et al: Relationships between biochemical markers of bone and carti-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 3: Articular Cartilage and Intervertebral Disk

    lage degradation with radiological progression in patients with knee osteoarthritis receiving risedronate: The
    Knee Osteoarthritis Structural Arthritis randomized
    clinical trial. Osteoarthritis Cartilage 2008;16(6):660666.
    This study (n = 2,483 patients) showed that urinary levels of CTX-II decreased with risedronate in patients
    with knee OA and levels reached after 6 months were
    associated with radiologic progression at 24 months.
    32.

    Chu Q, Lopez M, Hayashi K, et al: Elevation of a collagenase generated type II collagen neoepitope and proteoglycan epitopes in synovial fluid following induction
    of joint instability in the dog. Osteoarthritis Cartilage
    2002;10(8):662-669.
    Jordan KM, Syddall HE, Garnero P, et al: Urinary
    CTX-II and glucosyl-galactosyl-pyridinoline are associated with the presence and severity of radiographic knee
    osteoarthritis in men. Ann Rheum Dis 2006;65(7):871877.

    34.

    Jones P, Gardner L, Menage J, Williams GT, Roberts S:


    Intervertebral disc cells as competent phagocytes in vitro: Implications for cell death in disc degeneration. Arthritis Res Ther 2008;10(4):R86.
    Bovine intervertebral disk cells were competent phagocytes and worked as efficiently as dedicated phagocytes
    such as monocytes and macrophages in an in vitro
    model.

    35.

    36.

    37.

    Jnger S, Gantenbein-Ritter B, Lezuo P, Alini M, Ferguson SJ, Ito K: Effect of limited nutrition on in situ intervertebral disc cells under simulated-physiological
    loading. Spine (Phila Pa 1976) 2009;34(12):1264-1271.
    Glucose availability has implications to intervertebral
    disk cell viability in vitro. With limited availability, cell
    viability decreased and surviving cells did not compensate matrix production within the time frame studied.
    Arun R, Freeman BJ, Scammell BE, McNally DS, Cox
    E, Gowland P: 2009 ISSLS Prize Winner: What influence does sustained mechanical load have on diffusion
    in the human intervertebral disc? An in vivo study using
    serial postcontrast magnetic resonance imaging. Spine
    (Phila Pa 1976) 2009;34(21):2324-2337.
    Effects of sustained mechanical loading on transport of
    small solutes was investigated in vivo on normal human
    lumbar intervertebral disks using serial postcontrast
    MRI. The results suggested that supine creep loading
    (50% body weight) for 4.5 hours retards transport of
    small solutes into the center of human intervertebral
    disk, and it required 3 hours of accelerated diffusion in
    recovery state for loaded disks to catch up with diffusion in unloaded disks.
    Millward-Sadler SJ, Costello PW, Freemont AJ, Hoyland JA: Regulation of catabolic gene expression in normal and degenerate human intervertebral disc cells: Implications for the pathogenesis of intervertebral disc
    degeneration. Arthritis Res Ther 2009;11(3):R65.
    In vitro analysis of cells isolated from human IVDs indicated that TNF- may be an important initiating factor

    2011 American Academy of Orthopaedic Surgeons

    38.

    Iida R, Akeda K, Kasai Y, et al: Expression of


    proteinase-activated receptor-2 in the intervertebral
    disc. Spine (Phila Pa 1976) 2009;34(5):470-478.
    Proteinase-activated receptor-2 (PAR-2) is a G proteincoupled receptor identified in human intervertebral disk
    tissues. The expression of PAR-2 is regulated by IL-1
    stimulation. PAR-2 activation accelerates the expression
    of matrix-degrading enzymes. PAR-2 may play an important role in the cytokine-mediated catabolic cascade
    and consequently may be involved in intervertebral disk
    degeneration.

    39.

    Yoshida T, Park JS, Yokosuka K, et al: Up-regulation in


    receptor for advanced glycation end-products in inflammatory circumstances in bovine coccygeal intervertebral
    disc specimens in vitro. Spine (Phila Pa 1976) 2009;
    34(15):1544-1548.
    Employing a bovine coccygeal intervertebral disk model,
    the authors demonstrate that advanced glycation end
    products (AGEs) and receptors of AGE were localized
    within the bovine intervertebral disks. AGEs significantly
    decreased the aggrecan expression in bovine intervertebral disk as in human intervertebral disk, and the effect
    was enhanced further with the presence of IL-1.

    40.

    Sharp CA, Roberts S, Evans H, Brown SJ: Disc cell clusters in pathological human intervertebral discs are associated with increased stress protein immunostaining.
    Eur Spine J 2009;18(11):1587-1594.
    Based on increased expression of heat shock proteins
    hsp-27 and -72 in clustered cells of herniated disks, the
    authors suppose that clustered cells may be mounting a
    protective response to abnormal environmental factors
    associated with disk degeneration.

    41.

    Kaneyama S, Nishida K, Takada T, et al: Fas ligand expression on human nucleus pulposus cells decreases
    with disc degeneration processes. J Orthop Sci 2008;
    13(2):130-135.
    Human nucleus pulposus cells showed strong positive
    staining for FasL with a significant decrease in FasL expression in the degenerated group compared with the
    nondegenerated group indicating a potential mechanism
    of protection of the intervertebral disk against degeneration.

    42.

    Ali R, Le Maitre CL, Richardson SM, Hoyland JA,


    Freemont AJ: Connective tissue growth factor expression in human intervertebral disc: Implications for angiogenesis in intervertebral disc degeneration. Biotech
    Histochem 2008;83(5):239-245.
    Connective tissue growth factor plays a pivotal role in
    angiogenesis. Increased expression of connective tissue
    growth factordegenerated disks within areas of neovascularization may suggest their role in angiogenesis in the
    human degenerated intervertebral disk.

    43.

    Richardson SM, Knowles R, Tyler J, Mobasheri A,


    Hoyland JA: Expression of glucose transporters
    GLUT-1, GLUT-3, GLUT-9 and HIF-1alpha in normal
    and degenerate human intervertebral disc. Histochem
    Cell Biol 2008;129(4):503-511.

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    33.

    in matrix degeneration, IL-1 plays a greater role in established pathologic degradation.

    35

    Section 1: Principles of Orthopaedics

    degenerate human intervertebral disc. Arthritis Res Ther


    2009;11(2):R47.
    Human anulus fibrosus specimens were obtained from
    surgical subjects and control donors, and showed increased senescent cells with increasing grades of degeneration. A decreasing number of proliferative cells with
    increasing degeneration provides a rationale for increased incidence of degeneration with aging.

    Immunohistochemistry showed that human intervertebral disk cells express glucose transporters GLUT-1, -3
    and -9 in both the nucleus pulposus and anulus fibrosus
    with hypoxia inducible factor-1 co-expression only in
    the nucleus pulposus. GLUT expression also changed as
    degeneration progressed, suggesting metabolic changes
    with disease pathology.

    1: Principles of Orthopaedics

    44.

    45.

    46.

    47.

    48.

    36

    Heathfield SK, Le Maitre CL, Hoyland JA: Caveolin-1


    expression and stress-induced premature senescence in
    human intervertebral disc degeneration. Arthritis Res
    Ther 2008;10(4):R87.
    The expression of caveolin-1 in intervertebral disk tissue
    and its association with the senescent phenotype suggest
    that caveolin-1 and stress-induced premature senescence
    may play a prominent role in the pathogenesis of intervertebral disk degeneration.
    Gruber HE, Ingram JA, Davis DE, Hanley EN Jr: Increased cell senescence is associated with decreased cell
    proliferation in vivo in the degenerating human annulus. Spine J 2009;9(3):210-215.
    Asporin, also known as periodontal ligament-associated
    protein 1 (PLAP1), reported to have a genetic association with OA. Its D14 allele has recently been found to
    be associated with lumbar disk degeneration in patients
    of Asian descent. Immunohistochemical localization of
    asporin in the disk of Caucasian subjects and the sand
    rat showed that asporin was present in the outer anulus
    fibrosus, but not in the nucleus pulposus. Increased expression was observed in degenerated disks when compared to normal disks.
    Poveda L, Hottiger M, Boos N, Wuertz K: Peroxynitrite
    induces gene expression in intervertebral disc cells.
    Spine (Phila Pa 1976) 2009;34(11):1127-1133.
    Degenerated intervertebral disk tissue showed strong nitrosylation, especially in the nucleus pulposus. Isolated
    human nucleus pulposus cells showed a strong signal for
    nitrosylation and intracellular reactive oxygen species
    on stimulation with peroxynitrite or 3-morpholinosydnonimine (SIN-1), indicating that neutralizing peroxynitrite and its derivatives (for example, via the use of
    antioxidants) may be a novel treatment option for discogenic back pain.
    Videman T, Saarela J, Kaprio J, et al: Associations of 25
    structural, degradative, and inflammatory candidate
    genes with lumbar disc desiccation, bulging, and height
    narrowing. Arthritis Rheum 2009;60(2):470-481.
    The authors investigated associations of 99 genetic variants with quantitative magnetic resonance imaging measurements. Twelve of the 99 variants in 25 selected candidate genes provided evidence of association (P < 0.05)
    with disk signal intensity in the upper and/or lower lumbar regions. AGC1, COL1A1, COL9A1, and
    COL11A2 genes provided the most significant evidence
    of association with disk signal intensity, suggesting that
    genetic variants account for interindividual differences
    in disk matrix synthesis and degradation.
    Gruber HE, Ingram JA, Hoelscher GL, Zinchenko N,
    Hanley EN Jr, Sun Y: Asporin, a susceptibility gene in
    osteoarthritis, is expressed at higher levels in the more

    Orthopaedic Knowledge Update 10

    49.

    Wuertz K, Godburn K, MacLean JJ, et al: In vivo remodeling of intervertebral discs in response to shortand long-term dynamic compression. J Orthop Res
    2009;27(9):1235-1242.
    The authors demonstrate that in vivo dynamic compression maintains or promotes matrix biosynthesis without
    substantially disrupting disk structural integrity. Static
    compression, bending, or other interventions created
    greater structural disruption.

    50.

    Meir A, McNally DS, Fairbank JC, Jones D, Urban JP:


    The internal pressure and stress environment of the scoliotic intervertebral disca review. Proc Inst Mech Eng
    H 2008;222(2):209-219.
    With pressure profilometry, which provides stress profiles across the disk in mutually perpendicular axes, the
    authors show that abnormalities in high hydrostatic
    pressure profiles could influence both disk and end plate
    cellular activity directly, causing asymmetric growth and
    matrix changes.

    51.

    Michalek AJ, Buckley MR, Bonassar LJ, Cohen I,


    Iatridis JC: Measurement of local strains in intervertebral disc anulus fibrosus tissue under dynamic shear:
    Contributions of matrix fiber orientation and elastin
    content. J Biomech 2009;42(14):2279-2285.
    Alterations in the elastic fiber network, as found with
    intervertebral disk herniation and degeneration, can significantly influence the anulus fibrosus response to shear
    loading, making it more susceptible to micro failure under bending or torsion loading.

    52.

    Yang F, Leung VY, Luk KD, Chan D, Cheung KM:


    Injury-induced sequential transformation of notochordal nucleus pulposus to chondrogenic and fibrocartilaginous phenotype in the mouse. J Pathol 2009;
    218(1):113-121.
    This study is the first to use an injury-induced model to
    study disk degeneration in mouse. The disk degeneration induced using a needle puncture involves a transient transformation of nucleus pulposus from notochordal to chondrogenic and eventually into
    fibrocartilaginous phenotype, suggesting its relevance to
    human intervertebral disk pathology.

    53.

    Lotz JC, Hadi T, Bratton C, Reiser KM, Hsieh AH: Anulus fibrosus tension inhibits degenerative structural
    changes in lamellar collagen. Eur Spine J 2008;17(9):
    1149-1159.
    Annular tension is beneficial to maintain healthy lamellar appearance. Cell-mediated events and cellindependent mechanisms may contribute to the protective effect of tissue level tension in the anulus fibrosus.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 4

    Muscle, Tendon, and Ligament


    Lawrence V. Gulotta, MD

    Scott A. Rodeo, MD

    Skeletal Muscle
    The human body contains more than 400 skeletal muscles that comprise approximately 40% to 50% of the
    total body weight. Skeletal muscle serves to produce
    the force required for locomotion, breathing, and postural support as well as heat production during cold
    stress. As with most tissues, its structure is highly organized and accounts for its function. An appreciation of
    the structure and physiology of skeletal muscle is important because it serves as the foundation for understanding exercise physiology and muscle injuries.
    All muscles have a fibrous connective tissue network
    within and around the muscle that is important for
    overall function (Figure 1). Tendons originate from
    within the muscle, or from its surface, and provide a
    wide area for the attachment of muscle fibers. The
    epimysium is connective tissue that surrounds the entire
    muscle. This divides the muscle from the surrounding
    tissues and allows it to glide freely. The perimysium
    surrounds bundles of muscle fibers, called fascicles, and
    the endomysium surrounds each individual muscle fiber. This framework is continuous within the muscle
    and attaches to the tendon to increase the efficiency of
    movement.
    The microstructure of skeletal muscle is complex
    and accounts for the muscles ability to contract. During development, many muscle cells, called myoblasts,
    fuse to form myofibrils. Because myofibrils are not
    made up of a single cell, the nomenclature and structure is different than that of a normal cell. As such, the
    plasma membrane is referred to as the sarcolemma, the
    endoplasmic reticulum as the sarcoplasmic reticulum,
    the mitochondria as the sarcosome, and the cytoplasm
    as the sarcoplasm. Additionally, myofibrils are made up
    of many nuclei. Each myofibril is made up of arrays of
    parallel filaments. The thick filaments are composed of
    the protein myosin. Thin filaments are primarily composed of the proteins actin, troponin, and tropomyosin.

    Dr. Rodeo or an immediate family member serves as a


    paid consultant to or is an employee of Wyeth. Neither
    Dr. Gulotta nor an immediate family member has received anything of value from or owns stock in a commercial company or institution related directly or indirectly to the subject of this chapter.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    Structure and Function

    The characteristic striations of skeletal muscle seen


    with microscopy are the result of alternating light and
    dark bands of the myofibril. The light band, called the I
    band, is made up of thin filaments. The dark band,
    called the A band, is made up of thick filaments.
    Sarcomeres are the repeating subunit of a myofibril
    and are considered the smallest contractile unit of muscle. Perpendicular protein plates, called Z lines, form
    the boundaries of a sarcomere. From these Z lines, thin
    filaments extend inward toward the center of the sarcomere where they partially overlap with the thick filaments. M line proteins attach the thick myosin filaments to each other that aid in filament stabilization.
    Actin proteins have binding sites for a myosin crossbridge, or head. When a muscle fiber is at rest, the myosin binding sites are covered by tropomyosin proteins.
    These proteins are associated with troponin, another
    regulatory protein. When calcium is released from the
    sarcoplasmic reticulum in response to an action potential, it binds to troponin, causing tropomyosin to move
    away from the myosin binding site. This allows myosin
    to bind to actin at the expense of an adenosine triphosphate (ATP) molecule. Once bound to actin, the myosin
    head swivels and pulls the actin filament toward it, resulting in a contraction. During this process, the distance between Z lines is decreased. This process is referred to as the sliding filament model of muscle
    contraction.1
    The signal for skeletal muscle contraction originates
    from nerves at the motor end plate. The end plate is a
    pocket of sarcolemma that forms around the motor
    neuron. The number of nerve fibers controlled by a single motor end plate is highly variable. Muscle contraction is initiated when acetylcholine is released from the
    motor neuron resulting in an end-plate action potential
    that spreads along the surface membrane (sarcolemma)
    and the transverse tubular system (T tubules) until it
    reaches the sarcoplasmic reticulum. Once stimulated by
    the action potential, the sarcoplasmic reticulum releases
    the calcium, initiating a contraction as outlined above.
    The greater the number of actin-myosin crossbridges
    that form, the greater the force of the contraction.
    Therefore, the peak force a muscle can generate is directly related to the physiologic cross-sectional area of
    all the fibers.
    Muscle is made up of various types of fibers that
    have different functional properties, peak forces, contraction velocities, resistances to fatigue, and oxidative
    and glycolytic capacities. These fiber types can be
    37

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 1

    Schematic drawing of the structure of skeletal muscle. The endomysium is the connective tissue layer that surrounds
    the individual myofibers. The perimysium surrounds fascicles of myofibers. The epimysium is the outermost connective tissue layer that surrounds the entire muscle. When muscle is injured, satellite cells differentiate into myoblasts
    and then into differentiated myotubes and finally into mature myofibers. The histologic panels show the central
    location of nuclei in the immature or regenerating myotubes, but migrate to the periphery of the myofiber as it
    matures. (Reproduced from Beason DP, Soslowski LJ, Karthikeyan T, Huard J: Muscle, tendon, and ligament, in Fischgrund JS, ed: Orthopaedic Knowledge Update 9. Rosemont, IL. American Academy of Orthopaedic Surgeons, 2008,
    pp 35-48.)

    broadly characterized into two major classes, fast


    twitch and slow twitch (Table 1). Slow-twitch fibers are
    also called type I fibers. They have a slow contraction
    velocity but are relatively fatigue resistant. They have
    long twitch times, low peak forces, a high concentration of oxidative enzymes and myoglobin, and a low
    concentration of glycolytic markers. Their high oxidative capacity makes them appear red under the microscope. Type I fibers are used for aerobic activities requiring low-level force production, such as walking or
    maintaining posture. Fast-twitch fibers are also called
    type II fibers. They have a fast contraction velocity due
    to a faster rate of calcium release from the sarcoplasmic
    reticulum and higher levels of myosin ATPase. Type II
    fibers can be further subclassified into two groups.
    38

    Orthopaedic Knowledge Update 10

    Table 1

    The Three Main Types of Myofibers and Their


    Characteristics
    Fiber Type

    Contraction
    Velocity

    Fatigue Resistance

    Type I

    Slow

    Greatest

    Type II A

    Fast

    Intermediate

    Type II B

    Fast

    Least

    2011 American Academy of Orthopaedic Surgeons

    Chapter 4: Muscle, Tendon, and Ligament

    Muscle Injury and Repair


    Muscles can be injured by direct trauma, disease, medications, ischemia, and certain exercises, most notably
    ones that require eccentric contraction. Muscles that
    span two joints, such as the hamstrings and gastrocnemius, are particularly susceptible to injury. These injuries most commonly occur at the musculotendinous
    junction or the tendon-bone junction. Regardless of the
    insult, the muscles response to injury can be broken
    down into four phases: necrosis, inflammation, repair,
    and fibrosis2 (Figure 2). In the first phase, necrosis and
    degeneration of myofibrils occur due to breakdown of
    the sarcolemma, causing an ingress of calcium that results in fiber death. The injury site is then invaded by
    inflammatory cells, notably macrophages and T lymphocytes, that phagocytose and remove the debris created during the first phase. The inflammatory cells secrete growth factors and cytokines that promote
    vascularity and the migration of more inflammatory
    mediators. Muscle regeneration does not occur until
    phagocytic cells have cleared the necrotic debris. Blunting the inflammatory response (such as with nonsteroidal anti-inflammatory drugs [NSAIDs]) may have a
    detrimental effect on muscle healing by reducing the
    amount of growth factors secreted by macrophages.3-5
    These growth factors are thought to promote myoblast
    proliferation and regeneration and are essential for

    2011 American Academy of Orthopaedic Surgeons

    muscle healing. Muscle regeneration begins within 7 to


    10 days from the time of injury, peaks at 2 weeks, and
    declines after 3 to 4 weeks. This process is mediated by
    several trophic substances such as insulin growth
    factor-I (IGF-I), basic fibroblast growth factor (bFGF),
    and nerve growth factor (NGF), that are released by
    the injured cells and stimulate differentiation, proliferation, and fusion of myoblasts from the satellite cells
    located between the basal lamina and the plasma membrane of individual myofibrils. At the same time as regeneration, fibrosis also occurs. Fibrosis has been
    shown to occur in the presence of transforming growth
    factor1 (TGF-1). TGF-1 promotes differentiation
    and proliferation of myofibroblasts that in turn produce abundant amounts of types I and III collagen.
    During the repair process, muscle regeneration and fibrosis compete for muscle area. Unfortunately, scar tissue, which has inferior mechanical and contractile
    properties than that of normal tissue, is usually predominant.
    A few circumstances of muscle injury deserve special
    attention. Muscle lacerations heal by dense scar formation and no muscle regenerates across the injured tissue.6 Therefore, functional continuity is not restored
    and the muscle lacks the ability to produce tension.
    Muscle contusions, which are often seen in contact
    sports, result in hematoma formation and inflammation. A potential complication of muscle contusions is
    myositis ossificans, or the calcification or ossification
    of tissue at the site of injury.7 The pathogenesis is
    poorly understood, but may involve release of osteoblastic growth factors in the presence of muscle-derived
    stem cells. A major risk for the development of myositis
    ossificans is reinjury in the early stages of recovery. A
    third type of muscular injury is the fatty degeneration
    that occurs following tendon detachment, as seen in
    chronic rotator cuff tears. The exact cause is not fully
    appreciated, but one hypothesis is that this is caused by
    an increase in the space between muscle fibers that allows fat to form.8 Regardless of the cause, fatty degeneration makes the muscle-tendon unit less compliant,
    thereby putting tension on repairs. This increased tension is thought to make repairs prone to failure.

    1: Principles of Orthopaedics

    Type IIA fibers have a fast contraction velocity and are


    moderately fatigue resistant. These fibers represent a
    transition between the slow type I fibers and the type
    IIB fibers. They are used for prolonged anaerobic activities with relatively high force output, such as a 400-m
    run. Type IIB fibers also have a fast contraction velocity, but they have low fatigue resistance. They are used
    for short, anaerobic, high-force production activities
    such as sprinting or lifting weights. Most muscles contain a combination of these fibers.
    Muscles do not necessarily have to shorten to generate a force. Eccentric contractions occur when the muscle fibers lengthen as the muscle contracts. This occurs
    when the force generated by the muscle is not enough
    to overcome the external load. This type of contraction
    puts the most stress on muscles and is the most common mechanism for muscular and tendinous injuries.
    Isometric contractions, also called static contractions,
    occur when the muscle does not change length. In this
    case, the force generated by the muscle is equivalent to
    the external load. Isotonic contractions occur when the
    tension in the muscle remains constant despite a change
    in muscle length. This can occur only when a muscles
    maximal force of contraction exceeds the total load on
    the muscle (the weight lifted). An isokinetic contraction
    occurs when there is a constant force applied through a
    full range of motion. Because velocity does not change
    during this contraction, kinetic energy remains constant. Muscles also undergo concentric contraction in
    which the muscle shortens as it contracts. In this case,
    the force generated by the muscle is greater than the external load.

    New Developments in the


    Treatment of Muscle Injuries
    The mainstay of treatment of most muscular injuries is
    rest, ice, compression, elevation, NSAIDs, and mobilization. However, healing occurs slowly and is often incomplete. Therapies that can augment the healing process and drive it toward regeneration and away from
    scar formation would improve functional outcomes.2,9
    Strategies to achieve these goals can be broadly
    grouped according to those that limit fibrosis and those
    that promote regeneration.
    Antifibrotic agents such as decorin,10 relaxin,11 interferon,12 and the antiparasitic drug suramin13 have all
    been shown to limit the amount of fibrosis associated
    with muscle healing by inhibiting TGF-1. However,

    Orthopaedic Knowledge Update 10

    39

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 2

    Summary of biologic strategies to improve muscle healing. Following the initial injury, inflammation occurs. This appears to be a crucial step because NSAIDs appear to inhibit healing. Various growth factors such as IGF-1, bFGF, and
    NGF may play a role in enhancing regeneration. Following inflammation and regeneration, TGF-1 is released that
    induces fibrosis. Antifibrotic factors such as decorin, relaxin, suramin, and -interferon (-IFN) may inhibit TGF-1,
    thereby limiting fibrosis and improving the healing process. (Reproduced from Beason DP, Soslowski LJ, Karthikeyan
    T, Huard J: Muscle, tendon, and ligament, in Fischgrund JS, ed: Orthopaedic Knowledge Update 9. Rosemont, IL.
    American Academy of Orthopaedic Surgeons, 2008, pp 35-48.)

    these studies have only been conducted in animal models, and each of these agents has technical obstacles or
    severe adverse effects that would make their application to human patients difficult. Interestingly, the antihypertensive agent losartan has been shown to have
    significant antifibrotic effects. Losartan is a widely used
    angiotensin II receptor blocker (ARB) that also inhibits
    TGF-1mediated fibrosis in vitro and in vivo. One
    mouse study showed that the administration of losartan immediately following gastrocnemius laceration resulted in a dose-dependent increase in the number of
    regenerating myofibers and a decrease in fibrosis compared to controls at 3 and 5 weeks.14 Although these
    basic science studies are encouraging, trials in human
    patients are needed to recommend them for the augmentation of muscle healing and repair.
    Exogenously administered growth factors and stem
    cells may be able to promote muscle regeneration.
    IGF-I and bFGF have both been shown to increase the
    40

    Orthopaedic Knowledge Update 10

    number and diameter of regenerating myofibers in a


    mouse gastrocnemius laceration model.15 Musclederived stem cells (MDSCs) are multipotent stem cells
    found between the basal lamina and sarcolemma that
    are able to double 300 times before becoming senescent
    (compared with embryonic stem cells that double 130
    to 250 times).9 For these reasons, they provide great
    promise for muscle regeneration. Applications to the
    musculoskeletal system have been limited to animal
    models that have shown improved muscle quality when
    administered in models with Duchenne muscular dystrophy, and better muscle integrity when given in an ischemia model.16 Clinical studies using MDSCs have
    shown that they can improve the symptoms of urinary
    stress incontinence when implanted in the detrusor
    muscle in a small group of women.17 Future studies will
    focus on bioengineered scaffolds that are either impregnated with MDSCs, or with factors that are capable of
    recruiting host MDSCs. Furthermore, these cells can be

    2011 American Academy of Orthopaedic Surgeons

    Chapter 4: Muscle, Tendon, and Ligament

    genetically modified to overexpress growth factors at


    the healing site.

    Tendon and Ligament

    Structure and Function

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    In the simplest sense, tendons are the connective tissue


    structures that serve to transmit force from skeletal
    muscle to bone whereas ligaments connect one bone to
    another. However, their function is much more complex. Ligaments help guide the three-dimensional motion of the bones during joint function and therefore
    carry loads during daily activities. An understanding of
    the structure and composition of these materials is important to understanding their function. Both are primarily composed of water and type I collagen, as well
    as elastin, lipids, and several types of proteoglycans.
    Proteoglycans are negatively charged and attract water
    into the structure. The accumulation of water into the
    tissue largely accounts for its rate-dependent response
    to load, or viscoelasticity. 18 However, recent evidence
    suggests that viscoelasticity is also dependent on the
    cross-sectional area of the tissue tested, whereas smaller
    diameter tissues exhibit a higher tensile modulus, a
    slower rate of relaxation, and a lower amount of relaxation in comparison to larger specimens.19 The exact
    reason for this is uncertain.
    Although both are similar in terms of their structure
    and biomechanical properties, differences between tendons and ligaments do exist. Tendons contain less elastin than ligaments. Although most ligaments contain
    little elastin, some, like the ligamentum flava in the
    spine, have a relatively high content. However, the exact elastin content in most ligaments is unknown as is
    its exact function within the tissue. Ligaments also contain relatively less proteoglycan matrix than tendons.
    Tendons are also composed primarily of densely packed
    collagen fibrils in cords, whereas the collagen fibrils in
    ligaments are slightly less in volume fraction and are
    less organized.
    Tendons also differ from ligaments in that they are
    surrounded by a synovial-like membrane called the epitenon. The epitenon contains lymphatic vessels, blood
    vessels, and nerves. Some tendons have a loose areolar
    tissue around the epitenon called the paratenon,
    whereas in other tendons the paratenon is replaced by a
    bursa that is lined with synovial cells. Tendons receive
    nutrition through several sources such as the perimysium, periosteal attachments, and surrounding tissues.
    There is a distinction between vascular and relatively
    avascular tendons. Vascular tendons receive their blood
    supply directly from the vessels that run in their surrounding paratenon. Relatively avascular tendons are
    contained in tendinous sheaths and receive nutrition
    from vascular mesotenons called vincula. In addition to
    the vincula, these tendons receive blood from the musculotendinous and tendon-bone junctions. Tendons can
    also receive nutrition through diffusion from synovial
    fluid. Tendons that are intrasynovial, such as the flexor

    tendons of the hand, have different characteristics than


    those that are extrasynovial, such as the peroneal tendons around the ankle. Intrasynoval tendons are dependent on nutrition from the synovial fluid, and their
    ability to proliferate and remain metabolically active is
    decreased when removed from that environment. Extrasynovial tendons, on the other hand, are able to remain metabolically viable regardless of their environment.20 Exactly what accounts for these differences is
    not known at this time.
    The exact manner in which ligaments receive their
    nutrition is uncertain because most ligaments have not
    been studied. Some ligaments receive a direct supply
    from an artery, such as the anterior cruciate ligament
    (ACL), that receives nutrients from the middle geniculate artery. Most ligaments have an epiligament coat
    that is analogous to the epitenon seen in tendons. Ligaments that do not have an epiligament are usually surrounded by synovium, such as the ACL. It is thought
    that ligaments receive much of the nutrients needed
    from these surrounding structures.
    Tendon and ligament insertions into bone can be
    classified as being either indirect (or fibrous) or direct
    (or fibrocartilaginous). In indirect insertion sites, the
    collagen fibers of the tendon or ligament enter the bone
    through perforating collagen fibers (called Sharpey fibers) that are oriented perpendicular to the bone. At
    the insertion, the endotenon becomes continuous with
    the periosteum. An example of an indirect insertion site
    is the distal insertion of the medial collateral ligament
    (MCL) of the knee onto the proximal tibia. In direct insertion sites, the tendon enters bone through a highly
    organized fibrocartilaginous transition zone that consists of four layers: tendon, unmineralized fibrocartilage, mineralized fibrocartilage, and bone. This structure allows force to be dissipated gradually as it passes
    from the tendon to the bone. An example of a direct insertion site is the proximal insertion of the MCL on the
    distal femur.
    The molecular structure of tendons and ligaments is
    largely responsible for their biomechanical function of
    load transmission, as well as their characteristic response to tensile testing in the laboratory. Tendons
    have a stress-strain relationship similar but not identical to ligaments. They exhibit time-dependent, nonlinear viscoelastic properties such as stress relaxation (decreased stress with time under constant deformation)
    and creep (increased deformation with time under a
    constant load). Another characteristic of a viscoelastic
    tissue that is exhibited by ligaments and tendons is hysteresis, or energy dissipation. This means that when tissues are loaded and unloaded, the unloading curve will
    not follow the loading curve where the difference between the two curves is the energy that is dissipated
    during loading.
    Structural properties of the tissue can be determined
    by studying the load-elongation curve. Tensile testing
    reveals four distinct regions on the graph that correspond to the molecular structure of the ligament (Figure 3). The first region is the toe region, in which there
    is significant deformation for a given load. In the toe
    41

    Section 1: Principles of Orthopaedics

    vivo is unclear. This is especially true for ligaments that


    are composed of different bundles that take up load in
    various joint positions, such as the ACL and the posterior cruciate ligaments. These physiologic characteristics are important for understanding injury patterns, diagnosis, and surgical reconstruction.

    Tendon Injury and Repair

    1: Principles of Orthopaedics

    Figure 3

    Typical load-elongation curve for biomechanical


    testing of a tendon/ligament. This outlines the
    toe, linear, and yield/failure regions. (Reproduced
    from Beason DP, Soslowski LJ, Karthikeyan T,
    Huard J: Muscle, tendon, and ligament, in Fischgrund JS, ed: Orthopaedic Knowledge Update 9.
    Rosemont, IL. American Academy of Orthopaedic
    Surgeons, 2008, pp 35-48.)

    region, the crimped and relaxed fibers of the ligament


    are straightened and oriented to take up load. The second region is the linear region, in which the fibers are
    oriented longitudinal and parallel to the direction of
    the load. In this region, there is constant loadelongation behavior, and the tissue stiffness is represented by the slope of the load-elongation curve. The final region is nonlinear and begins at the yield point,
    which is the point where the tendon transitions from
    elastic (reversible) into plastic (irreversible) deformation. The final area of the curve is the ultimate failure
    of the tendon and is heralded by a steep decline in the
    load-deformation curve.
    The material properties of the tendon are represented by the stress-strain curve. The stress on the tissue is the force per unit area, whereas strain is the
    change in length relative to the original length. The
    slope of the linear portion of this curve is the Young
    modulus of elasticity. The material properties of repaired ligaments and tendons are important because
    they signify how strong the actual tissue is. Many biologic therapies that have been investigated for their
    ability to improve the strength of repairs result in improved structural properties. They do this by promoting the formation of more scar tissue. However, an
    analysis of the material properties shows that this tissue
    has inferior quality.
    Differences between tendons and ligaments can be
    seen in their stress-strain behavior, which depends on
    their exact physiologic roles. Tendons carry higher
    loads and thus recruit fibers much more quickly; therefore, they have a smaller toe region. Ligaments, on
    the other hand, have a longer toe region in uniaxial
    testing because their fibers have more of a wavy,
    crimped pattern and are recruited more gradually. Although uniaxial testing in vitro can determine some of
    the characteristics of ligaments, how they respond in
    42

    Orthopaedic Knowledge Update 10

    Tendon ruptures or lacerations can be divided into


    those that require tendon-tendon healing, such as
    flexor tendon repairs in the hand, and those that require tendon-bone healing, such as rotator cuff repairs.
    Similar to muscle, both types of healing follow the
    stages of inflammation, cellular proliferation, matrix
    formation, and remodeling. During the inflammatory
    phase, there is an influx of neutrophils and macrophages into the zone of injury. During this phase, there
    is abundant production of type III collagen that is replaced over the course of a few weeks with type I collagen. Tendons are thought to be weakest between 5 to
    21 days following repair that correlates with the inflammatory stage. Inflammatory cells and platelets then
    release several growth factors, such as TGF-1, IGF,
    platelet-derived growth factor (PDGF), bone morphogenetic proteins (BMPs)-12 and -13, and bFGF, and
    IGF-1, for example.21 These factors promote the differentiation and proliferation of fibroblasts that begin the
    reparative process. During this phase, there is a noticeable increase in cellularity and vascularity. In the final
    stage, remodeling, cellularity decreases and fibrosis ensues. The tissue continues to remodel over the course of
    1 year or longer, but at its conclusion the tissue never
    assumes the preinjury appearance. In tendon-bone healing, the bone grows into the fibrovascular scar tissue
    over time.22 This bone ingrowth coincides with significant increases in the strength of the healing tendon attachment. Tendons and ligaments heal with persistent
    scar tissue at the repair site that limits the ultimate
    strength of the repair and causes adhesions.
    There is a fine balance between limiting load across
    the repair to allow healing to occur and encouraging
    motion to limit adhesions and fibrosis and enhance the
    remodeling phase of healing. Studies have shown that
    stress deprivation of tendons results in increases in cellular apoptosis and the presence of matrix-degrading
    enzymes.23,24 Immobilization has also been shown to
    decrease the release of growth factors such as bFGF,
    NGF, and IGF-125 and decrease the expression of genes
    associated with tendon regeneration such as procollagen I, cartilage oligomeric matrix protein, tenascin-C,
    tenomodulin, and scleraxis.26 Some amount of load is
    clearly beneficial during the healing process. These basic science studies support the early initiation of gentle
    range of motion following tendon repairs. However,
    the amount and timing of application of load that is
    beneficial before becoming detrimental has yet to be
    determined.
    Several clinically relevant factors have also been
    shown to influence tendon and ligament healing. Smoking; NSAIDs such as indocin, celecoxib, and parecoxib;

    2011 American Academy of Orthopaedic Surgeons

    Chapter 4: Muscle, Tendon, and Ligament

    Figure 4

    diabetes; and ethanol intake all have led to adverse effects on healing following rotator cuff repairs in
    rats.27-32 The effects these factors have in patients remains to be seen.

    New Developments in the Treatment of Tendon


    and Ligament Injuries
    Several biologic strategies have been used in the laboratory to augment tendon and ligament healing. These
    strategies include those that limit inflammation and fibrosis and those that promote regeneration33 (Figure 4).
    Several studies have shown that blunting the immune
    response can actually improve tendon healing. Knockout mice for CD44, a surface receptor crucial for lymphocyte activation, experienced better healing after patellar tendon injury.34 Interleukin-10 (IL-10) is a potent
    anti-inflammatory cytokine that has been shown to improve healing when applied through lentivirus to injured patellar tendons.35 The depletion of macrophages,
    the main source for the profibrotic growth factor TGF1, resulted in improved tendon-bone healing in a rat
    ACL model.36 IL-1 is another inflammatory mediator
    present in healing tendons and ligaments. Its blockade
    with an IL-1 receptor antagonist inhibited the deterioration of mechanical properties of stress-shielded patellar tendons in a rabbit model.37 Although it appears
    that blunting of the inflammatory response may be
    beneficial for healing, it is unclear what role this strategy will play in the treatment of patients who undergo
    tendon or ligament repairs.
    Regenerative strategies have focused on the use of
    mesenchymal stem cells (MSCs) to promote healing.
    MSCs are pluripotent cells that differentiate into muscle, adipose, tendon, ligament, bone and cartilage tissues. Studies have shown that bone, marrowderived

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    The stages of tendon and ligament healing involve


    inflammation, repair, and remodeling. Growth
    factors are expressed during the repair phase
    because they promote cell proliferation and matrix production. This timeline must be kept in
    mind in growth factor therapies because the addition of growth factors too early or late in the
    healing process may decrease their effectiveness.
    (Reproduced with permission from Gulotta L, Rodeo S: Growth factors for rotator cuff repair. Clin
    Sports Med 2009;28(1):13-23. http://www.science
    direct.com/science/journal/02785919.)

    MSCs can improve healing of a tendon graft in a bone


    tunnel in rabbit and rat models based on the improved
    formation of the fibrocartilaginous transition zone with
    histology.38-40 Another study showed that MSCs were
    able to promote healing of partial tears of the superficial digital flexor tendons of racehorses based on ultrasound evaluation of the tendons.41 Although MSCs
    may improve tendon healing in a bone tunnel and
    tendon-tendon healing, these positive findings were not
    found in a rat model of rotator cuff repair.42 For this instance, in which the repair site has relatively little
    tendon-bone surface area and is exposed to high shear
    stresses, MSCs alone may be insufficient. A signal, by
    way of a growth or differentiation factor, is most likely
    needed to maximize the effect.
    Several growth factors have been evaluated for their
    ability to augment tendon and ligament healing. In an
    animal model of flexor tendon repair, PDGF-BB delivered in a fibrin/heparin-based carrier was able to increase cellular proliferation and activity and limit adhesions.43 However, no improvement in tensile strength
    was observed. Granulocyte colony-stimulating factor
    improved tendon incorporation into a bone tunnel in a
    dog model for ACL reconstruction.44 BMPs-2 and -12
    have also shown improved healing in animal rotator
    cuff repair models based on structural biomechanical
    properties.45,46 Although the application of various
    growth factors has shown improvements in the structural properties of the repairs, it has been difficult to
    demonstrate an increase in the material properties.
    These growth factors are already present during the
    normal healing process that results in fibrosis.33 Therefore, it stands to reason that the exogenous application
    of more growth factors will result in more fibrosis. Although an increase in fibrosis does provide greater mechanical strength, it comes at the hypothetical price of
    increased adhesions and impingement. Therapies that
    exploit the biology of tendon and ligament development during embryogenesis may provide the best hope
    of promoting regeneration of the repaired tissue. However, research into this field is still in its infancy.
    It appears that some combination of progenitor cells
    and growth or differentiation factors will be required
    to augment tendon and ligament repairs. Even when
    the proper combination is determined, there will be a
    challenge to deliver them to the repair site. Several scaffolds are currently being investigated that are designed
    to allow cell seeding and sustained-release growth factor delivery. One such scaffold has been used to promote primary ACL healing. The ACL has very little capacity to heal itself, which is why ligament
    reconstruction is the mainstay of treatment. Factors
    that prohibit healing are a lack of formation of a blood
    clot at the rupture site to serve as a scaffold for repair
    and its intra-articular location that contains several
    matrix-degrading enzymes. Research on primary ACL
    repair has focused on applying a scaffold with similar
    characteristics to the fibrin clot that normally forms to
    promote healing elsewhere in the body.47 The leading
    scaffold is a collagenplatelet-rich plasma hydrogel.
    Platelets release more than 20 known cytokines in a se43

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    quential fashion to promote healing. The collagen in


    the system stimulates platelets.48 Studies on the use of
    this scaffold in a porcine ACL transection model have
    shown encouraging results.49 Although the scaffoldenhanced repairs showed improved healing over suture
    repair alone, the final results were far from native ACL
    strength.
    An interesting new area of research into tendon and
    ligament healing has focused on the role of neuropeptides. Denervation degrades tendons and ligaments and
    impairs ligament healing.50 In vitro studies have shown
    that the application of neuropeptides such as substance
    P, neuropeptide Y, and calcitonin gene-related peptide
    to cultured fibroblasts increased the expression of several inflammatory mediators that may be responsible
    for initiating the healing cascade.51 Other studies have
    found that calcitonin gene-related peptide can improve
    healing in a medial collateral ligament transection
    model in a rabbit.52 The role and extent to which these
    neuropeptides play in tendon and ligament healing has
    yet to be determined.

    Tendinopathy
    In patients with chronic tendon pain, the pathology is
    usually secondary to a degenerative process caused in
    part by diminished blood flow, though the exact mechanism is still unknown. A recent study has shown evidence that microscopic collagen fiber failure may lead
    to local stress deprivation that causes the upregulation
    of catabolic matrix metalloproteinases (MMPs).53 Regardless of the cause, the formation of free radicals
    causes cellular apoptosis and the further release of
    MMPs. Histologic studies have shown the primary pathology is not inflammation. Instead of inflammatory
    cells, samples of diseased tendons show collagen degeneration, fiber disorientation, mucoid ground substance,
    hypercellularity, vascular ingrowth, and relative absence of inflammatory cells under light microscopy.
    Therefore, the terms tendinopathy or tendinosis have
    replaced tendinitis. The term angiofibroblastic hyperplasia has been used to refer to the hypercellularity and
    vascular ingrowth that is seen in biopsy specimens.
    The mainstay of treatment of tendinopathy is
    NSAIDs and physical therapy.54 Physical therapy
    should focus on controlled exercise with eccentric loading. Corticosteroid injections are another popular treatment option. However, studies have shown that steroid
    injections can decrease tenocyte proliferation, increase
    the amount of type III collagen present, and decrease
    the mechanical strength of the tendon.55,56 Although
    they remain a relatively safe and effective treatment,
    their use should be minimized whenever possible, as
    there are currently few data to support corticosteroid
    injection for tendinopathy. Other treatments such as nitric oxide patches,57 shock wave therapy,58,59 the MMP
    inhibitor aprotinin,60 and platelet-rich plasma injections61,62 have all been investigated and give inconsistent results. Clearly, further study is required in this
    area.
    44

    Orthopaedic Knowledge Update 10

    Summary
    Muscles, tendons, and ligaments are soft-tissue structures that work in concert to promote locomotion.
    Skeletal muscle is a complex tissue in which the macrostructures and microstructures reflect its specialized
    function. Tendons and ligaments are also specialized
    structures that are capable of withstanding high tensile
    loads from the muscle to the bone or from one bone to
    another, respectively. The microscopic structure of tendons and ligaments explains its response to tensile
    loading in the laboratory. All three tissues have a very
    similar response to injury. They undergo a period of degeneration and inflammation, followed by cell proliferation and matrix synthesis, remodeling, and fibrosis.
    Unfortunately, the end result of the healing process is
    predominated by fibrosis that makes the tissue weaker
    and less functional. Therapies that can promote the regeneration of the native tissue and limit the inflammation and resulting fibrosis would have a profound effect
    on the treatment of these injuries. In addition to determining the correct combination of cells and signals required to improve healing, the challenge of delivering
    them to the repair site remains. Bioengineered scaffolds
    are currently being designed to achieve this goal. However, most of the research on muscle, tendon, and ligament augmentation remains in the laboratory, with
    clinical application still years away.

    Annotated References
    1.

    Huxley AF: The origin of force in skeletal muscle. Ciba


    Found Symp 1975;31:271-290.

    2.

    Huard J: Regenerative medicine based on muscle stem


    cells. J Musculoskelet Neuronal Interact 2008;8(4):337.
    This is a review paper that outlines research into the use
    of muscle stem cells and future directions.

    3.

    Shen W, Prisk V, Li Y, Foster W, Huard J: Inhibited


    skeletal muscle healing in cyclooxygenase-2 genedeficient mice: The role of PGE2 and PGF2alpha. J
    Appl Physiol 2006;101(4):1215-1221.

    4.

    Shen W, Li Y, Zhu J, Schwendener R, Huard J: Interaction between macrophages, TGF-beta1, and the COX-2
    pathway during the inflammatory phase of skeletal
    muscle healing after injury. J Cell Physiol 2008;214(2):
    405-412.
    This study showed that macrophage depletion in a muscle injury model was detrimental to healing, thereby indicating a role for macrophages in the healing process.
    Furthermore, it showed that prostaglandin-E2 can inhibit the expression of TGF-1 and limit that amount of
    fibrosis. This implies that NSAIDs may be detrimental
    to muscle healing by increasing the amount TGF-1 and
    resulting fibrosis.

    5.

    Shen W, Li Y, Tang Y, Cummins J, Huard J: NS-398, a


    cyclooxygenase-2-specific inhibitor, delays skeletal mus-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 4: Muscle, Tendon, and Ligament

    cle healing by decreasing regeneration and promoting fibrosis. Am J Pathol 2005;167(4):1105-1117.


    6.

    7.

    Garrett WE Jr, Seaber AV, Boswick J, Urbaniak JR,


    Goldner JL: Recovery of skeletal muscle after laceration
    and repair. J Hand Surg Am 1984;9(5):683-692.
    Jackson DW, Feagin JA: Quadriceps contusions in
    young athletes: Relation of severity of injury to treatment and prognosis. J Bone Joint Surg Am 1973;55(1):
    95-105.
    Meyer DC, Hoppeler H, von Rechenberg B, Gerber C:
    A pathomechanical concept explains muscle loss and
    fatty muscular changes following surgical tendon release. J Orthop Res 2004;22(5):1004-1007.

    9.

    Quintero AJ, Wright VJ, Fu FH, Huard J: Stem cells for


    the treatment of skeletal muscle injury. Clin Sports Med
    2009;28(1):1-11.
    Another review paper that nicely outlines the role of
    stem cells for the treatment of skeletal muscle repair.

    10.

    Li Y, Li J, Zhu J, et al: Decorin gene transfer promotes


    muscle cell differentiation and muscle regeneration. Mol
    Ther 2007;15(9):1616-1622.
    This study showed that decorin gene transfer into myoblasts differentiated into myotubules at a higher rate
    than cells that did not undergo gene transfer. These cells
    displayed upregulation of myogenic genes Myf5, Myf6,
    MyoD, and myogenin. Therefore, decorin not only limits inflammation via inhibition of TGF-1 but may also
    promote myoblast differentiation.

    11.

    Negishi S, Li Y, Usas A, Fu FH, Huard J: The effect of


    relaxin treatment on skeletal muscle injuries. Am J
    Sports Med 2005;33(12):1816-1824.

    12.

    Foster W, Li Y, Usas A, Somogyi G, Huard J: Gamma


    interferon as an antifibrosis agent in skeletal muscle. J
    Orthop Res 2003;21(5):798-804.

    13.

    Nozaki M, Li Y, Zhu J, et al: Improved muscle healing


    after contusion injury by the inhibitory effect of
    suramin on myostatin, a negative regulator of muscle
    growth. Am J Sports Med 2008;36(12):2354-2362.
    Suramin was injected into the tibialis anterior muscle of
    mice 2 weeks following injury and was found to improve overall skeletal muscle healing. In an in vitro arm
    of the study, suramin enhanced myoblast and MDSC
    differentiation, which may explain the in vivo findings.

    14.

    Bedair HS, Karthikeyan T, Quintero A, Li Y, Huard J:


    Angiotensin II receptor blockade administered after injury improves muscle regeneration and decreases fibrosis in normal skeletal muscle. Am J Sports Med 2008;
    36(8):1548-1554.
    Mice underwent partial laceration of their gastrocnemius muscles and then were given the angiotensin II receptor blocker losartan or tap water. Those that received losartan healed with reduced fibrosis and an
    increased number of myofibers.

    2011 American Academy of Orthopaedic Surgeons

    Menetrey J, Kasemkijwattana C, Day CS, et al: Growth


    factors improve muscle healing in vivo. J Bone Joint
    Surg Br 2000;82(1):131-137.

    16.

    Bachrach E, Perez AL, Choi YH, et al: Muscle engraftment of myogenic progenitor cells following intraarterial transplantation. Muscle Nerve 2006;34(1):44-52.

    17.

    Carr LK, Steele D, Steele S, et al: 1-year follow-up of


    autologous muscle-derived stem cell injection pilot
    study to treat stress urinary incontinence. Int Urogynecol J Pelvic Floor Dysfunct 2008;19(6):881-883.
    This is a report of 1-year follow-up of eight women who
    underwent injection of autologous muscle-derived stem
    cells into the detrusor muscle for stress incontinence.
    Five of eight women had improvement in symptoms.

    18.

    Thornton GM, Shrive NG, Frank CB: Altering ligament


    water content affects ligament pre-stress and creep behaviour. J Orthop Res 2001;19(5):845-851.

    19.

    Atkinson TS, Ewers BJ, Haut RC: The tensile and stress
    relaxation responses of human patellar tendon varies
    with specimen cross-sectional area. J Biomech 1999;
    32(9):907-914.

    20.

    Abrahamsson SO, Gelberman RH, Lohmander SL:


    Variations in cellular proliferation and matrix synthesis
    in intrasynovial and extrasynovial tendons: An in vitro
    study in dogs. J Hand Surg [Am] 1994;19(2):259-265.

    21.

    Wrgler-Hauri CC, Dourte LM, Baradet TC, Williams


    GR, Soslowsky LJ: Temporal expression of 8 growth
    factors in tendon-to-bone healing in a rat supraspinatus
    model. J Shoulder Elbow Surg 2007;16(5, suppl):S198S203.
    In this study, rats underwent supraspinatus detachment
    and repair and were then sacrificed at 1, 2, 3, 8, and 16
    weeks. Immunohistochemical staining at each timepoint
    outlined the expression of bFGF, BMPs-12, -13, -14,
    cartilage oligomeric matrix protein, connective tissue
    growth factor, PDGF, and TGF-1.

    22.

    Rodeo SA, Arnoczky SP, Torzilli PA, Hidaka C, Warren


    RF: Tendon-healing in a bone tunnel: A biomechanical
    and histological study in the dog. J Bone Joint Surg Am
    1993;75(12):1795-1803.

    1: Principles of Orthopaedics

    8.

    15.

    23. Egerbacher M, Arnoczky SP, Caballero O, Lavagnino


    M, Gardner KL: Loss of homeostatic tension induces
    apoptosis in tendon cells: An in vitro study. Clin Orthop
    Relat Res 2008;466(7):1562-1568.
    This study showed that rat tail tendons that were stress
    deprived exhibited more apoptosis than those that were
    cyclically loaded. This highlights the need for homeostatic stress for overall tendon health.
    24.

    Gardner K, Arnoczky SP, Caballero O, Lavagnino M:


    The effect of stress-deprivation and cyclic loading on
    the TIMP/MMP ratio in tendon cells: An in vitro experimental study. Disabil Rehabil 2008;30(20-22):15231529.
    This study shows that stress deprivation increases the

    Orthopaedic Knowledge Update 10

    45

    Section 1: Principles of Orthopaedics

    Bug dayci G: The effect of ethanol intake on tendon


    healing: A histological and biomechanical study in a rat
    model. Arch Orthop Trauma Surg 2009;129(12):17211726.
    Rats were either given ethanol or served as control subjects. After 1 week, they underwent Achilles tendon laceration. At 4 weeks following injury, those that received
    ethanol had lower tensile strength and worse tenocyte
    histology scores. Therefore, ethanol has a detrimental
    effect on tendon healing.

    amount of MMP in rat tail tendons. This again emphasizes the idea that load is necessary to prevent tendon
    degeneration.

    1: Principles of Orthopaedics

    25.

    26.

    Eliasson P, Andersson T, Aspenberg P: Rat Achilles tendon healing: Mechanical loading and gene expression. J
    Appl Physiol 2009;107(2):399-407.
    Rat Achilles tendons were transected and were then randomized to receive botulinum toxin type A injections to
    unload the repair, or serve as a loaded control. Those
    that received botulinum toxin type A had less procollagen I, cartilage oligomeric matrix protein, tenascin-C,
    tenomodulin, and scleraxis at 14 and 21 days following
    injury. In the loaded samples there was increased crosssectional area at the healing site, but the material properties were unaffected. This led to the conclusion that
    tendon-specific genes are upregulated with loading and
    may promote regeneration rather than scar formation.

    27.

    Baumgarten KM, Gerlach D, Galatz LM, et al: Cigarette smoking increases the risk for rotator cuff tears.
    Clin Orthop Relat Res 2009;Mar 13:[Epub ahead of
    print].
    This study showed that smoking correlated with the rotator cuff tears in a dose- and time-dependent manner.

    28.

    Galatz LM, Silva MJ, Rothermich SY, Zaegel MA, Havlioglu N, Thomopoulos S: Nicotine delays tendon-tobone healing in a rat shoulder model. J Bone Joint Surg
    Am 2006;88(9):2027-2034.

    29.

    Cohen DB, Kawamura S, Ehteshami JR, Rodeo SA: Indomethacin and celecoxib impair rotator cuff tendonto-bone healing. Am J Sports Med 2006;34(3):362-369.

    30.

    Dimmen S, Engebretsen L, Nordsletten L, Madsen JE:


    Negative effects of parecoxib and indomethacin on tendon healing: An experimental study in rats. Knee Surg
    Sports Traumatol Arthrosc 2009;17(7):835-839.
    Rats underwent Achilles tendon laceration and then
    were given either parecoxib, indomethacin, or saline.
    Those that received parecoxib and indomethacin had
    lower tensile strength than control subjects at 14 days.

    31.

    Chen AL, Shapiro JA, Ahn AK, Zuckerman JD, Cuomo


    F: Rotator cuff repair in patients with type I diabetes
    mellitus. J Shoulder Elbow Surg 2003;12(5):416-421.

    32.

    46

    Bring D, Reno C, Renstrom P, Salo P, Hart D, Ackermann P: Prolonged immobilization compromises upregulation of repair genes after tendon rupture in a rat
    model. Scand J Med Sci Sports 2009;Jul 2:[Epub ahead
    of print].
    Rats underwent Achilles tendon rupture and then were
    randomized to cast immobilization or free mobilization.
    Those in the mobilized group had increased messenger
    RNA levels of brain-derived neurotrophic factor, bFGF,
    cyclooxygenase-1, and hypoxia-inducible factor-1 at
    17 days. This led to the conclusion that mobilization responded to increased expression of regenerative growth
    factors and may be beneficial to healing.

    Hapa O, Cakici H, Giderog lu K, Ozturan K, Kkner A,

    Orthopaedic Knowledge Update 10

    33.

    Gulotta LV, Rodeo SA: Growth factors for rotator cuff


    repair. Clin Sports Med 2009;28(1):13-23.
    The authors present a review of current research into
    the role of growth factors for the augmentation of rotator cuff repairs, as well as potential future directions.

    34.

    Ansorge HL, Beredjiklian PK, Soslowsky LJ: CD44 deficiency improves healing tendon mechanics and increases matrix and cytokine expression in a mouse patellar tendon injury model. J Orthop Res 2009;27(10):
    1386-1391.
    CD44 is a potent proinflammatory mediator. CD44
    knockout mice showed improved healing in a mouse patellar tendon injury model. This implies that blunting
    the inflammatory response may improve tendon and ligament healing by reducing fibrosis and promoting regeneration.

    35.

    Ricchetti ET, Reddy SC, Ansorge HL, et al: Effect of


    interleukin-10 overexpression on the properties of healing tendon in a murine patellar tendon model. J Hand
    Surg Am 2008;33(10):1843-1852.
    IL-10 is an anti-inflammatory cytokine. In this study,
    IL-10 overexpression was able to improve healing in a
    mouse patellar tendon defect model. This is further evidence that reducing the inflammatory response may be
    beneficial to healing.

    36.

    Hays PL, Kawamura S, Deng XH, et al: The role of


    macrophages in early healing of a tendon graft in a bone
    tunnel. J Bone Joint Surg Am 2008;90(3):565-579.
    Macrophages produce TGF-1 that results in fibrosis. In
    this study, macrophage depletion improved healing in a
    mouse ACL reconstruction model. Tendon grafts healed
    with less scar tissue and more fibrocartilage.

    37.

    Miyatake S, Tohyama H, Kondo E, Katsura T, Onodera


    S, Yasuda K: Local administration of interleukin-1 receptor antagonist inhibits deterioration of mechanical
    properties of the stress-shielded patellar tendon. J Biomech 2008;41(4):884-889.
    IL-1 is a potent proinflammatory mediator. In this study,
    application of an IL-1 receptor blocker was able to inhibit the deterioration of mechanical properties of
    stress-shielded patellar tendons. This signifies that inflammation is one pathway by which tendons degenerate during stress deprivation.

    38.

    Ouyang HW, Goh JC, Lee EH: Use of bone marrow


    stromal cells for tendon graft-to-bone healing: Histological and immunohistochemical studies in a rabbit
    model. Am J Sports Med 2004;32(2):321-327.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 4: Muscle, Tendon, and Ligament

    39.

    Chong AK, Ang AD, Goh JC, et al: Bone marrowderived mesenchymal stem cells influence early tendonhealing in a rabbit achilles tendon model. J Bone Joint
    Surg Am 2007;89(1):74-81.
    In this study, autologous bone marrowderived MSCs
    improved healing in a rabbit model of Achilles tendon
    healing.
    Lim JK, Hui J, Li L, Thambyah A, Goh J, Lee EH: Enhancement of tendon graft osteointegration using mesenchymal stem cells in a rabbit model of anterior cruciate ligament reconstruction. Arthroscopy 2004;20(9):
    899-910.

    41.

    Pacini S, Spinabella S, Trombi L, et al: Suspension of


    bone marrow-derived undifferentiated mesenchymal
    stromal cells for repair of superficial digital flexor tendon in race horses. Tissue Eng 2007;13(12):2949-2955.
    Eleven racehorses received MSCs to augment partial
    flexor tendon laceration healing. Nine of the 11 had significant clinical recovery that allowed them to return to
    racing.

    42.

    43.

    Gulotta LV, Kovacevic D, Ehteshami JR, Dagher E,


    Packer JD, Rodeo SA: Application of bone marrowderived mesenchymal stem cells in a rotator cuff repair
    model. Am J Sports Med 2009;37(11):2126-2133.
    Contrary to previous studies, this study failed to show
    improved healing in a rat rotator cuff repair model with
    the application of bone marrowderived MSCs. This
    highlights the need to determine a combination of pluripotent stem cells and growth or differentiation factors
    that can be effective to augment rotator cuff repairs.
    Thomopoulos S, Das R, Silva MJ, et al: Enhanced flexor
    tendon healing through controlled delivery of PDGFBB. J Orthop Res 2009;27(9):1209-1215.
    This study showed that PDGF-BB delivery on a fibrin/
    heparin-based delivery system increased tendon gliding,
    but failed to improve mechanical strength following
    flexor tendon repairs in dogs. This result occurred despite increases in cell activity, collagen crosslinks, and
    hyaluronic acid seen in the PDGF-BBtreated specimens.

    44.

    Sasaki K, Kuroda R, Ishida K, et al: Enhancement of


    tendon-bone osteointegration of anterior cruciate ligament graft using granulocyte colony-stimulating factor.
    Am J Sports Med 2008;36(8):1519-1527.
    ACL reconstruction was performed on dogs and either
    granulocyte colony-stimulating factor in a gelatin or the
    gelatin alone was applied to the tunnels. They found
    that bone-tendon healing strength was accelerated in
    specimens treated with granulocyte colony-stimulating
    factor by enhancing angiogenesis and osteogenesis.

    45.

    Hashimoto Y, Yoshida G, Toyoda H, Takaoka K: Generation of tendon-to-bone interface enthesis with use
    of recombinant BMP-2 in a rabbit model. J Orthop Res
    2007;25(11):1415-1424.
    In this study, BMP-2 was injected into the flexor digitorum communis tendon of rabbits to induce ectopic ossicle formation. The resultant tendon/ossicle complex was
    then transferred to the tibial surface. One month follow-

    2011 American Academy of Orthopaedic Surgeons

    46.

    Seeherman HJ, Archambault JM, Rodeo SA, et al:


    rhBMP-12 accelerates healing of rotator cuff repairs in
    a sheep model. J Bone Joint Surg Am 2008;90(10):
    2206-2219.
    This study evaluated the ability of BMP-12 on various
    carriers to improve infraspinatus healing in a sheep
    model. They showed that BMP-12 on a collagen or hyaluronan sponge was able to accelerate healing, and resulted in maximal loads to failure that were twice that
    of controls.

    47.

    Murray MM: Current status and potential of primary


    ACL repair. Clin Sports Med 2009;28(1):51-61.
    This is a review of the research into developing strategies to augment primary ACL repairs.

    48.

    Fufa D, Shealy B, Jacobson M, Kevy S, Murray MM:


    Activation of platelet-rich plasma using soluble type I
    collagen. J Oral Maxillofac Surg 2008;66(4):684-690.
    This study showed that soluble type I collagen is necessary for the release of growth factor from platelet-rich
    plasma.

    49.

    Murray MM, Spindler KP, Abreu E, et al: Collagenplatelet rich plasma hydrogel enhances primary repair
    of the porcine anterior cruciate ligament. J Orthop Res
    2007;25(1):81-91.
    The application of a platelet-rich plasma hydrogel was
    found to improve healing after primary ACL repair in a
    porcine model. However, the final strength of the ACL
    repairs was below that of the native ACL.

    50.

    Dwyer KW, Provenzano PP, Muir P, Valhmu WB,


    Vanderby R Jr: Blockade of the sympathetic nervous
    system degrades ligament in a rat MCL model. J Appl
    Physiol 2004;96(2):711-718.

    51.

    Salo P, Bray R, Seerattan R, Reno C, McDougall J, Hart


    DA: Neuropeptides regulate expression of matrix molecule, growth factor and inflammatory mediator mRNA
    in explants of normal and healing medial collateral ligament. Regul Pept 2007;142(1-2):1-6.
    This study showed that the application of the neuropeptides substance P, neuropeptide Y, and calcitonin generelated peptide to medial collateral ligaments induced
    several inflammatory mediators at 2 weeks. This shows
    that neuropeptides influence the metabolic activities on
    ligaments during the healing process.

    52.

    McDougall JJ, Yeung G, Leonard CA, Bray RC: A role


    for calcitonin gene-related peptide in rabbit knee joint
    ligament healing. Can J Physiol Pharmacol 2000;78(7):
    535-540.

    53.

    Arnoczky SP, Lavagnino M, Egerbacher M: The mechanobiological aetiopathogenesis of tendinopathy: Is it the


    over-stimulation or the under-stimulation of tendon
    cells? Int J Exp Pathol 2007;88(4):217-226.

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    40.

    ing transfer, those that were originally treated with


    BMP-2 had histology more representative of a direct insertion site, and this histology correlated with better
    biomechanical properties.

    47

    Section 1: Principles of Orthopaedics

    The authors studied the in vitro mechanobiologic response of tendon cells in situ to various tensile loading
    regimes in a rat tail tendon model.

    1: Principles of Orthopaedics

    54.

    55.

    Mikolyzk DK, Wei AS, Tonino P, et al: Effect of corticosteroids on the biomechanical strength of rat rotator
    cuff tendon. J Bone Joint Surg Am 2009;91(5):11721180.
    This study showed that a single dose of corticosteroids
    significantly weakened both intact and repaired rotator
    cuffs in a rat model. However, the strength returned to
    normal in 3 weeks.

    56.

    Wei AS, Callaci JJ, Juknelis D, et al: The effect of corticosteroid on collagen expression in injured rotator cuff
    tendon. J Bone Joint Surg Am 2006;88(6):1331-1338.

    57.

    Murrell GA: Using nitric oxide to treat tendinopathy. Br


    J Sports Med 2007;41(4):227-231.
    The author showed that nitric oxide enhances subjective
    and objective recovery of patients with tendon injury in
    three randomized clinical trials.

    58.

    48

    Andres BM, Murrell GA: Treatment of tendinopathy:


    What works, what does not, and what is on the horizon. Clin Orthop Relat Res 2008;466(7):1539-1554.
    The authors present a review article on the current status of the treatment of tendinopathy.

    Rompe JD, Furia J, Maffulli N: Eccentric loading compared with shock wave treatment for chronic insertional
    achilles tendinopathy: A randomized, controlled trial. J
    Bone Joint Surg Am 2008;90(1):52-61.
    This study showed that shock wave treatment was superior to physical therapy concentrating on eccentric loading in patients with insertional Achilles tendinopathy.

    Orthopaedic Knowledge Update 10

    59.

    Rompe JD, Furia J, Maffulli N: Eccentric loading versus


    eccentric loading plus shock-wave treatment for midportion achilles tendinopathy: A randomized controlled
    trial. Am J Sports Med 2009;37(3):463-470.
    This study showed that shock wave treatment was superior to eccentric loading in patients with midportion
    Achilles tendinopathy.

    60.

    Orchard J, Massey A, Brown R, Cardon-Dunbar A,


    Hofmann J: Successful management of tendinopathy
    with injections of the MMP-inhibitor aprotinin. Clin
    Orthop Relat Res 2008;466(7):1625-1632.
    This study showed that 76% of patients who received
    aprotinin injections for Achilles or patellar tendinopathy
    had improvement in their symptoms. The results were
    better for those who had Achilles tendinopathy (84%
    improvement) than those with patellar tendinopathy
    (69% improvement).

    61.

    Mishra A, Woodall J Jr, Vieira A: Treatment of tendon


    and muscle using platelet-rich plasma. Clin Sports Med
    2009;28(1):113-125.
    This is a review article outlining research into the use of
    platelet-rich plasma for the treatment of tendon and
    muscle injuries.

    62.

    Schnabel LV, Mohammed HO, Miller BJ, et al: Platelet


    rich plasma (PRP) enhances anabolic gene expression
    patterns in flexor digitorum superficialis tendons. J Orthop Res 2007;25(2):230-240.
    The application of platelet-rich plasma to flexor digitorum superficialis explants resulted in higher concentrations of TGF-1 and PDGF-BB, and higher expression
    of COL1A1, COL3A1, and cartilage oligomeric matrix
    protein.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 5

    Wound Management
    Jan Paul Ertl, MD

    Jeffrey Anglen, MD

    Introduction

    Dr. Ertl or an immediate family member serves as a


    board member, owner, officer, or committee member of
    Wishard Hospital and has received research or institutional support from Amgen, Synthes, and Wyeth. Dr. Anglen or an immediate family member serves as a board
    member, owner, officer, or committee member of The
    American Board of Orthopaedic Surgery, the American
    College of Surgeons, and the Orthopaedic Trauma Association; has received royalties from Biomet; serves as a
    paid consultant to or is an employee of Stryker; and has
    received research or institutional support from Stryker
    and Wyeth.

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    Extremity injuries with associated soft-tissue violation


    present challenges to fracture stabilization and, more
    importantly, the initial management of the soft tissues
    and timing of definitive coverage. A coordinated management team is necessary to address any lifethreatening injuries. Thorough dbridement techniques,
    consisting of removal of nonviable and contaminated
    tissues, have been the focus of wound management.1
    Extremity injuries should be seen as soft-tissue injuries that surround a central bone core. The soft-tissue
    injury in extremity trauma often dictates the outcome
    of fractures and takes priority in treatment to maintain
    a biologic barrier and blood supply to potentially exposed bone, and to avoid further tissue compromise
    and infection. Complications that occur during the
    course of fracture care ultimately increase morbidity,
    mortality, and treatment cost.2 Many factors that increase the risk of further soft-tissue compromise or infection in open or closed fractures are beyond the control of the surgeon. These factors include the severity of
    the injury, delay in initiation of medical care, and the
    health status of the patient. However, some treatment
    decisions, including timing of surgical treatment, use of
    systemic and local antibiotics, wound irrigation, adequacy of surgical dbridement, fracture stability, and
    early wound closure or flap coverage, are strongly believed to influence the incidence of infection.
    The development of a wound infection is a multistage process that is the result of contamination with
    sufficient numbers of viable bacteria, adhesion of the
    bacteria to wound surfaces, proliferation of bacterial
    colonies on the surface, and extension of the colonies

    beyond the original locations. The goals of initial


    wound care are to decrease the bacterial load, eliminate
    the devitalized tissue that serves as a medium for bacterial growth, and prevent further contamination,
    thereby facilitating the action of host defense systems.3
    The initial and continued management of wounds are
    critical in the ultimate successful outcome of fractures,
    and a multidisciplinary approach is usually required.

    Initial Management of Open Fracture Wounds


    Closed fractures with devitalized skin and all open fractures are considered contaminated. The severity of injury to the soft-tissue envelope may be difficult to assess in the emergency department, and the amount of
    contamination is further affected by additional factors
    such as patient age, energy absorbed, setting of injury
    (for example, barnyard), vascular disruption, and patient comorbidities. Initial wound management in the
    emergency department includes removal of splints and
    assessment of the extremity. Sterile dressings, if present,
    are left in place. It has been shown that redressing the
    wound in the emergency department causes a threefold
    to fourfold rise in the rate of infection.4 The extent of
    soft-tissue injury is greater than is evident upon simple
    inspection, and is best determined in the operating
    room. Factors that influence the development of infection include the involved area of the body, severity of
    soft-tissue damage, virulence of organisms introduced
    into the wound, treatment regimen, presence of foreign
    material in the wound, and host response to both injury and wound inoculation.
    Surgical wounds have been grouped into four types,
    based on the risk of surgical site infection: class I, clean;
    class II, clean-contaminated; class III, contaminated;
    and class IV, dirty-infected.5 Prophylactic antibiotics
    are indicated for class I and II wounds. Prospective6
    and meta-analysis review have demonstrated the efficacy and benefit of prophylactic antibiotics for class I
    and II wounds and therapeutic antibiotics are indicated
    for class III and IV wounds.

    Antibiotic Therapy
    For patients with class III and IV wounds, antibiotics
    are used perioperatively not for prophylaxis but for
    managing a contaminated or infected wound. In open

    Orthopaedic Knowledge Update 10

    49

    Section 1: Principles of Orthopaedics

    Table 1

    1: Principles of Orthopaedics

    Recommendations for Intravenous Antibiotic Therapy in Open Fracture Management


    Fracture Type

    Clinical Infection
    Rates

    Antibiotic Choice

    Antibiotic Duration

    1.4%

    Cefazolin

    every 8 h 3 doses

    II

    3.6%

    Piperacillin/azobactam or cefazolin and


    tobramycin

    24 h after wound closure

    IIIA

    22.7%

    Piperacillin/azobactam or cefazolin and


    tobramycin + penicillin for anaerobic,
    as required

    3 days

    IIIB

    10% to 50%

    Piperacillin/azobactam or Cefazolin and


    tobramycin + penicillin for anaerobic,
    as required

    Continue 3 days after wound


    closure

    IIIC

    10% to 50%

    Piperacillin/azobactam or cefazolin and


    tobramycin + penicillin for anaerobic,
    as required

    Continue 3 days after wound


    closure

    fractures, antibiotic therapy serves as an adjunct to surgical dbridement by reducing the bacterial load in the
    tissue. Multiple investigators have established the role
    of antibiotics in treatment and confirmed their efficacy
    in preventing infection after treatment of open fracture
    in prospective, randomized, controlled trials.7 Antibiotics should be initiated within 3 hours after injury because the risk of infection increases after that time.8 Although the efficacy of antibiotics in the management of
    open fractures is clear, length of therapy and the optimal antibiotic are not. Randomized controlled trials are
    needed to determine these variables.
    The suggested duration of antibiotic therapy is 1 to 3
    days for Gustilo-Anderson grade I and II open fractures
    and up to 5 days for grade III wounds.7,9-11 Antibiotic
    selection depends on the likely organisms contaminating the wound. For grade I and II open fractures, Staphylococcus aureus, streptococci, and aerobic gramnegative bacilli are the most common infecting
    organisms; thus, the use of a first- or second-generation
    cephalosporin has been proposed.12 A quinolone (for
    example, ciprofloxacin) might be a reasonable alternative given its broad-spectrum coverage, bactericidal activity, good oral bioavailability, and good adverse effect
    profile.13 More severe injuries should be managed with
    better coverage for gram-negative organisms, and the
    addition of an aminoglycoside to the cephalosporin is
    recommended.14 Alternatives to aminoglycosides may
    include third-generation cephalosporins or aztreonam.15
    For severe injuries with soil contamination and tissue
    damage with areas of ischemia, penicillin should be
    added to provide coverage against anaerobes, particularly Clostridium species (Table 1).

    move the devitalized tissue, foreign material, and contaminating bacteria in an attempt to decrease the
    bioburden that leads to wound infection.
    In a study of open fracture wounds of the lower extremity, patients were randomized to receive either bacitracin or castile soap added to the irrigation fluid.3 The
    results demonstrated no significant difference in infection rate between the two groups. Problems associated
    with wound healing (wound dehiscence or necrosis, incision breakdown, or flap or graft failure) occurred in
    9.5% of the bacitracin irrigation group and in 4% of
    the castile soap irrigation group. There were fewer infections and problems with fracture union in the group
    treated with the soap, although those differences were
    not significant. It was concluded that irrigation of open
    fracture wounds with antibiotic solution offered no advantage over the soap solution; in fact, use of the antibiotic may increase the risk of problems associated
    with wound healing. Irrigation of open fracture
    wounds with castile soap solution is advocated, particularly for the first irrigation and for wounds with gross
    contamination.
    The authors of a 2009 study compared pulsatile (19
    psi) irrigation with bulb syringe irrigation in an animal
    model and with multiple solutions.16 These data suggest
    that use of a low-pressure device and saline solution to
    irrigate wounds is the best choice. It was demonstrated
    that bulb syringe irrigation and normal saline produced
    improved results, with decreased bacterial rebound at
    48 hours using 6 L of solution. According to a 2006
    study in a goat model, it was demonstrated that potable water can also be used to reduce bacterial counts.17

    Timing to Irrigation and Dbridement


    Type of Irrigation and Volume
    The optimal care of open fracture wounds involves surgical dbridement and irrigation of the wound to re50

    Orthopaedic Knowledge Update 10

    The timing to irrigation and dbridement with luminescent Pseudomonas bacteria was studied, and it was
    concluded that earlier irrigation in a contaminated

    2011 American Academy of Orthopaedic Surgeons

    Chapter 5: Wound Management

    wound model resulted in superior bacterial removal.18


    A recent multicenter study concluded that the time
    from the injury to surgical dbridement is not a significant independent predictor of the risk of infection, and
    instead the timing of admission to a definitive trauma
    treatment center had a beneficial influence (with earlier
    admission leading to fewer infections).19 This finding
    should not be interpreted to mean that surgical dbridement of open fractures should not be accomplished urgently.

    Treatment

    Antibiotic Bead Pouch


    Beads made of polymethylmethacrylate (PMMA) containing antibiotic may be used to deliver an extremely
    high concentration of antibiotic to the wound, while simultaneously protecting the tissues against desiccation,
    contamination, and injury (Figure 1). Antibiotics including tobramycin, vancomycin, and cefazolin are
    commonly chosen because they are water soluble, heat
    stable, well tolerated, and broad spectrum. Vancomycin
    is not recommended as an initial agent because of concerns of overuse leading to development of resistant microorganisms. The wound is packed with the beads
    after dbridement and then covered with a semipermeable membrane dressing. Rubber bands or lacing can
    be used in conjunction with beads to prevent retraction
    of the wounds. The bead pouch allows diffusion of an-

    2011 American Academy of Orthopaedic Surgeons

    Figure 1

    1: Principles of Orthopaedics

    How much excisional dbridement should be done is


    difficult to assess in most contaminated injuries. Recent
    consensus opinion from the Extremity War Injury Symposium was that necrotic, devitalized, and contaminated tissue must be removed but that objective assessment of completeness of dbridement is difficult.20
    Contractility, color, consistency, and capacity to bleed
    are all important recognized indicators of viable tissue,
    but a great deal of experience is necessary to define
    nonviable tissue.20
    The management of wounds and open fractures continues to provide challenges for the orthopaedic surgeon. Despite the improvements in technology and surgical techniques, the rates of infection and nonunion
    are still troublesome. Early antibiotic administration
    coupled with early and meticulous irrigation and dbridement can lead to decreased rates of infection. Initial surgical intervention should be conducted as soon
    as possible, but the classic 6-hour rule does not seem to
    be supported in the literature.21 All open fractures
    should be assessed for the risk of contamination from
    Clostridium tetani. When possible, early closure of
    open fracture wounds, either by primary means or with
    flaps, can also decrease the rate of infection, especially
    from nosocomial organisms. Early skeletal stabilization
    is necessary, which can be accomplished easily with
    temporary external fixation. Adhering to these principles can help surgeons provide optimal patient care and
    an early return to function.20,21

    The antibiotic bead pouch is shown. Antibioticimpregnated PMMA beads are contained in an
    open fracture wound and then sealed with a
    semipermeable membrane until the soft-tissue
    coverage procedure is performed. (Reproduced
    with permission from Zalavras CG, Marcus RE,
    Levin LS, Patzakis MJ: Management of open
    fractures and subseqent complications. J Bone
    Joint Surg Am 2007;89:884-895.)

    tibiotic into the wound exudates. Antibiotic levels can


    reach very high local concentrations without systemic
    toxicity, even penetrating tissues with poor or absent
    vascularity. The bead pouch technique seals the wound
    from the external environment with a semipermeable
    barrier, thereby preventing secondary contamination by
    nosocomial pathogens and at the same time maintaining an aerobic wound environment.9-11
    An infection rate of 3.7% was reported in a group of
    patients with open fractures who received combined
    treatment with both systemic antibiotics and antibiotic
    beads.22 This rate was considerably lower than the
    12% infection rate associated with open fractures
    treated with systemic antibiotics alone.

    Negative Pressure Wound Therapy


    Negative pressure wound therapy (NPWT) is a relatively new, commercially available treatment that has
    been used across many disciplines and proved beneficial in various types of complex wounds.23-25 However,
    very little has been written regarding the use of NPWT
    in orthopaedics. Most of the articles in the literature
    are either case reports or small case series and many do
    not involve complex traumatic wounds.26-28
    NPWT has become widely accepted in orthopaedics
    and used routinely in acute wound management, preoperative temporizing, complex trauma, wound bed
    preparation, and treatment of chronic wounds. NPWT
    uses micromechanisms and macromechanisms of action
    to increase local blood flow, reduce edema, stimulate
    formation of granulation tissue, stimulate cell proliferation, reduce cytokines, reduce bacterial load, and
    draw wounds together.23,29 NPWT is thought to exert

    Orthopaedic Knowledge Update 10

    51

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 2

    Negative wound pressure therapy (wound vac)


    has improved the treatment of soft-tissue injuries in the polytrauma patient. The wound vac
    maintains wound coverage until definitive softtissue management can be completed.

    its biologic effects by first stimulating the release of local cell growth factors by induced mechanical strain
    similar to the mechanism of Ilizarov and then improving microcirculation by actively removing edema from
    injured tissue.30,31 NPWT has been indicated in chronic,
    acute, traumatic, subacute, and high-risk elective surgical wounds as well as partial-thickness burns, ulcers,
    flaps, and skin grafts. Contraindications to treatment
    with NPWT include wounds with necrotic tissues, exposed vital structures, untreated osteomyelitis, unexplored fistulae, and malignant wounds. In the management of orthopaedic wounds NPWT serves as an
    adjunct to soft-tissue defects as a method of reducing
    bacterial counts in wounds, as a bridge to definitive
    bone coverage, treating infections, wound bed preparation for split-thickness skin grafting (STSG) dermal replacements, or flap coverage. No significant complications have been noted in reported studies to date,
    although there have been case reports of erosion of
    NPWT into vascular structures, leading to hemorrhage.32,33
    NPWT uses application of subatmospheric pressure
    (less than 760 mm Hg) to the wound bed to promote
    healing. A range of pressures between 50 and 500 mm
    Hg were tested; the most efficient pressure was 125 mm
    Hg, which resulted in a fourfold increase in blood flow,
    a 63% increase in granulation tissue with continuous
    pressure, and a 103% increase in granulation tissue
    with intermittent pressure. 23,24 NPWT can be applied
    through both reticulated foam and gauze at the wound
    interface, although most published literature supports
    the use of reticulated foam.31,34 Further studies are
    needed to compare foam and gauze dressings and the
    effect of each on healing.
    The bacterial colonization of a wound is a recognized detrimental factor in the multifactorial process of
    52

    Orthopaedic Knowledge Update 10

    wound healing. The harmful effects on wound healing


    are recognized to correspond to a level of greater than
    105 colonies of bacteria per gram of tissue. NPWT has
    been applied to traumatic wounds for varying periods
    in an attempt to avoid infection and bridge the time until definitive coverage can be completed (Figure 2). The
    question of decreasing bacterial counts has been addressed in basic science animal studies and in clinical
    practice. 23,24 Wounds were infected with Staphylococcus aureus and Staphylococcus epidermidis and treated
    with foam NPWT. Sequential full-thickness punch biopsies obtained over a 2-week period demonstrated
    bacterial counts below 105 organisms per gram of tissue. Other investigators in a retrospective review of
    acute and chronic wounds did not consistently identify
    decreased bacterial colonization.35 Most of the patient
    subgroup studied was chronic nonorthopaedic wounds;
    despite these findings it was concluded that most
    wounds healed. In a prospective randomized study, the
    impact of NPWT after severe open fractures on infection was evaluated.36 Fifty-nine patients with 63 heavily
    contaminated types II, IIIA, IIIB, and IIIC fractures
    were included. All patients underwent identical treatment protocols except for the type of dressing placed
    over the open fracture wound. The control group received fine mesh gauze dressing and the other group received NPWT dressings. The study findings demonstrated that NPWT-treated patients were 20% less
    likely to develop infection in comparison with the control group.
    NPWT has been used in the treatment of combatrelated complex soft-tissue wounds and complex highenergy open fractures.37,38 The isolated soft-tissue injury
    cohort had less dbridement, faster time to closure, and
    no infections. NPWT was considered an important adjunct in the dbridement protocols of soft-tissue injuries. The open fractures were treated aggressively with
    multiple dbridements and NPWT was used to bridge
    the gap until wound closure was completed. Although
    there are many factors to consider, no infections were
    reported.
    It must be emphasized that NPWT/reticulated foam
    is not a substitute for thorough surgical dbridement of
    nonviable soft tissue and bony structures.34

    NPWT and STSG


    Multiple prospective, retrospective, and basic science
    studies have provided supporting evidence for the use
    of NPWT over STSG.39,40 Application of NPWT over
    the skin graft is intended to minimize shear forces, pull
    off wound bed edema, and hinder infection. NPWT
    also minimizes shear forces that may be particularly advantageous in the pediatric population and other patient subgroups with limited ability to self-immobilize.
    The primary advantages of using reticulated foam
    sponges applied to STSG sites are decreased shear
    forces on the STSG, compression of the STSG to the recipient bed, removal of any edema, and conformance
    with the STSG on uneven wound surfaces. The STSG
    recipient site can be covered with the nonadherent/

    2011 American Academy of Orthopaedic Surgeons

    Chapter 5: Wound Management

    Suture for Skin Closure


    The type of skin closure for compromised skin was
    studied in an animal model.42 The objective of this
    study was to determine the effect of suture patterns on
    the cutaneous blood supply with increasing tension applied to the suture. A porcine model was used to measure the suture tension of simple, horizontal mattress,
    vertical mattress (Donati) and the Allgower modification of the Donati sutures. It was determined that the
    Allgower-Donati suture had the least effect on cutaneous blood flow; the Allgower-Donati suture pattern can
    be used for traumatized or compromised soft-tissue injuries.

    Timing of Microsurgical Coverage


    A coordinated effort with a microvascular surgical service is necessary to address the timely coverage of bone
    with soft-tissue loss. The timing of posttraumatic microsurgical lower extremity reconstruction was described in 1986, with recommendations for flap coverage of Gustilo grade IIIB and IIIC fractures within 72
    hours of injury. 43 The highest risk of infection and flap
    loss occurred within the delayed period, defined as 72
    hours to 90 days. Lower rates of flap loss and infection
    have been cited when repair and coverage were performed in this defined early period.44 However, the definition of early remains vague. Many modern-day level
    I trauma and tertiary care centers often receive transfer
    patients more than 72 hours after injury, with some patients sustaining significant concomitant injury. Institutional factors also come into play, such as operating
    room availability and appropriate support staff, resulting in less optimal timing of immediate reconstruction
    of these injuries. In a 2008 retrospective study, 14
    lower extremity reconstructions with free flaps were reviewed over a 4-year period. 45 All patients underwent
    delayed reconstruction more than 72 hours after injury.

    2011 American Academy of Orthopaedic Surgeons

    There were no flap losses and one patient had late osteomyelitis. These results indicate that posttraumatic
    lower extremity reconstruction may be safely and reliably performed when the wound is adequately dbrided
    and when the patients other injuries have been stabilized. Reconstruction was possible an average of 22
    days after injury. Aggressive dbridement and liberal
    use of NPWT aided in decreasing the bacterial load and
    subsequent incidence of wound infections. It was concluded that lower extremity reconstruction can be performed safely and effectively in the delayed period
    (within 72 hours to 90 days of injury) to allow for
    wound dbridement, stabilization of other injuries, and
    transfer to a microsurgical facility.
    1: Principles of Orthopaedics

    nonpetroleum dressing stapled at the periphery to


    avoid unwanted tissue ingrowth. The NPWT can also
    be applied in a similar fashion without staples to the
    donor site, resulting in faster healing.39 The literature
    supports removing the NPWT over the skin graft by 5
    days and as early 3 days. The orthopaedic trauma patient often is in the hospital beyond the time required
    for NPWT, so leaving the NPWT (foam) in place for 3,
    5, or even 7 days does not impede discharge from the
    hospital.34,41 The use of NPWT over dermal substitutes
    has been used;41 however, more clinical investigation is
    required.
    In a study of the cost-effectiveness of NPWT, it was
    concluded that NPWT can reduce the need for expensive traditional soft-tissue reconstructions.28
    NPWT is a relatively simple supplement in the treatment of complex acute and chronic wounds. Although
    used extensively in these wounds, NPWT does not replace the surgical principles of dbridement, bony stabilization, and appropriate antibiotic therapy.

    Newer Soft-Tissue Coverage Options


    Limb replantation and free tissue flaps have been part
    of the limb reconstruction algorithm since the introduction of the operating room microscope in 1960. Recent
    developments and modifications in soft-tissue coverage
    include the fillet flaps, which apply a spare parts
    concept and can be customized for specific recipient
    sites. The so-called perforator flap makes use of feeder
    vessels, providing cutaneous and other composite flaps
    without sacrificing major vessels. The introduction of
    the sural flap has made it possible to avoid microsurgical reconstruction but still provide adequate, wellvascularized coverage, particularly in the distal third of
    the leg.46
    By definition, fillet flaps are axial-pattern flaps harvested from amputated, discarded, or otherwise nonfunctioning or nonsalvageable tissues and body parts
    that can also function as composite tissue transfers.
    They can be used as pedicled or free flaps and are a
    beneficial reconstruction strategy for major defects,
    provided tissue adjacent to these defects is available.47
    The expanded use of the fillet flap as either pedicle flap
    or free tissue transfer is a method for gaining more serviceable soft-tissue coverage and for preserving length
    of the residual limb when amputation is required. This
    concept highlights the principle of stabilizing and salvaging limbs as opposed to immediate amputation, and
    provides the surgeon performing the eventual reconstruction or amputation with more choices for wound
    closure or coverage.
    Another new advance for soft tissue coverage is the
    so-called perforator flap first described in 1987, in
    which the angiosomes that are distributed to skin territories can be followed to the feeder vessels, thereby increasing the armamentarium of cutaneous flaps and
    other composite flaps without sacrificing major vessels.
    These flaps based on perforating vessels, either in free
    or pedicled form, represent a new perspective for resolving complex wounds with lower morbidity, especially in the distal segment of the leg. The anterolateral
    thigh flap has become a workhorse for the treatment of
    upper and lower extremity defects during flap surgery.
    The anterolateral thigh flap is indicated for reconstruction of a diverse range of defects of various surface ar-

    Orthopaedic Knowledge Update 10

    53

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    eas and depths; it can be used as an ultrathin flap for


    resurfacing, rolled up for filling in dead space, or taken
    with muscle to obliterate spaces or provide bulk. The
    anterolateral thigh flap has been used in trauma salvage
    as a flow-through flap, as a tissue carrier, and to piggyback additional flaps. The flap can be a raised pedicle
    (proximally or distally) or free, suprafascial or subfascial, further thinned, or harvested with muscle or additional tissue components. The anterolateral thigh flap is
    robust and versatile enough to fulfill a wide variety of
    reconstructive requirements. Harvesting these flaps requires a high level of technical skill, but increases surgeon versatility and replaces similar flaps.48
    A distally-based fasciocutaneous flap from the sural
    region based on the sural artery anatomy has been described. The sural flap has progressively gained recognition as a suitable soft-tissue reconstruction alternative
    to microvascular free-flap transfer. The sural artery fasciocutaneous flap has become a standard for soft-tissue
    coverage of distal third open tibia fractures, exposed
    calcaneus fractures, and open wounds around the ankle
    when the overall wound is less than 6 cm in diameter.
    Most authors have described good results, with low
    partial and complete flap necrosis rates of between 0%
    and 17%.47,49

    Summary
    The philosophy of modern treatment of wounds dictates the use of methods believed to reduce the risk of
    complications. The adequacy of initial surgical wound
    care may be the most important factor under the surgeons control and may be the difference between success and failure. Adequate sharp dbridement with removal of all debris and devitalized tissue and thorough
    irrigation are vital. Therefore, the initial management
    and continued management of wounds are critical in
    the ultimate successful outcome of fractures and often
    require a multidisciplinary approach.

    WR; Hospital Infection Control Practices Advisory


    Committee: Guideline for prevention of surgical site infection, 1999. Infect Control Hosp Epidemiol 1999;
    20(4):250-278, quiz 279-280.
    6.

    Boxma H, Broekhuizen T, Patka P, Oosting H: Randomised controlled trial of single-dose antibiotic prophylaxis in surgical treatment of closed fractures: The
    Dutch Trauma Trial. Lancet 1996;347(9009):11331137.

    7.

    Olson SA, Finkemeier CF, Moehring HD: Open fractures, in Bucholz RW, Heckman JD (eds): Rockwood
    and Greens Fractures in Adults, ed 5. Philadelphia, PA,
    Lippincott-Williams & Wilkins, 2001, pp 285-318.

    8.

    Patzakis MJ, Wilkins J: Factors influencing infection


    rate in open fracture wounds. Clin Orthop Relat Res
    1989;243(243):36-40.

    9.

    Zalavras CG, Patzakis MJ: Open fractures: Evaluation


    and management. J Am Acad Orthop Surg 2003;11(3):
    212-219.

    10.

    Zalavras CG, Patzakis MJ, Holtom P: Local antibiotic


    therapy in the treatment of open fractures and osteomyelitis. Clin Orthop Relat Res 2004;427(427):86-93.

    11.

    Zalavras CG, Marcus RE, Levin LS, Patzakis MJ: Management of open fractures and subsequent complications. Instr Course Lect 2008;57:51-63.
    The authors discuss the need for early, systemic, widespectrum antibiotic therapy in the treatment of open
    fractures and avoidance of certain complications.

    12.

    Templeman DC, Gulli B, Tsukayama DT, Gustilo RB:


    Update on the management of open fractures of the tibial shaft. Clin Orthop Relat Res 1998;350(350):18-25.

    13.

    Patzakis MJ, Bains RS, Lee J, et al: Prospective, randomized, double-blind study comparing single-agent antibiotic therapy, ciprofloxacin, to combination antibiotic therapy in open fracture wounds. J Orthop Trauma
    2000;14(8):529-533.

    14.

    Sanders R, Swiontkowski M, Nunley J, Spiegel P: The


    management of fractures with soft-tissue disruptions.
    J Bone Joint Surg Am 1993;75(5):778-789.

    15.

    Zalavras CG, Patzakis MJ, Holtom PD, Sherman R:


    Management of open fractures. Infect Dis Clin North
    Am 2005;19(4):915-929.

    16.

    Owens BD, White DW, Wenke JC: Comparison of irrigation solutions and devices in a contaminated musculoskeletal wound survival model. J Bone Joint Surg Am
    2009;91(1):92-98.
    The authors describe an established goat model involving the creation of a reproducible complex musculoskeletal wound followed by inoculation with Pseudomonas
    aeruginosa (lux) bacteria. This genetically altered luminescent bacterium provides the ability for quantitative
    analysis with a photon-counting camera system. For

    Annotated References

    54

    1.

    Bowyer G: Dbridement of extremity war wounds.


    J Am Acad Orthop Surg 2006;14(10 Spec No.):S52S56.

    2.

    Fry DE: The economic costs of surgical site infection.


    Surg Infect (Larchmt) 2002;3(Suppl 1):S37-S43.

    3.

    Anglen JO: Comparison of soap and antibiotic solutions


    for irrigation of lower-limb open fracture wounds: A
    prospective, randomized study. J Bone Joint Surg Am
    2005;87(7):1415-1422.

    4.

    Browner BD: Skeletal Trauma: Basic Science, Management, and Reconstruction, ed 3. Philadelphia, PA, WB
    Saunders, 2003.

    5.

    Mangram AJ, Horan TC, Pearson ML, Silver LC, Jarvis

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 5: Wound Management

    study 1, wound irrigation was performed 6 hours after


    the injury and inoculation; the goats were assigned to
    four treatment groups: normal saline solution, bacitracin solution, castile soap, and benzalkonium chloride.
    All wounds received sharp dbridement and irrigation
    with use of a pulsatile lavage device (19 psi). Images and
    photon counts were obtained prior to irrigation, after irrigation, and 48 hours after injury and inoculation. For
    study 2, the same animal model was used, and bulb syringe and pulsatile lavage irrigation was compared with
    saline solution. In study 1, the irrigation treatment lowered the bacterial counts in all treatment groups. The
    greatest reduction was seen with castile soap. In study 2,
    both treatment methods were effective in removing 75%
    of the bacteria initially.

    18.

    19.

    Svoboda SJ, Bice TG, Gooden HA, Brooks DE, Thomas


    DB, Wenke JC: Comparison of bulb syringe and pulsed
    lavage irrigation with use of a bioluminescent musculoskeletal wound model. J Bone Joint Surg Am 2006;
    88(10):2167-2174.
    Owens BD, Wenke JC: Early wound irrigation improves
    the ability to remove bacteria. J Bone Joint Surg Am
    2007;89(8):1723-1726.
    The authors evaluated the effect of different delays in irrigation on bacterial removal in an animal model.
    Pollak AN, Jones AL, Castillo RC, Bosse MJ, MacKenzie EJ; LEAP Study Group: The relationship between
    time to surgical debridement and incidence of infection
    after open high-energy lower extremity trauma. J Bone
    Joint Surg Am 2010;92(1):7-15.
    The authors evaluated the relationship between the timing of the initial treatment of open fractures and the development of subsequent infection as well as assess contributing factors. Eighty-four patients (27%) had
    development of an infection within the first 3 months
    after the injury. No significant differences were found
    between patients who had development of an infection
    and those who did not when the groups were compared
    with regard to the time from the injury to the first dbridement, the time from admission to the first dbridement, or the time from the first dbridement to softtissue coverage.

    20.

    Ficke JR, Pollak AN: Extremity war injuries: Development of clinical treatment principles. J Am Acad Orthop Surg 2007;15(10):590-595.
    The authors discussed four specific areas: prehospital
    management of extremity wounds, initial dbridement,
    early stabilization, and postoperative wound management during air evacuation.

    21.

    Okike K, Bhattacharyya T: Trends in the management


    of open fractures: A critical analysis. J Bone Joint Surg
    Am 2006;88(12):2739-2748.

    22.

    23.

    Ostermann PA, Seligson D, Henry SL: Local antibiotic


    therapy for severe open fractures: A review of 1085
    consecutive cases. J Bone Joint Surg Br 1995;77(1):9397.
    Morykwas

    MJ,

    Argenta

    LC,

    Shelton-Brown

    2011 American Academy of Orthopaedic Surgeons

    EI,

    24.

    Argenta LC, Morykwas MJ: Vacuum-assisted closure: A


    new method for wound control and treatment. Clinical
    experience. Ann Plast Surg 1997;38(6):563-576, discussion 577.

    25.

    Wongworawat MD, Schnall SB, Holtom PD, Moon C,


    Schiller F: Negative pressure dressings as an alternative
    technique for the treatment of infected wounds. Clin
    Orthop Relat Res 2003;414(414):45-48.

    26.

    Bihariesingh VJ, Stolarczyk EM, Karim RB, van Kooten


    EO: Plastic solutions for orthopaedic problems. Arch
    Orthop Trauma Surg 2004;124(2):73-76.

    27.

    Herscovici D Jr , Sanders RW, Scaduto JM, Infante A,


    DiPasquale T: Vacuum-assisted wound closure (VAC
    therapy) for the management of patients with highenergy soft tissue injuries. J Orthop Trauma 2003;
    17(10):683-688.

    28.

    Webb LX: New techniques in wound management:


    vacuum-assisted wound closure. J Am Acad Orthop
    Surg 2002;10(5):303-311.

    29.

    Gustafsson R, Sjgren J, Ingemansson R: Understanding


    topical negative pressure therapy, in European Wound
    Management Association Position Document Topical:
    Negative Pressure in Wound Management. London, England: Medical Education Partnership Ltd, 2007, pp
    2-4.

    30.

    Webb LX, Pape HC: Current thought regarding the


    mechanism of action of negative pressure wound therapy with reticulated open cell foam. J Orthop Trauma
    2008;22(10, Suppl):S135-S137.

    1: Principles of Orthopaedics

    17.

    McGuirt W: Vacuum-assisted closure: A new method


    for wound control and treatment: animal studies and
    basic foundation. Ann Plast Surg 1997;38(6):553-562.

    There are currently two main theories regarding the


    mechanism of action of negative pressure wound therapy with reticulated open cell foam (NPWT/ROCF).
    The first is based on the stimulatory effect of microstrain on cellular mitogenesis, angiogenesis, and
    elaboration of growth factors. This same mechanism is
    operational in controlled Ilizarovian distraction or in
    tissue expansion. The second is based on the enhancement of the dynamics of microcirculation by active
    evacuation of excess interstitial fluid in the form of
    edema. The use of NPWT/ROCF has found a place in
    the management of high-energy traumatic wounds and
    certain high-risk elective surgical wounds.
    31.

    Saxena V, Hwang CW, Huang S, Eichbaum Q, Ingber


    D, Orgill DP: Vacuum-assisted closure: Microdeformations of wounds and cell proliferation. Plast Reconstr
    Surg 2004;114(5):1086-1096, discussion 1097-1098.

    32.

    White RA, Miki RA, Kazmier P, Anglen JO: Vacuumassisted closure complicated by erosion and hemorrhage
    of the anterior tibial artery. J Orthop Trauma 2005;
    19(1):56-59.

    Orthopaedic Knowledge Update 10

    55

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    33.

    34.

    Flack S, Apelqvist J, Keith M, Trueman P, Williams D:


    An economic evaluation of VAC therapy compared with
    wound dressings in the treatment of diabetic foot ulcers.
    J Wound Care 2008;17(2):71-78.
    The authors evaluated the cost-effectiveness of vacuumassisted closure therapy and found that it is less costly
    and more effective than both traditional and advanced
    dressings.

    35.

    Weed T, Ratliff C, Drake DB: Quantifying bacterial


    bioburden during negative pressure wound therapy:
    Does the wound VAC enhance bacterial clearance? Ann
    Plast Surg 2004;52(3):276-279, discussion 279-280.

    36.

    37.

    56

    Schlatterer D, Hirshorn K: Negative pressure wound


    therapy with reticulated open cell foam-adjunctive treatment in the management of traumatic wounds of the
    leg: A review of the literature. J Orthop Trauma 2008;
    22(10, Suppl):S152-S160.
    This article reviews the evidence-based medicine in
    terms of NPWT/reticulated open cell foam (ROCF), as a
    method of reducing bacterial counts in wounds, as a
    bridge until definitive bony coverage, for treating infections, and as an adjunct to wound bed preparation and
    for bolstering split-thickness skin grafts, dermal replacement grafts, and over muscle flaps. Evidence supports a
    decrease in complex soft tissue procedures in grade IIIB
    open fractures when NPWT/ROCF is used. NPWT/
    ROCF appears to provide clinical benefit for the treatment of complex lower extremity wounds.

    Stannard JP, Volgas DA, Stewart R, McGwin G Jr,


    Alonso JE: Negative pressure wound therapy after severe open fractures: A prospective randomized study.
    J Orthop Trauma 2009;23(8):552-557.
    The impact of NPWT after severe open fractures on
    deep infection was evaluated. This treatment represents
    a promising new therapy for severe open fractures after
    high-energy trauma.
    Helgeson MD, Potter BK, Evans KN, Shawen SB: Bioartificial dermal substitute: A preliminary report on its use
    for the management of complex combat-related soft tissue wounds. J Orthop Trauma 2007;21(6):394-399.
    Bioartificial dermal substitute grafting, when coupled
    with subatmospheric dressing management and delayed
    split-thickness skin grafting, is an effective technique for
    managing complex combat-related soft tissue wounds
    with exposed tendon that can potentially lessen the need
    for local rotational or free flap coverage.

    spective, blinded, randomized, controlled clinical trial of


    topical negative pressure use in skin grafting. Plast Reconstr Surg 2004;114(4):917-922.
    41.

    Brandi C, Grimaldi L, Nisi G, et al: Treatment with


    vacuum-assisted closure and cryo-preserved homologous de-epidermalised dermis of complex traumas to
    the lower limbs with loss of substance, and bones and
    tendons exposure. J Plast Reconstr Aesthet Surg 2008;
    61(12):1507-1511.
    The authors concluded that the combination of vacuumassisted closure therapy and deepidermalized dermis
    could, in selected cases, constitute an effective treatment
    for complex lower limb traumatic injuries with bone
    and tendon exposure.

    42.

    Sagi HC, Papp S, Dipasquale T: The effect of suture pattern and tension on cutaneous blood flow as assessed by
    laser Doppler flowmetry in a pig model. J Orthop
    Trauma 2008;22(3):171-175.
    The authors objective was to determine the effects of
    various suture patterns on cutaneous blood flow at the
    wound edge as increasing tension is applied through the
    suture. The Allgower-Donati suture pattern had the
    least effect on cutaneous blood flow with increasing tension in this model.

    43.

    Godina M: Early microsurgical reconstruction of complex trauma of the extremities. Plast Reconstr Surg
    1986;78(3):285-292.

    44.

    Hertel R, Lambert SM, Mller S, Ballmer FT, Ganz R:


    On the timing of soft-tissue reconstruction for open
    fractures of the lower leg. Arch Orthop Trauma Surg
    1999;119(1-2):7-12.

    45.

    Karanas YL, Nigriny J, Chang J: The timing of microsurgical reconstruction in lower extremity trauma. Microsurgery 2008;28(8):632-634.
    In a retrospective review of 14 lower extremity reconstructions with free flaps undertaken over a 4-year period, all patients underwent reconstruction in the delayed (longer than 72 hours) period. Lower extremity
    reconstruction can be performed safely and effectively
    during this delayed period to allow for wound dbridement, stabilization of other injuries, and transfer to
    a microsurgical facility.

    46.

    Levin LS: New developments in flap techniques. J Am


    Acad Orthop Surg 2006;14(10 Spec No.):S90-S93.

    38.

    Leininger BE, Rasmussen TE, Smith DL, Jenkins DH,


    Coppola C: Experience with wound VAC and delayed
    primary closure of contaminated soft tissue injuries in
    Iraq. J Trauma 2006;61(5):1207-1211.

    47.

    Kntscher MV, Erdmann D, Homann HH, Steinau HU,


    Levin SL, Germann G: The concept of fillet flaps: Classification, indications, and analysis of their clinical
    value. Plast Reconstr Surg 2001;108(4):885-896.

    39.

    Genecov DG, Schneider AM, Morykwas MJ, Parker D,


    White WL, Argenta LC: A controlled subatmospheric
    pressure dressing increases the rate of skin graft donor
    site reepithelialization. Ann Plast Surg 1998;40(3):219225.

    48.

    40.

    Moisidis E, Heath T, Boorer C, Ho K, Deva AK: A pro-

    Ali RS, Bluebond-Langner R, Rodriguez ED, Cheng


    MH: The versatility of the anterolateral thigh flap. Plast
    Reconstr Surg 2009;124(6, Suppl):e395-e407.
    The authors discuss anatomy, planning, flap harvest, donor morbidity, and clinical applications of the anterolateral thigh flap. An algorithm is proposed that facilitates
    a clear, problem-based approach for the use of this ver-

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 5: Wound Management

    satile reconstructive option. The flap has been extremely


    useful in skin resurfacing and even functional reconstruction in traumatic wounds.
    49.

    Follmar KE, Baccarani A, Baumeister SP, Levin LS, Erdmann D: The distally based sural flap. Plast Reconstr
    Surg 2007;119(6):138e-148e.

    The distally based sural flap offers an alternative to free


    tissue transfer for reconstruction of the lower extremity.
    The flaps indications and composition and a variety of
    modifications are described. Technical aspects are discussed and clinical insight to minimize complications is
    provided.

    1: Principles of Orthopaedics

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    57

    Chapter 6

    Musculoskeletal Biomechanics
    Michael Bottlang, PhD

    Daniel C. Fitzpatrick, MD

    Introduction

    principles governing orthopaedic biomechanics are


    available in the literature.1 This chapter outlines principal engineering and test parameters used in current biomechanical research to aid the reader in assessing the
    relevance and limitations of biomechanical studies. The
    engineering quantities that describe the principal structures of the musculoskeletal system are defined (the
    properties of bones and the function of joints) and experimental and numeric test methods in biomechanical
    research for evaluating orthopaedic interventions are
    explained.

    1: Principles of Orthopaedics

    Biomechanics is an engineering science that describes


    the complex structure and function of the musculoskeletal system in terms of simplified engineering parameters. These parameters serve to quantify functional aspects of orthopaedic interventions and implants in
    biomechanical studies with defined, reproducible,
    bench-test conditions. By reducing the number of uncontrolled variables compared with clinical studies,
    biomechanical studies have a higher sensitivity for detecting performance differences between interventions.
    Conversely, simplifying and reducing variables and outcome measures too much may limit the relevance of a
    biomechanical study by oversimplifying the clinical scenario. Hence, the challenge both in designing and in interpreting biomechanical studies is in selecting simplified, well-defined test parameters while avoiding
    inappropriate oversimplification of the clinical disorder.
    Detailed descriptions of the many parameters and

    Peter Augat, PhD

    Biomechanics of Bone
    Bones represent the primary load-bearing structural elements of the musculoskeletal system. Bones must be
    sufficiently stiff and strong to fulfill their principal
    function of load transmission. The stiffness and
    strength of bones depend on their material properties
    and geometric structure.

    Material Properties
    Dr. Bottlang or an immediate family member has received royalties from EBI, Synthes, and Zimmer; is a
    member of a speakers bureau or has made paid presentations on behalf of Zimmer and Synthes; serves as a
    paid consultant to or is an employee of Zimmer and Synthes; and has received research or institutional support
    from Zimmer and Synthes. Dr. Fitzpatrick or an immediate family member serves as a board member, owner,
    officer, or committee member of the Slocum Orthopedic
    Group and ASC Board of Directors LIPA; has received
    royalties from Synthes CMF and Zimmer; is a member of
    a speakers bureau or has made paid presentations on
    behalf of Synthes CMF; serves as a paid consultant to or
    is an employee of Synthes CMF; and has received research or institutional support from Synthes and the National Institutes of Health (NIAMS and NICHD). Dr.
    Augat or an immediate family member serves as a board
    member, owner, officer, or committee member of the International Society for Fracture Repair and German Society for Biomechanics; is a member of a speakers bureau
    or has made paid presentations on behalf of Stryker and
    Synthes; serves as a paid consultant to or is an employee
    of Stryker; serves as an unpaid consultant to Aesculap/B.
    Braun, Eli Lilly, and Orthofix; and has received research
    or institutional support from Aesculap/B. Braun, Boehringer, Eli Lilly, Stryker, and Zimmer.

    2011 American Academy of Orthopaedic Surgeons

    Material properties characterize the mechanical function and functional limits of a material. To measure
    material properties, a small cube of the material in
    question can be gradually compressed in a controlled
    manner (Figure 1). The height of the cube will decrease
    with increasing amounts of compressive loading. The
    ratio of the applied load to the resulting compression of
    the cube represents the material stiffness; for a given
    compressive load, stiffer materials undergo less compression than more elastic materials.
    For example, if a load of 10 N is required to compress the cube by 1 mm, the compressive stiffness of the
    cube is 10 N/mm. However, this stiffness depends not
    only on the material property but also on the height
    and cross-sectional area of the cube. To define stiffness
    independent of the cube size, loading is expressed in
    terms of stress (), which is calculated by dividing the
    load by the area the load is acting on (Table 1). Likewise, the resulting compression of the cube can be expressed in terms of strain (), which represents the
    amount of compression divided by the original height
    of the cube. Stiffness can thus be expressed in terms of
    the elastic modulus (E-modulus or E; E = /), which is
    independent of the cube size.
    Assuming that the cube in the example has a side
    length of 10 mm (0.01 m), 10 N loading will induce a

    Orthopaedic Knowledge Update 10

    59

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    compressive stress of = 10 N/0.0001 m2 = 100,000


    N/m2 on the cube surface. The resulting compression
    by 1 mm represents a compressive strain of = 1
    mm/10 mm = 0.1, which it typically expressed as 10%.
    The compressive E-modulus of the cube is expressed as

    Figure 1

    Illustration showing the assessment of material


    properties in a compression test. A compressive
    force is applied to a small cube of the material
    being tested. The height (l) of the cube decreases under the compressive loading (by I .
    The dotted lines represent the cube before
    compression.

    E = 100,000 N/m2/0.1 = 1,000,000 N/m2. Because


    strain has no units, and E-modulus have the same
    units of N/m2 or Pascal (Pa). These units are very small
    and are often expressed in MPa (106 Pa) and GPa (109
    Pa).
    The E-modulus for titanium (E = 110 GPa) is approximately half that of stainless steel (E = 200 GPa)
    (Table 2). Because the stiffness of these metal alloys can
    be sufficiently described by a single E-modulus value,
    they are said to have isotropic material properties.
    Bone tissue has anisotropic material properties,
    whereby the stiffness of a cortical bone cube is approximately 50% greater when loaded in the longitudinal
    direction (parallel to its osteon orientation) (E = 17
    GPa) than in the transverse direction (E = 12 GPa). Regardless of the loading direction, stainless steel is more
    than 10 times stiffer than cortical bone; however, cortical bone is more than 4 times stiffer than polymethylmethacrylate bone cement (E = 3 GPa).
    The E-modulus describes deformation in response to
    loading within the elastic working region of a material, where loads remain sufficiently small to allow
    complete elastic reversal of deformation after load removal. To determine the strength of a material, it must
    be loaded beyond its elastic region to induce failure.
    The load at which permanent plastic deformation begins to occur represents the yield strength of a material

    Table 1

    Basic Engineering Units for Material Property Characterization


    Parameter

    Formula
    m/s2

    Unit

    Example

    [N] Newton

    1-2 N force required to lift


    an apple

    Force

    F = m[kg] 9.81

    Moment

    M=Fd

    [Nm] Newton-meter

    1-2 Nm torque required


    to rotate door knob

    Strain

    = 1/1

    [unitless]; 0.01% to 1%

    1% maximal cortex strain


    before fracture

    Stress; Pressure

    = F/A

    [N/m2; Pa] Pascal

    1,000 Pa pressure to push


    keyboard key

    E-Modulus

    E = /

    [Pa] 1 GPa = 1 109

    110 GPa = 100 109 Pa


    stiffness of titanium

    Table 2

    Representative Values of Material Properties in Compression

    Stainless steel

    E-Modulus
    (GPa)

    Yield Strength
    (MPa)

    Ultimate
    Strength (MPa)

    Failure Strain
    (%)

    200

    700

    820

    12

    Titanium alloy

    110

    800

    860

    10

    Bone cortex

    17

    200

    200

    PMMA

    74

    74

    PMMA = polymethylmethacrylate bone cement

    60

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 6: Musculoskeletal Biomechanics

    Structural Properties

    Stress-strain curves reflect the properties of representative materials in compression tests. The
    slope of the initial linear region of curves (continuous lines) represents stiffness (E = /).
    Steeper slopes represent stiffer materials. Yield
    points indicate limits of the elastic working
    region. Brittle materials such as cortical bone fail
    abruptly, whereby the yield point coincides with
    failure. PMMA = polymethylmethacrylate.

    (Figure 2). The load at which the material fractures


    represents its ultimate strength. The ultimate strength
    of titanium (860 MPa) is similar to that of stainless
    steel (820 MPa), demonstrating that a less stiff material
    is not necessarily weaker than a stiffer material. Because of its anisotropic behavior, cortical bone has a
    higher ultimate strength when compressed in the longitudinal direction (193 MPa) than in the transverse direction (133 MPa). Additionally, cortical bone is nearly
    50% stronger in compression than in tension. These
    values have several clinical implications. Fractures of
    long bones typically are initiated in the region of highest tensile stress, resulting in a predicable fracture pattern for a given loading mode. These strength values
    also show that the ultimate strength of stainless steel is
    more than four times that of cortical bone. This is important for a single peak loading event, such as a fall,
    which may induce a periprosthetic fracture in the bone
    near an implant rather than an implant fracture. Repetitive loading below the ultimate strength limit induces
    microcracks that can also lead to fatigue failure. In
    healthy bone, remodeling continuously repairs these
    microcracks, making bone tissue highly resistant to fatigue failure. Unlike bone, microcracks in implant materials accumulate under repetitive loading and propagate until fatigue failure occurs. For example, if a bone
    fracture fails to unite, the osteosynthetic construct will
    be subjected to prolonged loading cycles that may lead
    to fatigue fracture of the fixation hardware.
    Analogous to the characterization of material under
    compressive and tensile loading, the stiffness, yield
    strength, and ultimate strength of a material also can
    be determined under bending and torsional loading to
    gain a comprehensive assessment of material properties
    specific to each principal loading mode, as described in
    the literature.1

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    Figure 2

    Structural properties depend not only on material properties but also on the objects size and shape. For geometrically simple structures with well-defined material
    properties, structural properties can be calculated without the need for mechanical testing. For example, the
    stiffness and strength of an osteosynthetic plate depends only on its material property and cross-sectional
    geometry. Assuming an osteosynthetic plate of width
    (w) = 15 mm and thickness (t) = 5 mm, the bending
    stiffness (EI) of the plate can be calculated as the product of its E-modulus and the second moment of inertia
    expressed by the formula (I) = (w t3)/12 (Figure 3). In
    this formula, bending stiffness correlates linearly with
    plate width but relates to the third order with plate
    thickness. Therefore, doubling the plate width results in
    twice the plate stiffness, whereas doubling the plate
    thickness increases plate stiffness eightfold (23). Similarly, the bending stiffness of a solid cylinder such as an
    intramedullary nail of diameter d is the product of its
    E-modulus and I = d4 /64. Doubling the nail diameter will cause a 16-fold increase (24) in bending stiffness. The bending stiffness of a cylinder can be increased without increasing its cross-sectional area by
    introducing a hollow core while expanding the outer
    diameter. The resulting cylindrical tube will have
    gained bending stiffness while maintaining the same
    weight and axial stiffness and strength as a solid cylinder of equivalent cross-sectional area. This weightoptimized tubular structure represents the principal diaphyseal geometry of long bones. However, closedform equations for calculating stiffness and strength are
    limited to simple and regular geometries, and such
    equations cannot accurately predict properties of bone
    structures.
    Density is another important structural property of
    bone. Because the mineral composition of bone is fairly
    consistent, the stiffness and strength of an individual
    area of trabecular bone is within 10% to 15% of cortical bone. However, trabecular bone as a structure is
    far weaker than cortical bone. The three-dimensional
    matrix of trabecular bone has a porosity of 30% to
    90%, making it much less dense than cortical bone.
    The stiffness and strength of trabecular bone depends
    primarily on its density. Osteoporosis is diagnosed by
    radiographically estimating bone density. The density
    of trabecular bone varies by approximately one order
    of magnitude, from approximately 0.1 g/mL to 1.0
    g/mL; however, the corresponding stiffness and strength
    of trabecular bone varies by three orders of magnitude.
    Therefore, even a small decrease in density can considerably reduce the structural properties of trabecular
    bone. Because of variability in the geometric organization of the trabecular structure, the stiffness and
    strength of trabecular bone with the same apparent
    density can vary tenfold. The most promising approach
    for in vivo assessment of bone mechanical properties
    combines quantitative CT with microfinite element
    analysis, whereby quantitative CT is used to acquire
    high-resolution images of the trabecular structure and
    61

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 3

    Illustration showing the influence of cross-sectional geometry on bending stiffness of basic structures. For example,
    increasing the outer diameter of a cylindrical structure from 10 mm to 12 mm while retaining a wall thickness of 2
    mm increases bending stiffness (I) by 82%.

    microfinite element analysis is used to calculate bone


    stiffness and strength, while accounting for both density and structural organization. This microfinite element analysis approach has been shown to yield a
    strong correlation (R2 = 0.75) between predicted and
    experimentally tested fracture loads, whereas strength
    prediction based on density alone had a considerably
    lower correlation (R2 = 0.45).2
    Clinical scenarios frequently involve more complex
    interactions between multiple structures, such as implants and bones, whereby load transfer and strength
    also depend on the contact interface and method of fixation between the structures. To analyze the stiffness,
    strength, and failure modes of these complex structures
    and constructs, bench-top biomechanical testing remains the gold standard. Numeric simulation by means
    of finite element analysis can provide distinct advantages over biomechanical testing for mechanical evaluation of structures and constructs. In most instances,
    these numeric approaches rely on biomechanical testing
    for model validation.

    Clinical Correlation
    Examining proximal femoral and femoral diaphyseal
    fracture risks in elderly individuals provides a good example of the clinical application of musculoskeletal
    biomechanics. Osteoporosis is a systemic disease and
    should affect the metaphyseal and diaphyseal bone in a
    similar manner. However, unlike proximal femoral
    fractures, an increased rate of femoral diaphyseal fractures is not observed in elderly patients. The structural
    properties of bone discussed in this section play a role
    62

    Orthopaedic Knowledge Update 10

    in the etiology of this observation. As an individual


    ages, the diameter of the femoral diaphysis increases
    and the thickness of the cortex decreases. Using the second moment of inertia principle discussed in this section, the bending stiffness of a tubular bone increases
    as the outer diameter increases, even as the cortical
    thickness and material properties of the bone decrease
    (Figure 3). The aggregate increase in strength realized
    by increasing the diameter of the shaft is adequate to
    protect elderly individuals from osteoporotic diaphyseal femoral fractures. In contrast, trabecular thinning
    of the metaphysis cannot be compensated by structural
    changes of the proximal femur, resulting in an increased risk of hip fractures in individuals with osteoporosis.

    Biomechanics of Joints

    Joint Loading
    Joints enable functional mobility between bone segments. Joint motion is controlled by the forces and moments acting across the joint. Forces acting on a joint
    are typically represented by vectors, depicting the magnitude and line of action of a force. If a force vector of
    magnitude F is acting at a distance d from a joint, it
    will also create a rotational moment M around the
    joint. This moment has a magnitude of M = F d,
    whereby M linearly increases with the perpendicular
    distance or lever arm of the force vector from the
    joint. Unless it is counteracted by a moment of equal

    2011 American Academy of Orthopaedic Surgeons

    Chapter 6: Musculoskeletal Biomechanics

    A free-body diagram of the elbow in static equilibrium while holding a gallon of milk, which exerts
    a downward force of 37 N. Because this force
    acts at a distance of 0.2 m to the elbow, it also
    induces an extension moment (M = 37 N 0.2 m
    = 7.4 Nm) around the elbow. Assuming that the
    biceps is the sole elbow flexor, the biceps muscle
    must create a flexion moment of equal magnitude for static equilibrium to exist. Because the
    biceps force acts at a distance of only 0.02 m to
    the elbow joint, it must generate a force (F = 7.4
    Nm/0.02 m = 370 N) to counteract the extension
    moment. To complete the free-body diagram,
    the sum of all forces must also be zero. Because
    the biceps induces an upward force of 370 N,
    but the gallon exerts a downward force of only
    37 N, an additional downward force (F = 370 N
    37 N = 333 N) must be generated as compression
    at the elbow joint to equalize forces.

    magnitude but opposite direction, this moment will induce rotation at the joint.
    Joint forces and resulting moments are induced by
    external loads such as the weight of an object held in a
    hand, and by internal loads such as the muscle forces
    required to hold the object. External forces can readily
    be measured with scales and load sensors that determine the force acting on the body. Assessing internal
    loads is far more complicated because muscles cannot
    be instrumented with load sensors and because multiple
    muscles (activated to various degrees) act across the
    same joint. However, when a joint is at rest or in a
    static equilibrium, joint forces can be calculated based
    on the facts that the sum of all forces and the sum of all
    moments acting on a nonmoving joint must be zero.
    For this purpose, known external forces are entered
    into a free-body diagram along with the line of action
    of muscles that must generate the internal loads to
    achieve static equilibrium.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    Figure 4

    For example, a free-body diagram can be drawn to


    calculate the forces in the elbow joint while holding a
    gallon of milk (Figure 4). The free-body diagram,
    which illustrates the fact that holding a gallon of milk
    induces a force equal to approximately one half body
    weight of loading in the elbow joint, shows that internal forces tend to be far greater than external forces because of the small lever arms by which muscles can induce moments around joints.
    In the previous example, it was necessary to assume
    that the biceps was the only elbow flexor. This illustrates the limitation of free-body diagram analysis; such
    analysis can only approximate joint forces under simplified, static loading conditions. In reality, several muscles act across the elbow joint to produce motion. Each
    of these muscles is activated to various degrees to produce elbow flexion. Because it is not possible to know
    the exact contribution that each muscle provides for elbow flexion, classic free-body diagram analysis has limited value. In this situation, optimization algorithms are
    used to calculate the most likely distribution of muscle
    forces during each instant of joint motion. Optimization is driven by the assumption that energy consumption of muscles for a given task is minimized.
    In vivo assessment of joint loads and muscle forces
    during active motion requires a combination of five advanced biomechanical techniques. (1) In vivo instrumented implants with telemetric data transmission are
    used to capture joint forces and moments during typical activities of daily living. (2) Load sensors are used
    to assess external forces acting on the body, such as
    ground reaction forces during gait. (3) Video-based motion analysis is used to acquire the corresponding
    movement of body segments by skin marker tracking.
    (4) Patient-specific reconstruction of bone and muscle
    geometry from CT data enables translation of body
    segment motion into motion of bone segments around
    joints. (5) Synchronized data of joint loads, external
    loads, and skeletal motion are applied to a musculoskeletal computer model for the calculation of muscle
    forces and muscle activation patterns. The calculated
    muscle activation patterns can then be validated using
    electromyogram recordings. This comprehensive assessment of joint loading has been performed for the hip,
    knee, shoulder, and spine for a range of daily activities
    such as walking, running, stair climbing, sitting, and
    lifting.3-7
    Using this approach, a series of clinically relevant
    observations on joint loading have been obtained in recent studies. In the hip, representative peak loads are
    270% of body weight (body weight, approximately
    700 N) during walking and 520% of body weight during running.3 Interestingly, wearing soft-soled shoes or
    running on soft surfaces does not appreciably reduce
    peak loads; the lowest peak loads are recorded when
    walking barefoot. Tripping can induce peak loads of
    870% of body weight. Compared with walking, stair
    climbing induces similar peak loads, but with more
    than 80% higher rotational moments. Because hips
    have the highest loads during walking and stair climbing, and because walking represents the most frequent
    63

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 5

    Illustration of joint classification based on the geometric constraints of diarthrodial joints.

    loading event (180,000 walking cycles/month),8 implants should be tested with loading that simulates
    walking and stair climbing. In the shoulder, glenohumeral contact forces remain less than 100% of body
    weight for most daily activities but range up to 130%
    of body weight when lifting an object at arms length.6
    Moments can reach up to 5.2 Nm and are attributed to
    friction at the bearing surface. In the knee, level walking induces peak axial forces of 280% of body weight.5
    Stair descending produces the highest forces of up to
    350% of body weight in axial loading, 35% of body
    weight in mediolateral loading, and 36% in anteroposterior loading. It furthermore induces a considerable
    varus-valgus moment of 4.6% body weight x meter.
    This emerging body of in vivo loading data from instrumented implants provides a unique opportunity to
    refine and unify loading schemes in biomechanical tests
    for the evaluation and systematic optimization of implant performance in bench-top studies.

    Joint Characterization
    Joints can be characterized by the geometric and ligamentous constraints that define joint stability and by
    the type and range of joint motion. Geometric constraints are provided by articulating surfaces that transmit compressive forces to effect motion during load
    bearing. Ligaments transmit tensile loads, preventing
    joint dislocation while allowing a defined amount of
    joint laxity. As a first approximation, diarthrodial
    joints may be categorized by their apparent geometric
    64

    Orthopaedic Knowledge Update 10

    constraints into pivot joints (such as the proximal radioulnar joint), hinge joints (such as the ulnohumeral
    joint), saddle joints (such as the carpometacarpal joint),
    and spheroidal joints (such as the hip) (Figure 5). However, such a simplified geometry-based classification
    system does not reflect ligamentous constraints that are
    biomechanically crucial for joint function.
    The hip joint resembles a ball and socket or spheroidal joint. The acetabular socket geometrically constrains translation of the femoral head in all three directions while permitting rotation (flexion-extension,
    internal-external, and abduction-adduction) around
    three axes. The high congruency of the spherical bearing interface provides load distribution over a large
    contact area, resulting in low contact pressure. The relatively high geometric constraint combined with a low
    contact pressure makes the hip joint particularly suitable for joint arthroplasty that can restore geometric
    constraints but not ligamentous constraints. In contrast, the bicondylar knee joint provides only modest
    geometric constraints of convex condyles that articulate
    on a substantially flat tibial plateau. The cruciate and
    collateral ligaments are essential stabilizers that guide
    knee flexion, concomitant internal-external rotation,
    and anteroposterior translation. These modest geometric constraints present considerable challenges for knee
    arthroplasty. The strong reliance on ligamentous constraints makes correct implant placement crucial to balancing tension in the medial and lateral collateral ligaments; deficient balancing may cause instability or
    excessive joint loading and wear. These examples show
    that a biomechanical analysis of joint motion and joint
    constraints is essential to understanding the complex
    function of native joints and to improving the function
    of joint arthroplasty.

    Joint Kinematics
    Joint kinematics describes the motion of one bone segment relative to the adjoining bone segment. Two adjoining bone segments exhibit six degrees of freedom
    bone translation in three orthogonal directions and
    rotation around three orthogonal axes. To simplify the
    description of motion, it is usually assumed that one
    bone segment is fixed in space. A local reference frame
    is defined in the fixed segment, typically along the anatomic axes (Figure 6). For example, a joint coordinate
    system can be used to describe motion of the femur relative to a fixed tibia in terms of three translations (anteroposterior, mediolateral, and proximodistal) and
    three rotations (flexion-extension, internal-external,
    and abduction-adduction).
    A variety of electromagnetic, ultrasonic, and optical
    motion tracking systems are available to automatically
    track the spatial motion of sensors or markers attached
    to motion segments at resolutions of better than 1 mm
    of translation and 1 of rotation. These systems allow
    convenient in vivo assessment of joint kinematics by
    tracking skin markers; however, accuracy is limited by
    skin-to-bone motion artifacts. To avoid these artifacts,
    in vivo joint kinematics can be directly assessed using

    2011 American Academy of Orthopaedic Surgeons

    Section 1: Principles of Orthopaedics

    Bench-Top Testing

    1: Principles of Orthopaedics

    Figure 8

    Illustrations showing isolated testing of a plating


    construct in the three principal loading modes:
    axial, torsional, and bending. Axial test results
    can considerably differ, depending on whether
    the specimen ends are rigidly fixed or loaded
    through joints. Bending is shown for a fourpoint-bending setup, which induces a constant
    bending moment between points A and B. Loadinduced actuator displacements represent deformation of the entire construct and can be considerably larger than displacement (d) at the
    fracture zone.

    represents the translation of the tibia relative to the femur in response to anteroposterior loading of the tibia,
    clinically known as the Lachman test. Translational laxity is measured in millimeters of translation per Newton
    loading, whereas rotational laxity is measured in degrees of rotation per Newton-meter torsion. If laxity is
    measured at joint motion increments throughout the
    range of motion, an envelope of joint laxity can be defined. Clinically, biomechanical measurements of joint
    laxity over a range of motion are important in determining safe and effective rehabilitation protocols after
    reconstructive surgery. For example, a recent study of
    medial collateral ligament sectioning suggests that after
    a medial collateral ligament repair at the elbow, passive
    range of motion with the forearm in supination is safer
    than passive motion with the elbow in pronation.11

    Clinical Correlation
    The interplay between geometric constraints and ligamentous stability discussed in this section is evident in
    the clinical case of an elbow dislocation. The elbow behaves mainly as a hinge joint with the trochlear groove
    and radial head providing inherent bony stability while
    allowing motion along the flexion-extension axis. The
    muscle forces acting on the elbow also provide a constant compressive force, while the medial and lateral
    collateral ligaments provide additional stability to the
    joint. After a traumatic elbow dislocation, the ligamentous constraints are disrupted. However, if the geometric (bony) constraints are intact, the elbow is stable and
    external splinting is not required. Conversely, if both
    the geometric constraints and ligamentous restraints
    are damaged, as occurs with a concomitant coronoid or
    radial head fracture, the elbow is rendered unstable and
    usually requires surgical repair.12
    66

    Orthopaedic Knowledge Update 10

    Biomechanical testing provides a time- and costeffective strategy to analyze implant performance in a
    controlled bench-top environment. Different from clinical outcome studies, biomechanical testing uses simplified test conditions to describe specific aspects of implant performance. This biomechanical testing strategy
    relies on the definition of a specific performance criterion or a clinically relevant failure mode that will subsequently guide the experimental design and choice of
    outcome parameters. A clear understanding of these
    generally simple implant evaluation parameters is helpful in assessing the clinical relevance of results obtained
    in biomechanical studies.

    Specimens
    Implants are typically tested in either cadaver or surrogate specimens. Nonembalmed cadaver specimens realistically reflect the complex structure and material
    properties of bone. However, cadaver specimens can
    greatly vary in geometry and material properties, even
    when specimens of similar bone density are selected.
    Variability can be reduced by using paired specimens,
    whereby interventions are randomly assigned to either
    right or left specimens; however, this necessarily confines testing to a comparison between two groups. Alternatively, whole-bone synthetic surrogates of the femur, tibia, humerus, radius, and ulna are commercially
    available (Pacific Research Laboratories, Vashon Island, WA). These surrogate specimens, consisting of a
    glass fiber-reinforced epoxy cortex and cancellous bone
    replicated by rigid polyurethane foam, are designed to
    have structural properties in the physiologic range of
    healthy bone. Different from cadaver bone, the variability between surrogate femurs is within 2% to 10%.
    Polyurethane foam, however, does not replicate the
    density gradients and load-optimized architecture of
    the trabecular structure specific to cadaver bone. Also,
    these synthetic surrogates do not represent osteoporotic
    bone in which complications associated with implants
    are most prevalent. For this purpose, a validated surrogate of the osteoporotic femoral diaphysis has recently
    been introduced.13

    Loading Mode
    All bones are exposed to complex loading composed of
    three principal loading modesaxial, torsional, and
    bending. Testing implant performance individually for
    each of these principal loading modes simplifies the
    load application and enables isolation of failure mechanisms specific for each principal loading mode (Figure
    8). To reduce the number of loading scenarios, testing is
    sometimes only performed in the dominant loading
    modes for the anatomic site being studied. For example,
    because the femur is loaded primarily in axial compression and bending, unicortical locked plating of femoral
    fractures was initially tested in axial compression and
    bending only, which yielded encouraging results. However, the clinically observed failure mechanism of screw

    2011 American Academy of Orthopaedic Surgeons

    Chapter 6: Musculoskeletal Biomechanics

    Figure 6

    A tibia-fixed local reference frame is centered on


    the tibial plateau with the orthogonal coordinate axis directed laterally (X-axis), anteriorly (Yaxis), and proximally (Z-axis). Translation of the
    femur relative to the tibia can now be expressed
    in terms of three discrete displacements along
    the X, Y, and Z axes. Rotation of the femur relative to the tibia can be defined by three discrete
    rotations , , and around the X, Y, and Z axes,
    respectively.

    Figure 7

    Illustration showing a characterization of joints. A, A series of SDAs obtained from incremental joint motion represents the location and dispersion of rotation axes over the elbow range of motion. The smaller the axes dispersion,
    the closer the joint resembles an ideal hinge joint. The angles between the average SDA and the ulnar and humeral
    shaft axes are denoted by 1 and 2, respectively. B, Graph showing joint laxity of the elbow, represented by the
    permissible varus-valgus rotation from a neutral motion path in response to defined varus-valgus loads over the
    flexion range of motion. (Reproduced with permission from Bottlang M, Madey SM, Steyers CM, Marsh JL, Brown
    TD: Assessment of elbow joint kinematics in passive motion by electromagnetic motion tracking. J Orthop Res
    2000;18:197-198.)

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    fluoroscopy with model- or image-matching based on


    CT-derived models of bone segments or arthroplasty
    components.9
    Analysis of the six degrees of freedom joint kinematic data can be graphically represented by six individual curves. Because of the high volume of data represented in motion curves, datasets often must be
    reduced to clinically relevant parameters or to a small
    number of joint positions to enable statistical comparison of kinematic performance between experimental
    groups. If the research questions seek to identify the location or axis around which motion occurs, helical
    axes or screw displacement axes (SDAs) can be calculated from the six degrees of freedom motion data.
    SDAs represent the fact that any arbitrary motion of a
    bone segment can be accomplished by rotation around
    and translation along a unique axis. For example, SDA
    can be calculated from the six degrees of freedom data
    of the ulna relative to the humerus obtained at 10 and
    20 of elbow flexion. This SDA will intersect the trochlea and directly represents the axis around which ulnar
    rotation occurred during elbow flexion from 10 to
    20. A series of SDAs obtained from incremental joint
    rotations spanning the range of joint motion can provide a detailed and intuitive characterization of joint
    function (Figure 7, A). Recent SDA analysis of the knee
    during running showed both a translation of up to 20
    mm and a change of up to 15 in inclination of the instantaneous axis of rotation during the flexion cycle, a
    finding that suggests a single axis knee prosthesis may
    oversimplify native knee motion.10
    Joints also can be characterized in terms of their
    range of motion and joint laxity (Figure 7, B). Laxity
    defines the constraints to motion in response to an external load. For example, anteroposterior knee laxity

    65

    Chapter 6: Musculoskeletal Biomechanics

    1: Principles of Orthopaedics

    Figure 9

    Graphs showing test load patterns. After application of a preload (LPRE), testing may be conducted statically for assessing stiffness and failure load (LMAX) (A), dynamically for assessing the number of loading cycles until fatigue failure occurs (B), or with progressive dynamic loading for assessing the failure load level under dynamic loading (C).

    pullout was subsequently linked to the poor fixation


    strength of unicortical locking screws in torsion.14
    Therefore, results obtained in one loading mode cannot
    be extrapolated to alternate loading modes.
    Specimen constraints highly influence the load imparted to a specimen under a principal loading mode.
    For example, if the ends of a plating construct are not
    rigidly constrained but suspended between ball joints,
    axial loading will primarily impart plate bending.
    Therefore, both the loading mode and specimen constraint must be considered when comparing results between studies.
    As an alternative to simplified testing under the principal loading modes, implants may be tested under
    joint-specific complex loading modes representative of
    the activities of daily living. As previously mentioned,
    physiologic loading data for a range of activities have
    been obtained for the hip, knee, shoulder, and spine using implants instrumented with load sensors and telemetry for wireless data transfer.4-7 For load application in
    biomechanical tests, these loading data can be combined into a resultant load vector that changes in magnitude and orientation throughout a specific loading
    task. Reproducing these physiologic transient load vectors in bench-top testing requires sophisticated joint
    simulators or the use of robotic equipment capable of
    inducing arbitrary motion and forces in space. Quasiphysiologic load application can be achieved using
    more standard testing systems by positioning specimens
    at a specific angle and offset relative to the vertical actuator of a standard material testing system to yield a
    specific resultant load vector and loading moment.
    Physiologic loading and joint motion may also be facilitated by muscle force simulation through tendons.
    For this purpose, muscle force distributions and activation patterns have been computed from loading data of
    instrumented implants for the hip, knee, and shoulder.
    These recent advances in joint and muscle load assessment based on instrumented prostheses are crucial for

    2011 American Academy of Orthopaedic Surgeons

    resolving the apparent lack of consensus on test configurations and loading conditions in biomechanical studies.

    Loading Patterns
    Test loads can be applied statically or dynamically.
    Static loading is used to assess stiffness, constraints,
    and load transfer but may also be used for strength assessment, whereby loading is gradually increased until
    failure occurs (Figure 9, A). However, clinical failure
    rarely occurs from a single loading event and most often is better simulated by dynamic loading. Traditionally, dynamic loading has been used for wear and fatigue testing of arthroplasty implants by repeating a
    load pattern for millions of cycles to simulate multiyear
    loading histories in an accelerated manner (Figure 9,
    B). Dynamic loading is increasingly being applied for
    testing osteosynthetic constructs to simulate fixation
    failure, implant migration, and fatigue. Failure may not
    consistently occur at a given dynamic load amplitude
    under a standard cyclic loading regimen. For this reason, several recent studies have applied progressive dynamic loading in which the amplitude of the dynamic
    load is increased in a stepwise manner to induce construct failure within a controlled number of loading cycles (Figure 9, C).
    Testing can be conducted using displacement or load
    control. Displacement-controlled tests prescribe a defined linear or rotational displacement and assess the
    resulting forces and moments. Load controlled tests apply a force or moment and measure the resulting deformation or motion of the loaded specimen. Most biomechanical tests are conducted using load control to
    simulate physiologic loading regimens. However, displacement control remains an attractive alternative because of the relative simplicity of applying accurate cyclic displacements with the camshaft or screw-type
    actuators that are frequently used in mechanoactive tissue engineering applications.

    Orthopaedic Knowledge Update 10

    67

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    Figure 10

    A, Under dynamic loading, specimens undergo elastic, recoverable deformation as well as subsidence or migration,
    which represents the accumulation of unrecoverable displacement. Progression of subsidence is indicative of failure, which can be defined by selection of an appropriate subsidence threshold. B, Under static loading, a sudden
    drop in displacement defines failure and allows identification of strength in terms of peak load (LMAX). C, Specimens that gradually fail will complicate detection of failure for strength determination.

    Outcome Parameters
    Stiffness
    Stiffness is frequently used to represent the deformation
    of a test specimen in response to loading; however, higher
    stiffness does not necessarily correlate with improved implant performance. Excessive stiffness can increase the
    risk of periprosthetic fracture because of increased stress
    risers at the implant-bone interface, especially in the
    presence of osteoporotic bone. For osteosynthetic constructs, deficient stiffness can lead to hypertrophic nonunions, whereas excessive stiffness can suppress secondary bone healing. Because bone healing depends on the
    stiffness at the fracture site rather than the entire testing
    apparatus, reports of the stiffness of osteosynthetic constructs should reflect displacement measured across the
    fracture site. Stiffness or degradation of stiffness under
    dynamic loading is sometimes used to infer strength. Although intuitive, inferring strength without testing to
    failure remains speculative.
    Stability
    Stability is not an engineering quantity but is frequently
    used to describe the amount of displacement across a
    fracture or a bone-implant interface in response to a
    given loading event. Subsidence or migration represents
    the amount of unrecovered displacement after the loading event (Figure 10, A). Subsidence during dynamic
    loading provides a sensitive parameter of implant performance. Stabilization of initial subsidence typically
    indicates successful settling of an implant into a stable
    position, whereas progression of subsidence reflects the
    rate of damage accumulation that eventually will lead
    to implant or fixation failure.
    Stress
    Stress () in implants and bone cannot be measured directly, but is typically inferred from measurements of
    stress-induced material deformation and strain (). The
    resulting stress depends on the induced strain as well as
    68

    Orthopaedic Knowledge Update 10

    on the apparent stiffness of the deforming material ( =


    E). A softer material will exhibit less stress than a
    stiffer material for a given deformation. Strain gauges
    have been used since 1938 and remain the most common strain sensors because of their high sensitivity and
    accuracy. They are glued onto a surface of interest and
    contain a conductive filament that changes electrical resistance when strained. Standard strain gages measure
    strain in only one direction. Rosette strain gauges contain three filaments to sense the magnitude and orientation of the highest compressive and tensile strains at
    the strain gage location. Contemporary optical systems
    can capture continuous strain maps by correlating digital images of a surface obtained before and after deformation. These image correlation systems track the displacement of individual surface markers or the
    deformation of a speckle pattern projected by lasers
    onto the object surface. The high sensitivity and noncontact approach of these optical strain sensors enables
    acquisition of strain distributions on hard and soft tissues, reflecting load transfer mechanisms and stress
    concentrations.15 However, all strain sensors are confined to measuring surface strain. Strain in structures
    and at interfaces can only be estimated by numeric simulation, typically with finite element analysis.
    Strength
    Strength provides a clear indicator of implant performance, which correlates clinically with a reduced risk
    of implant failure. Although strength simply represents
    the ultimate load at which a structure fails, strength assessment is highly dependent on the choice of failure
    criterion. For a sudden catastrophic fracture of a structure, the instance of failure is defined by the fracture
    (Figure 10, B). When specimens fail gradually, the instance of failure may be less clear (Figure 10, C). In
    such cases, defining a failure criterion based on a subsidence threshold under dynamic loading can be advantageous. When strength is assessed under dynamic

    2011 American Academy of Orthopaedic Surgeons

    Chapter 6: Musculoskeletal Biomechanics

    Figure 11

    loading it also can be expressed in terms of fatigue


    strength, which represents the number of loading cycles
    of a given magnitude that can be sustained before failure occurs. The highest dynamic load amplitude at
    which no failure will occur regardless of the number of
    loading cycles is called the endurance limit. Most importantly, the failure modes induced in a simplified
    bench-top environment should correlate with clinically
    observed failures to support the relevance of strength
    results.
    Kinematic Representations of
    Musculoskeletal Movements
    Kinematic representations of musculoskeletal movements, such as displacements and rotation angles
    around joints, require a clearly defined, physically
    meaningful, and reproducible reference frame or coordinate system. For any given joint, reference frames can
    be aligned based on a variety of anatomic landmarks
    and planes, whereby kinematic representation of the
    same motion will differ when expressed in different reference frames. A direct comparison of kinematic results
    between studies is only possible when the same reference frame is used to describe motion. The effects of interventions on joint kinematics also should be evaluated for all permissible translations and rotations
    around a joint because an intervention may restore one
    particular kinematic parameter while having a detrimental effect on other kinematic parameters.

    Clinical Correlation
    Mechanical studies can isolate clinically relevant but
    rarely observed failure modes. Locked-plate constructs
    provide excellent fixation in osteoporotic bone; however, the difference in stiffness between the osteoporotic
    bone and plate is magnified in the presence of anglestable locked screws. A recent bench-top study, which
    investigated the effect of a mismatch between implant
    and bone stiffness, reported that angle-stable, locked
    screws at the end of the plate increased the risk of a
    periprosthetic fracture relative to nonlocked screws.16
    This complication is so rare that it is unlikely to be rec-

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    Chart showing the process of finite element analysis. A central part of finite element analysis is the validation process. The results of the model must be validated internally (verification and sensitivity) and also externally by comparing the computed results with bench-top experiments.

    ognized in any reasonably sized clinical study. The


    bench-top study was valuable because it isolated and
    identified the problem and proposed a simple but effective solution.

    Numeric Simulation
    Numeric models have been developed to solve complex
    loading scenarios to determine stress and strain in implants and musculoskeletal structures.17,18 Although the
    loading of a cantilever beam by a single force can be
    solved analytically, the deformation during walking of a
    cephalomedullary nail that fixes a subtrochanteric fracture can be considered a complex loading scenario requiring a numeric solution. Finite element analysis is the
    method of choice to solve these types of problems. Finite
    element analysis is defined as a numeric method to solve
    partial differential equations; practically, it is a technique
    to compute stress, strain, and deformation in a digitized
    structure (Figure 11). The digitized structure consists of
    thousands of individual elements that are connected to
    each other. The numeric approach is to consider each individual element and calculate its mechanical behavior
    as a response to all neighboring elements.
    The most time-consuming aspects of a finite element
    analysis are correctly preprocessing the mechanical
    problem and verifying and validating the results. For
    the preprocessing of the mechanical problem, the geometry of the object (bone, implant, or device) must be
    provided in digital form with sufficient accuracy and
    spatial resolution of the locations of interest to permit
    visualization of the results. Mesh or element generation
    is strongly supported by finite element analysis software but must be tailored to the specific mechanical
    problem. The material properties, applied loads, and
    moments must be provided and often must be estimated. In the example of the cephalomedullary nail
    that fixes a subtrochanteric fracture (Figure 12), the list
    of boundary conditions to be described includes the external load situation, the geometry of the nail, the bone
    and the fracture, the contact conditions between the
    implants (nail, screws) and the bone, and the material

    Orthopaedic Knowledge Update 10

    69

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 12

    Finite element analysis of cephalomedullary nail fixation of a subtrochanteric fracture of the proximal femur.
    A, The bone and the implant are represented by a mesh of individual elements. Arrows point to the fracture. B,
    The model can show locations of stress concentrations in the nail depending on the type of fracture pattern. C, To
    validate the model, the results of the numeric calculations are compared with results of a biomechanical test
    setup, which includes strain measurements on the nail by strain gauges.

    properties of the bone and the implants.


    The results of a finite element analysis should not be
    presented before verification and validation of the
    model. Verification of the model requires careful examination of the procedures (such as equation solving and
    model building) and techniques used. It ensures that the
    numeric model has no technical flaws and is capable of
    generating reasonable results. Verification involves determining if things were done correctly. Validation by contrast challenges the model or the concept itself. To validate a numeric model, it is evaluated to determine if the
    theoretic model is suitable for the real-world problem.
    Validation involves determining if the correct things were
    done.
    In the example of the cephalomedullary nail, the verification process would ensure the accuracy of the geometry and whether the geometric changes caused by
    the surgical procedure (holes, cavities, implant placement) are properly represented by the model. The constraints, the loads that act on the bone, the material
    properties, and the types of numeric contacts between
    the different parts of the assembly (such as the nail, the
    lag screw, and the bone fragments) would be checked
    for reasonability. The final and most important part of
    the verification is the so-called convergence analysis.
    This analysis ensures that the type of finite elements
    and the mesh density have no influence on the results.
    The validation of the model would be accomplished by
    comparing the numeric calculations with experimentally determined measurements. In the example, the osteosynthetic stiffness measured by the testing machine
    and strains measured on different parts of the implant
    by strain gauges could be used for validation.
    Although the development of a numeric model is an
    elaborate and time-consuming process, a valid finite element analysis model has several advantages over lab70

    Orthopaedic Knowledge Update 10

    oratory experiments. The finite element analysis model


    provides a much larger variety of results than experiments. The typical outcome measures, such as strain
    (), stress (), or deformation (), can be determined at
    every location in the model. For example, it is possible
    to find the location of the largest stress that occurs at
    the implant (Figure 12, B) or to determine the threedimensional deformation on each aspect of the fracture
    gap. It also is possible to obtain measurements from the
    inside of the model (for example, from the nail in the
    medullary canal or the endosteal bone surface). Experimental measurements are restricted to limited and predefined measurement locations on the specimen surface
    and are often only one-dimensional. The most significant advantage of finite element analysis models is the
    possibility to perform parameter studies in which the
    model geometry, the material properties, or the boundary conditions can be iteratively changed. In the example of the cephalomedullary nail, there would be interest in determining how the outcome measurements
    change for different types of hip fracture, after modification of the lag screw diameter, or with the additional
    use of locking bolts.17 The effects of different loading
    scenarios could easily be observed by changing the load
    direction and amplitude to account for muscle activities
    during different activities of daily living. Therefore, a
    validated finite element analysis model is perfectly
    suited to study the effect of parameter modifications on
    the mechanical performance of complex geometries and
    complex loading conditions.

    Summary
    A sound understanding of basic biomechanical principles provides a strong tool for the orthopaedic surgeon

    2011 American Academy of Orthopaedic Surgeons

    Chapter 6: Musculoskeletal Biomechanics

    to evaluate the results of bench-top studies and to integrate this information into clinical practice. Biomechanical testing allows specific aspects of the musculoskeletal system to be evaluated in a quantitative
    manner, without including confounding factors that often make clinical studies difficult. Biomechanical research also enables systematic optimization of orthopaedic implants and interventions, and thereby forms
    the foundation for innovations that drive the biomedical device industry and that expand a surgeons ability
    to improve patient care.

    tact force remained below one body weight for most activities of daily living. Moments due to friction in the
    joint reached 5.2 Nm.
    Rohlmann A, Graichen F, Bender A, Kayser R, Bergmann G: Loads on a telemeterized vertebral body replacement measured in three patients within the first
    postoperative month. Clin Biomech (Bristol, Avon)
    2008;23(2):147-158.
    The forces and moments acting in the lumbar spine during activities of daily living were measured in vivo with
    telemeterized vertebral body replacements. Sitting or upper body flexion caused resultant forces in excess of 400
    N. When working with elevated arms against the resistance of a physiotherapist, forces exceeded 700 N, and
    moments remained below 4 Nm.

    8.

    Morlock M, Schneider E, Bluhm A, et al: Duration and


    frequency of every day activities in total hip patients. J
    Biomech 2001;34:873-881.

    9.

    Bingham J, Li G: An optimized image matching method


    for determining in-vivo TKA kinematics with a dualorthogonal fluoroscopic imaging system. J Biomech Eng
    2006;128(4):588-595.

    10.

    van den Bogert AJ, Reinschmidt C, Lundberg A: Helical


    axes of skeletal knee joint motion during running. J Biomech 2008;41(8):1632-1638.
    Intracortical markers were used to determine the helical
    axis of the knee during the stance phase of running. The
    axis began at the midepicondylar point at the beginning
    of the stance phase and moved posteriorly and distally
    as the knee moved into flexion.

    11.

    Armstrong AD, Dunning CE, Faber KJ, Duck TR, Johnson JA, King GJ: Rehabilitation of the medial collateral
    ligament-deficient elbow: An in vitro biomechanical
    study. J Hand Surg Am 2000;25(6):1051-1057.

    12.

    Pollock JW, Brownhill J, Ferreira L, McDonald CP,


    Johnson J, King G: The effect of anteromedial facet
    fractures of the coronoid and lateral collateral ligament
    injury on elbow stability and kinematics. J Bone Joint
    Surg Am 2009;91(6):1448-1458.
    Anteromedial facet coronoid fractures were simulated in
    cadaver elbows with and without lateral ligament repair.
    In the varus position, type I fractures were stable after
    lateral ligament repair, whereas type II and III fractures
    were unstable regardless of the repair status.

    13.

    Sommers MB, Fitzpatrick DC, Madey SM, Vande


    Zanderschulp C, Bottlang M: A surrogate long-bone
    model with osteoporotic material properties for biomechanical testing of fracture implants. J Biomech 2007;
    40(15):3297-3304.
    A physical model of the osteoporotic femoral diaphysis
    was developed and tested to determine five key structural properties: torsional rigidity and strength, bending
    rigidity and strength, and screw pullout strength. Results demonstrated that all five structural properties
    were within the lower 16% of those reported for cadaver femurs. Therefore, the model is suitable for im-

    Annotated References
    1.

    Mow VC, Huiskes R: Basic Orthopaedic Biomechanics


    and Mechano-Biology, ed 3. Philadelphia, PA, Lippincott Williams & Wilkins, 2005.

    2.

    Pistoia W, van Rietbergen B, Lochmller EM, Lill CA,


    Eckstein F, Regsegger P: Estimation of distal radius
    failure load with micro-finite element analysis models
    based on three-dimensional peripheral quantitative
    computed tomography images. Bone 2002;30(6):842848.

    3.

    Heller MO, Bergmann G, Deuretzbacher G, et al:


    Musculo-skeletal loading conditions at the hip during
    walking and stair climbing. J Biomech 2001;34(7):883893.

    4.

    Mndermann A, Dyrby CO, DLima DD, Colwell CW


    Jr, Andriacchi TP: In vivo knee loading characteristics
    during activities of daily living as measured by an instrumented total knee replacement. J Orthop Res 2008;
    26(9):1167-1172.
    An instrumented knee prosthesis was used to measure
    knee joint force simultaneously with motion capture
    during activities of daily living. The maximum total
    compressive load at the knee was highest during stair
    ascending and descending. Total compressive load exceeded 2.5 times body weight for most activities.

    5.

    6.

    Heinlein B, Kutzner I, Graichen F, et al: ESB Clinical


    Biomechanics Award 2008: Complete data of total knee
    replacement loading for level walking and stair climbing
    measured in vivo with a follow-up of 6-10 months. Clin
    Biomech (Bristol, Avon) 2009;24(4):315-326.
    A telemetric tibial tray was used to measure the three
    forces and three moments acting on the implant, providing in vitro loading data of the knee joint for a range of
    activities. Stair descending was found to produce the
    highest loads, with peak force occurring in an axial direction, and peak moments occurring in the frontal
    plane.
    Bergmann G, Graichen F, Bender A, Kb M, Rohlmann A, Westerhoff P: In vivo glenohumeral contact
    forces: Measurements in the first patient 7 months postoperatively. J Biomech 2007;40(10):2139-2149.
    A telemetric shoulder implant was used to measure for
    the first time glenohumeral contact forces in vivo. Con-

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    7.

    71

    Section 1: Principles of Orthopaedics

    A locked plate with a locking screw in the last hole was


    compared with a locked plate with a nonlocking screw
    in the last hole for fixation in osteoporotic diaphyseal
    bone. Results showed a higher periprosthetic fracture
    risk in plates with a locked screw at the end.

    plant evaluation in osteoporotic bone where implant


    fixation is most challenging.
    14.

    1: Principles of Orthopaedics

    15.

    16.

    72

    Fitzpatrick DC, Doornink J, Madey SM, Bottlang M:


    Relative stability of conventional and locked plating fixation in a model of the osteoporotic femoral diaphysis.
    Clin Biomech (Bristol, Avon) 2009;24(2):203-209 Epub
    2008 Dec 12.
    Stiffness and strength of bridge plating with unicortical
    and bicortical locking plate fixation was compared with
    that of a nonlocked construct in a model of osteoporotic
    femoral diaphysis. Fixation strength was improved with
    the locked plate under axial loading but may be reduced
    in bending and torsion.
    Bottlang M, Mohr M, Simon U, Claes L: Acquisition of
    full-field strain distributions on ovine fracture callus
    cross-sections with electronic speckle pattern interferometry. J Biomech 2008;41(3):701-705.
    An electronic speckle pattern interferometry system was
    used to evaluate the possibility of assessing continuous
    strain distributions on fracture callus cross-sections.
    Strain acquisition based on this system facilitates reproducible quantification of strain distributions on callus
    cross-sections.
    Bottlang M, Doornink J, Byrd GD, Fitzpatrick DC,
    Madey SM: A nonlocking end screw can decrease fracture risk caused by locked plating in the osteoporotic diaphysis. J Bone Joint Surg Am 2009;91(3):620-627.

    Orthopaedic Knowledge Update 10

    17.

    Eberle S, Gerber C, von Oldenburg G, Hungerer S,


    Augat P: Type of hip fracture determines load share in
    intramedullary osteosynthesis. Clin Orthop Relat Res
    2009;467(8):1972-1980.
    A finite element model of a pertrochanteric fracture, a
    femoral neck fracture, and a subtrochanteric fracture all
    fixed with a cephalomedullary nail was developed to
    evaluate the mechanical performance of the nail. Results
    showed similar construct stiffness with the lowest peak
    stress in the fixed femoral neck fracture.

    18.

    Li W, Anderson DD, Goldsworthy JK, Marsh JL,


    Brown TD: Patient-specific finite element analysis of
    chronic contact stress exposure after intraarticular fracture of the tibial plafond. J Orthop Res 2008;26(8):
    1039-1045.
    Patient-specific finite element analysis models of fractured ankle and the uninjured contralateral ankle were
    developed. Results showed areas of chronic stress overload in the fractured ankles relative to the uninjured ankles.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 7

    Bearing Surface Materials for Hip,


    Knee, and Spinal Disk
    Replacement
    Javad Parvizi, MD, FRCS

    Michael Bercik, MD

    Todd Albert, MD

    Total joint arthroplasty represents one of the most successful surgical procedures in orthopaedics. Joint replacement surgery, especially total hip arthroplasty
    (THA) and total knee arthroplasty (TKA), often enable
    patients who were limited by pain and decreased range
    of motion to return to higher states of function. In the
    past, total joint arthroplasty was generally indicated for
    geriatric patients with low activity demands; however,
    its success has recently expanded its use into treatment
    plans for more active patients younger than 65 years.1
    The acceptance of more liberal indications for total
    joint arthroplasty also has highlighted the complication
    of prosthetic failure. Aseptic loosening and osteolysis
    secondary to wear has been identified as the primary

    1: Principles of Orthopaedics

    Introduction

    cause of prosthetic failure.2 Much research currently is


    focused on increasing the longevity of prostheses by increasing wear resistance, which then reduces the overall
    rate of prosthetic failure and the need for revision surgery. Attempts at wear reduction have involved altering
    the structure of polyethylene, primarily through the
    process of cross-linking. Another strategy avoids the
    use of polyethylene and instead uses bearing surface
    materials, such as metal and ceramic, which are intrinsically more resistant to wear. This chapter will discuss
    the basic principles of bearing surfaces and wear; the
    advantages and disadvantages of the bearing surfaces
    used in THA and TKA (Table 1); and total disk arthroplasty (TDA), a relatively new tool in the orthopaedic
    repertoire.

    Bearing Surfaces
    Dr. Parvizi or an immediate family member serves as a
    board member, owner, officer, or committee member of
    the American Association of Hip and Knee Surgeons,
    American Board of Orthopaedic Surgery, British Orthopaedic Association, Orthopaedic Research and Education
    Foundation, and SmartTech; serves as a paid consultant
    to or is an employee of Stryker; and has received research or institutional support from KCI, Medtronic, the
    Musculoskeletal Transplant Foundation, Smith &
    Nephew, and Stryker. Dr. Bercik or an immediate family
    member is a board member, owner, officer, or committee member of the American Academy of Orthopaedic
    Surgeons. Dr. Albert or an immediate family member
    serves as a board member, owner, officer, or committee
    member of the Cervical Spine Research Society and Scoliosis Research Society; has received royalties from DePuy;
    is a member of a speakers bureau or has made paid
    presentations on behalf of DePuy and Biomet; serves as
    a paid consultant to or is an employee of DePuy; has received research or institutional support from DePuy, AO,
    Biomet, Medtronic Sofamor Danek, and Synthes; and
    has stock or stock options held in K2M, Gentis, In Vivo
    Therapeutics, Vertech, Biomerix, Breakaway Imaging,
    Paradigm Spine, Pioneer, Invuity, and Crosstree Medical.

    2011 American Academy of Orthopaedic Surgeons

    In engineering terms, a bearing surface represents the


    area of contact between two objects. In total joint arthroplasty, bearing surfaces are the areas on the prosthesis that articulate within the joint. In THA, the femoral head and the acetabular component are the
    primary bearing surfaces, whereas modular junctions
    represent secondary bearing surfaces. In TKA, the femoral component, the tibial base plate, and the polyethylene insert are all areas of contact. In TDA, the core
    replacing the disk and the end plates are the articulating contact areas. These surfaces lie perpendicular to
    the force transmitted through the joint and are subject
    to relative motion; consequently, these bearing surfaces
    are subject to wear.

    Wear Defined

    Wear Mechanisms
    Wear is the removal of material from opposing surfaces
    under an applied load that occurs when they are put
    into relative motion. The primary mechanisms of wear
    that occur with total joint arthroplasty are abrasion,

    Orthopaedic Knowledge Update 10

    73

    Section 1: Principles of Orthopaedics

    Table 1

    1: Principles of Orthopaedics

    Summary of Bearing Surfaces Available for THA and TKA


    Bearing Surface

    Advantages

    Disadvantages

    Conventional polyethylene

    Nontoxic
    Lower cost
    Multiple liner options
    Better fatigue resistance than cross-linked
    polyethylene

    Most bioactivity and osteolysis


    Not suitable for long-term use or active
    patients

    Highly cross-linked polyethylene

    High wear resistance


    Nontoxic
    Lower cost
    Multiple liner options
    Proven history

    Reduced fatigue resistance


    Increased bioactivity and osteolysis
    compared with metal and ceramic

    Ceramic on ceramic

    Highest wear resistance


    Bioinert
    Long in vivo experience
    Wettability
    Decreased surface roughness
    Resistance to oxidative wear

    Acetabular liner chipping


    Fracture risk
    Squeaking
    Increased cost
    Limited neck lengths

    Metal on metal

    Very high wear resistance


    Larger head diameters
    Long invivo experience

    Increased ion levels


    Delayed-type hypersensitivity response
    Corrosion at metal junctions
    Precise machining required
    Potential carcinogen

    Oxidized zirconium on polyethylene Wear resistance similar to ceramic


    Fatigue resistance similar to metal

    Limited clinical data to support use


    Susceptible to damage after dislocation
    and closed reduction attempts

    Ceramic on metal

    Limited clinical data to support use

    Reduced wear
    Reduced friction
    Less metal ion release

    adhesion, fatigue, and third-body wear. Abrasion is a


    mechanical process in which asperities of a harder surface remove material from a softer surface by cutting
    into and driving through that surface. Adhesion occurs
    when two materials are pressed against one another, resulting in a bond. When the surfaces are subsequently
    separated, material is pulled from the softer surface.
    Fatigue is the progressive local damage inflicted on a
    material after repeated cyclic loadings. Material is released from a surface when local stresses exceed the fatigue strength of the material.3 Fatigue damage can
    range from microscopic pitting to large areas of delamination. Third-body wear is a form of abrasive wear
    that occurs when particulates such as cement and bone
    become entrapped in an articular surface and act as asperities. The microscopic materials released from bearing surfaces through the aforementioned mechanisms
    of wear are called wear particles.

    Wear Modes
    Wear modes describe the conditions under which the
    prosthesis is functioning when wear occurs.4 Mode 1
    occurs when two articulating surfaces move relative to
    each other. This is the primary source of wear in a wellfunctioning prosthesis. Mode 2 describes wear that occurs when a primary bearing surface moves relative to
    a secondary surface that was not intended to be part of
    74

    Orthopaedic Knowledge Update 10

    the articulation. Mode 3 wear occurs when third-party


    bodies interpose between the primary surfaces. Mode 4
    wear describes the relative motion between two secondary bearing surfaces, such as the motion that occurs between the tibial base plate and the undersurface on the
    polyethylene insert in a TKA prosthesis.

    Differences Between Hip, Knee, and Spine


    Wear Characteristics
    The biomechanics and kinematics differ between the
    hip, the knee, and the spine because of differences in
    anatomy and movement. Consequently, the bearing surfaces in knee, hip, and spinal disk prostheses are subject to a different milieu of forces and motions that lead
    to wear. These variations are clinically important because properties of bearing surfaces necessary for function and longevity in one prosthesis may not be as applicable in another prosthesis.
    The hip is a congruent ball-in-socket joint, with surface motion primarily occurring as the femoral head
    slides within the acetabulum. In THA, this sliding
    movement at the articulation of components produces
    microabrasion and microadhesion of the bearing surfaces.5 Although most wear particles arise from the articulating surface, unintentional impingement and motion at the modular junctions also contribute to wear.
    Currently, the leading cause of THA failure is aseptic

    2011 American Academy of Orthopaedic Surgeons

    Chapter 7: Bearing Surface Materials for Hip, Knee, and Spinal Disk Replacement

    2011 American Academy of Orthopaedic Surgeons

    Tribology
    Tribology is the science of interactive surfaces in relative motion. It incorporates the concepts of wear, friction, and lubrication. Wear is the removal of material
    from a surface through the mechanisms of adhesion,
    abrasion, and fatigue. Friction is the force that resists
    the relative motion of two surfaces in contact; it is described by the coefficient of friction. The coefficient of
    friction in the native joint is 0.008 to 0.02. Prostheses
    are designed to replicate (or better) this value to reduce
    frictional forces across the joint. Lubricant interposed
    between two opposing surfaces helps carry the existing
    load between those surfaces. The lambda () ratio describes the ratio of fluid-film thickness to surface
    roughness. A higher ratio is desirable because it translates into reduced friction and wear. A ratio greater
    than 3 is ideal because it represents fluid-film lubrication; in this setting, asperities of opposing surfaces are
    completely separated and the load is entirely carried by
    the lubricant. In vivo, mixed film lubrication (defined
    by a ratio between 1 and 3) predominates, and the
    surfaces are only partially separated.3
    Biomechanical studies attempt to explore tribology
    by in vitro simulation of movement at a joint in its natural environment. To better understand and predict
    wear mechanisms in hip prostheses, hip joint simulators have been used to mimic both the movements of
    the hip and the lubrication of synovial fluid. Physiologic knee simulators attempt to closely mimic the natural movement and lubrication of a knee over the
    course of several million cycles to simulate the in vivo
    wear that occurs in knee prostheses. Unidirectional and
    multidirectional disk movement simulators have been
    used to predict wear patterns in vivo. Multidirectional
    methods appear to more closely reflect the activities of
    daily living.11 A variety of methods can be used to analyze wear, including measuring the weight loss of the
    component, deviation from a reference geometry, and
    visualization with an electron microscope.

    1: Principles of Orthopaedics

    loosening and osteolysis that develops secondary to the


    release of wear particles.6
    The knee is a complex pivotal hinge joint that allows
    flexion and extension as well as some internal and external rotation. As with THA, osteolytic loosening of
    components secondary to the host response to wear particles is one of the leading causes of prosthetic failure.
    There are two type of bearing surface wear in TKA: articular wear and undersurface wear. Articular wear occurs secondary to contact stresses at the primary bearing surfaces coupled with movement at the articulation.
    Undersurface wear occurs in knee prostheses between
    the tibial insert and the tibial base plate. When inserted
    onto the tibial base plate, current tibial inserts used in
    fixed-bearing knee prostheses incorporate some type of
    locking mechanism to prevent motion; however, no system can completely diminish movement between these
    two components. The resultant micromotion between
    the insert and the base plate produces some polyethylene particles, which may then contribute to an inflammatory osteolytic response.7 Mobile-bearing prostheses,
    which allow free movement between the tibial insert
    and the base plate, seek to reduce undersurface wear by
    reducing joint loads. Also, mobile-bearing prostheses
    permit the use of highly polished cobalt-chromium
    baseplates, which, because of manufacturing constraints, are more difficult to produce with suitable intraoperative locking mechanisms for standard polyethylene inserts.8
    In addition to aseptic loosening, TKA may also fail
    because of fatigue damage and gross fracture. This
    complication occurs more commonly in TKA than in
    THA. Because of the hinge-like nature of the knee, contact zones move with respect to the polyethylene component during knee flexion and extension. At one point
    during gait an area of contact may be under compression, whereas the same area may be under tension at
    another point during gait. This alternation of forces
    produces cyclic loading, fatigue, and ultimately, delamination at the bearing surface. Gross failure and fracture of the bearing surface may develop as the end
    point of this process.9
    TDA is a relatively recent procedure that was developed to relieve pain associated with degenerative diseases of the spine. Although degrees of motion in vertebral disks are relatively small compared with those seen
    in knee and hip joints, vertebral disks are subject to axial loads and relative movement during rotation, flexion, and extension of the spine. At the central bearing
    surface of the polyethylene core, microabrasion and microadhesion are the primary mechanisms of wear. At
    the rims, fatigue and gross fracture predominate.10 Interestingly, the components used in TDA incorporated
    features of both THA and TKA. Under neutral alignment, the axial load is distributed mainly across the
    central region of the core, and the sliding motion of the
    disk is similar to that of the hip. During bending movements, compression and tension forces act primarily
    along the edges of the artificial disk, producing fatigue
    and failure. Currently, much less is known about the
    clinical importance of wear in TDA than is understood
    about the role of this factor in THA and TKA.

    Polyethylene

    History and Structure


    Polyethylene is a viscoelastic and thermoplastic polymer consisting of long chains of the monomer ethylene.
    It is composed of the repeating unit (C2H4)n, in which
    all carbon-carbon and carbon-hydrogen bonds are single. First discovered in a reproducible set of chemical
    conditions in 1935, polyethylene has since become one
    of the most commercially used plastics in the world.
    Depending on its density and the branching of its
    chains, polyethylene can be classified into several different categories. High-density polyethylene is defined by
    a density greater than 0.941 g/cm3 and is used in packaging (such as detergent bottles). Low-density polyethylene is defined by a density of 0.910 to 0.940 g/cm3
    and is more suited for the production of plastic bags
    and film. These two examples hint at the applicability

    Orthopaedic Knowledge Update 10

    75

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    of polyethylene to biologic engineering. Polyethylene


    has the capacity to be both a sturdy, tough solid that is
    resistant to wear as well as a material that is ductile
    and conformable into appropriate geometries. Both
    properties have clear benefit in the design of replacement components for the complex movements and
    anatomy of human joints. Sterilization was historically
    performed with gamma radiation. This also produced
    free radicals that could participate in cross-linking or
    oxidation. In an attempt to avoid oxidative damage,
    sterilization in an oxygen-free environment, usually
    with ethylene oxide or gas plasma, was performed.
    Polyethylene components sterilized in this manner
    showed increased wear by avoiding cross-linking.

    Ultra-HighMolecularWeight Polyethylene
    Ultra-highmolecularweight polyethylene (UHMWPE)
    is the product of polyethylene catalyzation and is defined by an average molecular weight of greater than 3
    million g/mol. It has been the preferred bearing material in orthopaedic joint arthroplasty for more than 40
    years. UHMWPE consists of extremely long chains of
    polyethylene. Its microstructure consists of crystalline
    domains embedded within an amorphous matrix. The
    crystalline phase is created by rows of folded carbon
    chains, whereas the amorphous surrounding is a randomly oriented and entangled environment of polymer
    chains. Tie molecules connect these sets of chains, providing resistance to mechanical deformation.12 Despite
    favorable properties for use in bioengineering, polyethylene remains an imperfect product for bearing surfaces
    because it is not impervious to wear and inevitably fails
    after repeated use. This limitation has motivated the
    search for other materials that produce better clinical
    results via improved wear resistance. Alternative bearing surfaces with better wear resistance, such as metal
    and ceramic bearing surfaces, have their own advantages and disadvantages.

    Alternative Bearing Surfaces

    Bearing Surface Problems


    The primary cause of failure in THA and TKA is aseptic
    loosening secondary to osteolysis. At one time,
    periprosthetic weakening of the bone and its associated
    finding on radiographic imaging (such as lytic lesions
    around the prosthesis) were considered a response to
    the cement used in implantation. Referred to as cement
    disease, this process is now better understood and attributed to wear particles. These particles incite a complex inflammatory response in the body involving cytokines, chemokines, and multiple cell types. Although
    the steps have not been entirely elucidated, osteoclastic
    maturation in response to the presence of wear particles
    is known to lead to resorption of the bone surrounding
    the prosthesis. All wear particles are not equally responsible for inciting an inflammatory response. In THA,
    macrophages appear most sensitive to submicron-sized
    particles.13 Different bearing surfaces produce different
    76

    Orthopaedic Knowledge Update 10

    ratios in the sizes of created microscopic wear particles.


    Polyethylene bearing surfaces produce wear particles
    within the size ranges that are ideal for inciting an inflammatory response. Metals and ceramics produce particles in the less active ranges of inflammatory incitation, which should result in less osteolysis.14
    The search for clinically superior alternative bearing
    surfaces has intensified because the proportion of patients younger than 65 years (and perhaps even those as
    younger than 45 years) who are being treated with
    joint replacement surgery is increasing.1 In THA, metal
    on polyethylene remains the most common type of implant. The realization that polyethylene wear and subsequent osteolysis is the leading cause of prosthetic failure has encouraged some surgeons to use alternative
    bearing surfaces, most notably metal-on-metal and
    ceramic-on-ceramic implants, which currently are the
    second and third most commonly used bearing surfaces, respectively.15 These bearing surfaces have their
    own limitations; however, both are more wear resistant
    than polyethylene.

    Metal-on-Metal Prostheses
    Metal-on-metal hip prostheses have been in clinical use
    longer than any bearing surface. In 1938, an entire hip
    was replaced with stainless steel components. Improvements were made on this initial design because stainless
    steel is not optimal for use in an articular surface. In
    the 1960s, the McKee-Farrar metal-on-metal prosthesis
    was introduced using a cobalt-chromium alloy. Metalon-metal hip prostheses were the most commonly used
    hip replacement option until the 1970s, when the
    Charnley polyethylene-on-metal hip prosthesis almost
    universally supplanted their use. The Charnley model
    gained favor for several reasons, including the early
    success of the Charnley prosthesis, known failures of
    metal prostheses, and concerns regarding metal sensitivity and carcinogenesis.16 As the role of polyethylene
    wear in prosthetic failure became better understood,
    the search for clinically superior alternative bearing surfaces rejuvenated the use of metal-on-metal prostheses.
    Recent retrieval analyses have shown that the metal-onmetal prostheses achieve excellent long-term results.17
    Long-term survivorship of metal-on-metal prostheses
    compare favorably with the Charnley and other metalon-polyethylene prostheses.18 The Metasul (Zimmer,
    Warsaw, IN) hip replacement, a cobalt-alloy bearing reintroduced in the 1980s, is still a commonly used
    metal-on-metal prosthesis. The Metasul incorporates a
    polyethylene acetabular cup with a metal inlay that directly articulates with the metallic alloy of the femoral
    head. Other improvements on first-generation metalon-metal prostheses include better bearing geometry
    and an enhanced surface finish.
    The most apparent advantage of the metal-on-metal
    hip prosthesis is its greater resistance to wear compared
    with polyethylene. Run-in wear represents a period of
    increased wear, usually during the first million cycles,
    which is followed by a longer period with a lower rate
    of consistent wear (steady-state wear). Modern metal-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 7: Bearing Surface Materials for Hip, Knee, and Spinal Disk Replacement

    2011 American Academy of Orthopaedic Surgeons

    the components. In most instances, the patient is asymptomatic. Pseudotumors are thought to occur with greater
    wear and in the presence of higher concentrations of
    metal ions. A recent study investigating the wear characteristics of implants revised for the presence of pseudotumors, as compared with a control group revised for
    other reasons, showed increased wear associated with
    the presence of pseudotumors. Edge loading and its associated loss of fluid-film lubrication appeared to be the
    dominant mechanism of wear. The authors of this study
    suggest that inadequate coverage of the femoral head
    component from the outset may have led to increased
    wear and subsequent pseudotumor formation.25
    Perhaps more concerning is the systemic distribution
    of metal ions in the body. Increased levels of metal ions,
    particularly cobalt and chromium, have been observed
    in the blood and urine of patients treated with metalon-metal hip prostheses. Postoperatively, these ions can
    increase in concentration fivefold to tenfold.26 As
    metal-on-metal prostheses are more often considered
    for younger and more active patients because of their
    resistance to wear and potential longevity, the relationship between activity level and metal ion release is becoming more important. Unfortunately, a definitive answer regarding this relationship has not been
    determined. One study showed little variability in metal
    ion levels over the course of 2 weeks with varying
    amounts of activity,27 whereas a later study reported a
    direct relationship between increased ion levels after
    short periods of activity.28 Current studies, however,
    have not proven a direct relationship between ion levels
    and primary malignancies.29
    Because the implantation of metal-on-metal prostheses is a relatively recent trend, there are few long-term
    studies showing efficacy. Two recent studies have
    shown survivorship rates of 93% to 98% after 10 years
    of implantation.29,30 This remains an area of active investigation.

    1: Principles of Orthopaedics

    on-metal prostheses have shown a yearly run-in wear


    rate of approximately 25 m, and steady-state wear of
    3 to 7 m. This rate represents only 2% of the wear
    rate typically seen in historic (such as noncross-linked)
    polyethylene.19 Metal-on-metal prostheses also have
    shown a unique ability to self-polish. Given the ductility of metal components, larger scratches on the component surface may be polished down to smaller
    scratches with continued use.20 Reducing wear increases the potential longevity of a prosthesis by keeping the wear particle concentration and size below the
    threshold for osteolysis.11 Theoretically, a metal-onmetal prosthesis should last the lifetime of a patient,
    even a younger and more active patient.
    Another advantage of the metal-on-metal prosthesis
    is its tolerance of larger femoral heads. This factor is
    clinically important because larger diameter articulating couples are more stable and allow greater range of
    motion. With polyethylene components, larger femoral
    heads lead to increased wear rates; therefore, to optimize wear resistance and longevity, overall stability is
    compromised with the use of a smaller femoral head. In
    contrast, metal-on-metal femoral heads allow for less
    exclusivity between wear resistance and stability because metal-on-metal components have reduced wear
    with larger femoral heads.21 A larger femoral head pulls
    more fluid into the articulation, leading to an increased
    state of fluid-film lubrication and a reduction of frictional forces in the prosthesis.
    Concerns remain regarding the long-term biologic
    effects of metal ions released from metal-on-metal prostheses. For example, elevated levels of chromium have
    been found in patients with metal-on-metal implants,
    with the prosthetic component indicated as the primary
    source of the ions.22 Theoretically, increased metal ions
    carry risks for carcinogenesis, delayed hypersensitivity
    reactions, and organ toxicity. In the local periprosthetic
    tissue, evidence of hypersensitivity and unusual lymphocytic aggregates have been reported. The term acute
    lymphocytic vasculitis associated lesions (ALVAL) has
    been used to describe the lymphocyte proliferation and
    associated vasculitis that occur in response to the release of metal particles.23 One study evaluating metalon-metal prostheses reported a unique perivascular
    lymphocytic infiltrate.23 Although an immunologic response was evident, it was unlike that seen with macrophagic response to polyethylene debris, which is characterized by a foreign body response and granuloma
    formation. Rather, this response was more indicative of
    a type IV delayed hypersensitivity reaction. Notably,
    osteolysis was reported as a cause of implant failure;
    replacement with more inert metals was required for
    successful revision. Similar cases of metallic hypersensitivity necessitating revision have been reported, including a case report of two revisions that describe a similar
    type IV hypersensitivity reaction as well as tissue hyperreactivity caused by gross wear.24
    Another concern with the use of a metal-on-metal
    bearing surface has been the development of joint effusion and local soft-tissue reaction (pseudotumor) that is
    known to occur independent of failure or loosening of

    Ceramic-on-Ceramic Prostheses
    Alumina ceramic-on-ceramic prostheses have been in
    use since the early 1970s. Historically, ceramic-onceramic prostheses did not fare as well initially as their
    counterparts. The underperformance of first-generation
    ceramic prostheses was associated with the complications of excessive wear, fracture, and migration.31 These
    complications were attributed to the inadequate production of materials and poor surgical technique. To increase fracture resistance and overall strength, material
    was inserted into second-generation ceramics to limit
    grain size, thereby reducing cracking and fracture propagation. Ceramic-on-ceramic prostheses, now in their
    third generation of production, have continued to improve. Proof testing, the process by which ceramics are
    subjected to stresses greater than those expected in
    their routine use, helps ensure quality; weaker components are removed from circulation prior to distribution and clinical implementation.
    Advantageous properties of third-generation ceramics and better clinical results can be primarily attributed

    Orthopaedic Knowledge Update 10

    77

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 1

    The impingement between the femoral neck and


    the acetabular rim is believed to lead to metal
    transfer and patch wear that, when combined
    with other factors (such as the type and position of components), may lead to squeaking.

    to improvements in purity, grain microstructure, and


    strength. Advances in ceramic manufacturing include
    the ability to produce very pure, fully dense ceramics
    with a small grain size; this reduces crack propagation
    and fracture. Third-generation ceramics have the lowest wear rates of all the currently used bearing surfaces
    and produce low rates of osteolysis.32 Given their hardness, ceramics can maintain polish in the presence of
    third body particles. Ceramics also are hydrophilic,
    which leads to higher wettability of the surface and better lubrication within the joint. Ceramics, unlike metal
    prostheses, are biologically inert. They are fully oxidized and thus do not release ions or further oxidize in
    vivo.18 Of the two most commonly used ceramics, zirconia and alumina, zirconia appears to be harder and
    stronger but may be less thermostable. Reports of
    phase transformation of zirconia have been reported.33
    Ceramic-on-ceramic prostheses also have limitations. To prevent excessive wear and fracture, ceramics
    must be inserted with optimal positioning, which can
    be complicated by the reduced head size options for ceramic prostheses. Wear, surface damage, and rarely,
    fracture can occur. When gross fracture occurs, total revision with removal of all components is often necessary.34 The most unusual complication of ceramic-onceramic prostheses is squeaking. Reports of squeaking
    rates vary from less than 3% to more than 10%.35 Currently, the etiology of squeaking remains unclear, but a
    multifactorial cause is likely.36 It is believed that a contact (impingement) between the femoral neck and the
    metal rim of the acetabulum may lead to generation of
    metal particles, which if transmitted into the bearing
    surface, may result in squeaking (Figure 1). The latter
    may explain why the incidence of squeaking is much
    higher with a particular ceramic-on-ceramic prosthetic
    design that encases the ceramic bearing in a metal
    housing on the acetabular side. Other factors are be78

    Orthopaedic Knowledge Update 10

    lieved to play a role in noise generation with ceramicon-ceramic bearing surfaces, including component positions, which increases the likelihood of impingement;
    the type of components (a specific design of femoral
    stem made of titanium, molybdenum, zirconium, and
    ferrous alloy [TMZF; Stryker, Kalamazoo, MI] is currently implicated); and possibly, the thickness of the acetabular shell. It is important to note that the etiology
    of squeaking associated with a ceramic-on-ceramic
    bearing surface remains unknown and the aforementioned factors are mere speculations. The problem of
    squeaking is generally a curious annoyance for most
    patients, but for some it may necessitate revision. Ceramic components also are notably more expensive
    than are their polyethylene counterparts.
    Clinical results of modern ceramic-on-ceramic prostheses are generally encouraging. In comparison with
    metal-on-polyethylene hip replacements, ceramics have
    shown no significant difference in patient satisfaction
    but have resulted in fewer revisions and less evidence of
    osteolysis.37 Fracture rates have generally been reported
    as very low, although one recent study showed a 1.7%
    rate of alumina bearing surface failure caused mainly
    by impingement and acetabular cup chipping.38 The extrapolation of these numbers to other alumina prostheses is uncertain.

    Highly Cross-Linked Polyethylene


    UHMWPE has been the most commonly used acetabular component in hip prostheses for the past 30 years.
    UHMWPE is less suitable for younger, active patients
    because component wear causes failure secondary to
    osteolysis and loosening around the prosthesis. In an
    effort to improve the wear properties of polyethylene
    cups, highly cross-linked UHMWPE was introduced in
    the 1990s.
    Cross-linking is performed via a series of steps that
    includes irradiation, thermal processing, and sterilization. Radiation breaks carbon-hydrogen bonds in polyethylene chains, creating free radicals that then participate in covalent bonds. Formation of these covalent
    bonds makes polyethylene more resistant to wear and
    deformation. A relationship between dose irradiation,
    cross-linking, and wear resistance has been reported.39
    The most rapid decrease in wear rate occurs with irradiation of 0 to 5 mrad, and then further decreases, becoming too small to measure after 10 mrad. Although
    the created free radicals may form covalent bonds, they
    may also react with oxygen if they remain in the plastic. Oxidation weakens the plastic and can be viewed as
    an opposing force to cross-linking. Thermal processing
    of irradiated polyethylene reduces the amount of free
    radicals present. This can be accomplished via remelting (heating to a point above the melting point of the
    plastic) or annealing (heating to a point just below the
    melting point). Remelting completely removes the free
    radicals from the plastic but in doing so changes the
    crystalline structure and consequently reduces its mechanical and fatigue properties. Annealing does not
    change mechanical properties but leaves free radicals

    2011 American Academy of Orthopaedic Surgeons

    Chapter 7: Bearing Surface Materials for Hip, Knee, and Spinal Disk Replacement

    Other Options
    A ceramic-on-metal combination prosthesis has been
    developed to incorporate the benefits of hard bearing
    surfaces while reducing the risks associated with both
    metal and ceramic components. More specifically,
    ceramic-on-metal prostheses reduce metal ion release
    and ceramic fracture. Comparisons of tribology and
    ion release of ceramic-on-metal THAs compared with
    ceramic-on-ceramic and metal-on-metal THAs showed
    reduced friction, wear, and metal ion release in laboratory studies, and a reduction of ion release in early clinical studies.44 Oxidized zirconium represents another
    attempt to create the ideal bearing surface. These surfaces are derived from a zirconium base that is heated
    and then infused with oxygen, transforming the outermost layer into a ceramic shell. This surface essentially
    combines the fracture resistance of metal with the wear
    resistance of ceramics. The major advantage of oxidized zirconium is its apparent capacity for reduced
    wear when coupled as a femoral head component to a
    polyethylene cup.45 No clinical studies to date have
    identified any clinical benefit. There is a case report describing damage to the oxidized zirconium head after
    recurrent dislocations.46 Although the oxidized zirconium shell is strong, the zirconium base may be less
    suitable as a bearing surface based on the reported femoral head damage.

    2011 American Academy of Orthopaedic Surgeons

    Total Disk Arthroplasty


    TDA began in the 1960s.47 Although the original TDA
    prosthesis ultimately failed, newer models have been
    developed as alternatives to fusion for alleviating back
    pain. Although lumbar fusion has been successful in
    treating back pain, it has been associated with complications such as pseudarthrosis and adjacent-level disk
    disease (the exact etiology of the latter is not yet fully
    understood, but altered biomechanics after fusion are
    thought to play a role). TDA is based on the theory of
    replacing the diseased disk, thereby relieving pain and
    reproducing functional movement. This would have
    two advantages over fusion: removing the need for fusion and the risk of pseudarthrosis, and possibly reducing adjacent-level disk disease. There are three categories of disk replacements currently in use in lumbar
    TDA: unconstrained, semiconstrained, and constrained
    prostheses. The Charit prosthesis (DePuy Spine, Raynham, MA) is composed of cobalt-chromiummolybdenum alloy end plates and a polyethylene core
    (Figure 2, A). This unconstrained model theoretically
    parallels the natural motion of a native disk. The
    ProDisc-L (Synthes, West Chester, PA) prosthesis is a
    semiconstrained model (Figure 2, B). The core is locked
    into the inferior end plate, reducing the risk of extrusion, but perhaps at the cost of a decreased range of
    motion. The ProDisc-L contains a polyethylene core.
    The constrained FlexiCore (Stryker) represents the
    newest TDA implant.47
    Much less is known concerning the in vivo biomechanics of the spine than is known about the in vivo
    biomechanics of the hip and the knee. As TDA is a relatively young science, the tribologic behavior of disk
    prostheses requires further investigation. In vitro studies simulating multidirectional wear seem to more accurately reflect the activities of daily living and induce
    more profound wear than unidirectional studies.11 Despite the finding of a higher proportion of wear than
    originally anticipated, osteolysis does not seem to be as
    serious a concern in TDA as it is in THA and TKA. In
    one study, periprosthetic tissue inflammation and activated macrophages were observed; however, osteolysis
    was not evident in 96.6% of the revisions.48 For the allmetal disk replacements, there is concern regarding
    metal ion release locally and systemically. Cobalt and
    chromium metal ion release in TDA may be similar to
    that which occurs in THA.49
    The primary cause of failure in THA and TKA, aseptic loosening, is rare in TDA. As mentioned, osteolysis
    seems to be a much more rare complication in TDA. In
    one study of 18 patients treated with TDA revision surgery, osteolysis was reported in only 1 patient.10 Subsidence was the most common complication. Anterior
    migration, core dislocation, and subluxation also were
    more common than osteolysis in this study. This study
    involved only short- and medium-term follow-up. With
    longer follow-up, the prevalence of osteolysis may become more frequent. Also, because TDA is still a very
    new procedure, inadequate surgical technique and infe-

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    available for oxidation. Another strategy to reduce oxidation is the addition of antioxidant agents, such as vitamin E, to the polyethylene; these agents appear to
    quench the free radicals.
    Attempts to resolve these problems has led to the
    current process of polyethylene manufacturing. Polyethylene is initially cross-linked via irradiation, then
    thermally processed to remove remaining free radicals,
    then sterilized in a nonoxidative environment to avoid
    reintroducing free radicals and subsequent oxidation.40
    In vitro studies have shown the increased wear resistance of highly cross-linked polyethylene cups.41 When
    this wear resistance is considered along with the established benefits of polyethylenea proven history of
    clinical satisfaction, nontoxicity, affordable cost, and
    multiple liner options providing increased flexibility
    highly cross-linked polyethylene continues to be a popular bearing surface option. Clinical studies have
    shown no significant clinical differences in early and intermediate follow-up periods but have supported laboratory data showing increased wear resistance as compared with conventional polyethylene.42 It is hoped that
    longer-term studies will show an extrapolation of these
    positive results, with clinically superior end results.
    Increasing wear resistance via cross-linking weakens
    fatigue strength. This compromise in mechanical properties has been verified as a potential factor leading to
    fatigue failure in highly cross-linked components.43 The
    clinical success of UHMWPE components will depend
    on striking a balance between wear, fatigue, and fracture resistance.

    79

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 2

    A, Oblique view of the SB Charit III artificial disk. Anterior (a), lateral (b), cobalt-chromium-molybdenum alloy end
    plates (c), fixation fins (d), and polyethylene core (e). (Courtesy of DePuy Spine, Raynham, MA.) B, Oblique view of
    the ProDisc-L prosthesis. Superior fixation keel (a), lateral (b), polyethylene core (c), and anterior (d). (Courtesy of
    Synthes, West Chester, PA.)

    rior products are almost certainly more ubiquitous and


    clinically relevant than in THA or TKA. As TDA
    evolves and surgeon familiarity increases, the current
    leading complications may become more infrequent
    and osteolysis more prominent. It also must be noted
    that because of the proximity of the disk prosthesis to
    the spine and the more invasive surgical approach necessary to reach the spine, TDA failure may induce more
    morbidity than THA or TKA.
    There is a dearth of clinical data supporting TDA.
    One study found lumbar TDA to be more efficacious
    and superior to fusion in certain patients.50 Similar conclusions have been reached in trials of cervical TDA.51
    These studies have not yet provided long-term data.
    Other TDA procedures that initially were deemed successful have produced poor results when observed over
    longer periods. One study reported good clinical shortterm results; however, longer follow-up showed that
    the patient ultimately required revision secondary to
    massive osteolysis.52 Further investigation into the longterm clinical results of lumbar and cervical TDA are
    necessary before definitive statements can be made regarding their efficacy.

    defined. More extensive investigations into the biologic


    and tribologic properties of disk prostheses are under
    way; findings from these studies will help predict and
    build on in vivo outcomes.

    Annotated References
    1.

    Kurtz SM, Lau E, Ong K, Zhao K, Kelly M, Bozic KJ:


    Future young patient demand for primary and revision
    joint replacement: National projections from 2010 to
    2030. Clin Orthop Relat Res 2009;467(10):2606-2612.
    The authors used the Nationwide Inpatient Sample between 1993 and 2006 to project the upcoming demands
    for total joint replacement. They predict that younger
    populations (younger than 65 years) will exceed 50% of
    all total hip replacements and total knee replacements
    by 2011.

    2.

    Clohisy JC, Calvert G, Tull F, McDonald D, Maloney


    WJ: Reasons for revision hip surgery: a retrospective review. Clin Orthop Relat Res 2004;429(429):188-192.

    3.

    Heisel C, Silva M, Schmalzried TP: Bearing surface options for total hip replacement in young patients. Instr
    Course Lect 2004;53:49-65.

    4.

    McKellop HA: The lexicon of polyethylene wear in artificial joints. Biomaterials 2007;28(34 ):5049-5057.
    The author defines the vocabulary pertaining to polyethylene wear in artificial joints. Broad categories include modes, mechanisms, damage, and debris.

    5.

    McKellop HA, Campbell P, Park SH, et al: The origin


    of submicron polyethylene wear debris in total hip arthroplasty. Clin Orthop Relat Res 1995;311(311):3-20.

    6.

    Ulrich SD, Seyler TM, Bennett D, et al: Total hip arthroplasties: what are the reasons for revision? Int Orthop
    2008;32(5):597-604.

    Future Directions
    The quest continues for optimal bearing surfaces for total joint arthroplasty. The evolution of bearing surfaces
    in the hip, the knee, and for disk replacement surgery
    will strive to develop components with more resistant
    surfaces and improved fatigue strength. For polyethylene components, alternative mechanisms for neutralizing free radicals, including vitamin E quenching and
    multistage annealing, are being incorporated. More
    studies are needed to follow up on the long-term clinical results of metal and ceramic components and the
    frequency and outcomes of potential complications. Indications and contraindications for TDA must be better
    80

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 7: Bearing Surface Materials for Hip, Knee, and Spinal Disk Replacement

    This study evaluated the indications for revision hip arthroplasty in patients requiring revision surgery less
    than 5 years after the index THA and more than 5 years
    after the index THA.
    7.

    8.

    9.

    Amstutz HC, Grigoris P: Metal on metal bearings in hip


    arthroplasty. Clin Orthop Relat Res 1996;329(suppl):
    S11-S34.

    17.
    Wasielewski RC, Parks N, Williams I, Surprenant H,
    Collier JP, Engh G: Tibial insert undersurface as a contributing source of polyethylene wear debris. Clin Orthop Relat Res 1997;345:53-59.

    Brown SR, Davies WA, DeHeer DH, Swanson AB:


    Long-term survival of McKee-Farrar total hip prostheses. Clin Orthop Relat Res 2002;402:157-163.

    18.

    Callaghan JJ, Insall JN, Greenwald S, et al: Mobilebearing knee replacement. J Bone Joint Surg Am 2000;
    82:1020-1041.

    Jacobson SA, Djerf K, Wahlstrm O: Twenty-year results of McKee-Farrar versus Charnley prosthesis. Clin
    Orthop Relat Res 1996;329(suppl):S60-S68.

    19.

    Wright TM, Bartel DL: The problem of surface damage


    in polyethylene total knee components. Clin Orthop
    Relat Res 1986;205:67-74.

    Dumbleton JH, Manley MT: Metal-on-Metal total hip


    replacement: What does the literature say? J Arthroplasty 2005;20(2):174-188.

    20.

    Sieber HP, Rieker CB, Kottig P: Analysis of 118 secondgeneration metal-on-metal retrieved hip implants.
    J Bone Joint Surg Br 1999;81:46-50.

    21.

    Dowson D, Hardaker C, Flett M, Isaac GH: A hip joint


    simulator study of the performance of metal-on-metal
    joints: Part I: the role of materials. J Arthroplasty 2004;
    19(8, suppl 3):118-123.

    22.

    Maezawa K, Nozawa M, Matsuda K, Sugimoto M, Shitoto K, Kurosawa H: Serum chromium levels before and
    after revision surgery for loosened metal-on-metal total
    hip arthroplasty. J Arthroplasty 2009;24(4):549-553.
    The authors analyzed the serum chromium levels in 10
    patients with metal-on-metal articulations before and
    after revision surgery. Mean serum chromium levels decreased from 2.53 g/L to 0.46 g/L in patients with no
    residual metal articulations, and decreased from 2.85
    g/L and 1.90 g/L in patients with retained metal articulations on the contralateral side.

    23.

    Willert HG, Buchhorn GH, Fayyazi A, et al: Metal-onmetal bearings and hypersensitivity in patients with artificial hip joints. A clinical and histomorphological
    study. J Bone Joint Surg Am 2005;87(1):28-36.

    24.

    Mikhael MM, Hanssen AD, Sierra RJ: Failure of metalon-metal total hip arthroplasty mimicking hip infection.
    A report of two cases. J Bone Joint Surg Am 2009;
    91(2):443-446.
    The authors describe a case report of prosthetic failure
    secondary to metal hypersensitivity reactions in two patients with similar clinical presentations that were suggestive of periprosthetic infection.

    25.

    Kwon YM, Glyn-Jones S, Simpson DJ, et al: Analysis of


    wear of retrieved metal-on-metal hip resurfacing implants revised due to pseudotumours. J Bone Joint Surg
    Br 2010;92(3):356-361.
    The authors quantified the wear in vivo of implants revised for pseudotumors and for those revised for other
    reasons. They found a significantly higher rate of median linear wear in both the femoral and acetabular
    components of implants revised for pseudotumors.

    26.

    MacDonald SJ: Metal-on-metal total hip arthroplasty:


    The concerns. Clin Orthop Relat Res 2004;429:86-93.

    Kurtz SM, van Ooij A, Ross R, et al: Polyethylene wear


    and rim fracture in total disc arthroplasty. Spine J 2007;
    7(1):12-21.
    The authors analyzed 21 implants from 18 patients
    treated with TDA to evaluate the magnitude and rate of
    polyethylene wear and surface damage.

    11.

    Grupp TM, Yue JJ, Garcia R Jr, et al: Biotribological


    evaluation of artificial disc arthroplasty devices: influence of loading and kinematic patterns during in vitro
    wear simulation. Eur Spine J 2009;18(1):98-108.
    The authors of this study reported in vitro wear differences in total disk prostheses with multidirectional versus unidirectional moving patterns. There was increased
    wear associated with the multidirectional group. The
    authors suggest that in vivo loading likely follows a
    multidirectional path.

    12.

    Kurtz SM, Muratoglu OK, Evans M, Edidin AA: Advances in the processing, sterilization, and crosslinking
    of ultra-high molecular weight polyethylene for total
    joint arthroplasty. Biomaterials 1999;20(18):16591688.

    13.

    Holt G, Murnaghan C, Reilly J, Meek RM: The biology


    of aseptic osteolysis. Clin Orthop Relat Res 2007;460:
    240-252.
    This literature review describes the biochemical processes leading to aseptic osteolysis, with emphasis on the
    receptor activator of nuclear factor-kappa ligand
    (RANKL)receptor activator of nuclear factor (RANK)kappa pathway.

    14.

    Campbell P, Shen FW, McKellop H: Biologic and tribologic considerations of alternative bearing surfaces. Clin
    Orthop Relat Res 2004;418(418):98-111.

    15.

    Bozic KJ, Kurtz S, Lau E, et al: The epidemiology of


    bearing surface usage in total hip arthroplasty in the
    United States. J Bone Joint Surg Am 2009;91(7):16141620.
    The authors reviewed the Nationwide Inpatient Sample
    database to determine the prevalence of each type of hip
    replacement in 112,095 primary THAs.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    10.

    16.

    81

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    27.

    Heisel C, Silva M, Skipor AK, Jacobs JJ, Schmalzried


    TP: The relationship between activity and ions in patients with metal-on-metal bearing hip prostheses.
    J Bone Joint Surg Am 2005;87(4):781-787.

    28.

    Khan M, Takahaski T, Kuiper JH, Sieniawska CE, Takagi K, Richardson JB: Current in vivo wear of metal-onmetal bearings assessed by exercise-related rise in
    plasma cobalt level. J Orthop Res 2006;24(11):20292035.

    29.

    Grbl A, Marker M, Brodner W, et al: Long-term


    follow-up of metal-on-metal total hip replacement.
    J Orthop Res 2007;25(7):841-848.
    The authors investigated the rate of primary malignancies in 98 patients with 105 metal-on-metal primary
    THAs over a 10-year period. Malignancies did not occur at a greater rate than seen in the general population.

    30.

    31.

    32.

    33.

    82

    Neumann DR, Thaler C, Hitzl W, Huber M, Hofstadter


    T, Dorn U: Long-term results of a contemporary metalon-metal total hip arthroplasty: A 10-year follow-up
    study. J Arthroplasty 2009; Jul 10. [Epub ahead of
    print]
    One hundred metal-on-metal prostheses were prospectively analyzed up to 126 months postoperatively. Implant survivorship was measured using component removal secondary to aseptic loosening as the end point.
    Winter M, Griss P, Scheller G, Moser T: Ten- to 14-year
    results of a ceramic hip prosthesis. Clin Orthop Relat
    Res 1992;282:73-80.
    Lusty PJ, Tai CC, Sew-Hoy RP, Walter WL, Walter WK,
    Zicat BA: Third-generation alumina-on-alumina ceramic bearings in cementless total hip arthroplasty.
    J Bone Joint Surg Am 2007;89(12):2676-2683.
    The authors report on a 5-year study investigating the
    rates of wear and osteolysis associated with modern ceramic hip prostheses; 301 third-generation alumina-onalumina cementless primary hip replacements in 283 patients performed at one center using the same surgical
    technique and implant were investigated.
    Kim YH, Kim JS: Tribological and material analyses of
    retrieved alumina and zirconia ceramic heads correlated
    with polyethylene wear after total hip replacement.
    J Bone Joint Surg Br 2008;90(6):731-737.
    The surface characteristics and penetration rates of alumina versus zirconia ceramic heads were compared with
    ceramic-on-polyethylene components. Phase transformation in the zirconia heads was also examined.

    34.

    Barrack RL, Burak C, Skinner HB: Concerns about ceramics in THA. Clin Orthop Relat Res 2004;429:73-79.

    35.

    Jarrett CA, Ranawat AS, Bruzzone M, Blum YC, Rodriguez JA, Ranawat CS: The squeaking hip: a phenomenon of ceramic-on-ceramic total hip arthroplasty.
    J Bone Joint Surg Am 2009;91(6):1344-1349.
    The authors reviewed 149 ceramic-on-ceramic hips in
    131 patients at a minimum 1-year follow-up. Fourteen
    patients described a squeaking noise, squeaking was re-

    Orthopaedic Knowledge Update 10

    producible in four patients, and one patient reported


    squeaking before prompting by the questionnaire. Level
    of evidence: Therapeutic level IV.
    36.

    Restrepo C, Parvizi J, Kurtz SM, Sharkey PF, Hozack


    WJ, Rothman RH: The noisy ceramic hip: is component
    malpositioning the cause? J Arthroplasty 2008;23(5):
    643-649.
    In 999 patients treated with THA, 28 reported squeaking postoperatively. Radiographic analyses of acetabular
    positioning in squeaking and nonsqueaking prostheses
    were compared. No significant difference was found in
    cup inclination. Four retrieved components were analyzed for stripe wear.

    37.

    Capello WN, DAntonio JA, Feinberg JR, Manley MT,


    Naughton M: Ceramic-on-ceramic total hip arthroplasty: Update. J Arthroplasty 2008;23(7, suppl)S39S43.
    The authors report on a prospective, randomized, multicenter study of alumina-on-alumina hip prostheses
    that included 475 hips in 452 patients. The authors suggest clinically superior results compared with conventional polyethylene-on-metal bearings.

    38.

    Park YS, Hwang SK, Choy WS, Kim YS, Moon YW,
    Lim SJ: Ceramic failure after total hip arthroplasty with
    an alumina-on-alumina bearing. J Bone Joint Surg Am
    2006;88(4):780-787.

    39.

    Ries MD, Pruitt L: Effect of cross-linking on the microstructure and mechanical properties of ultra-high molecular weight polyethylene. Clin Orthop Relat Res 2005;
    440:149-156.

    40.

    Jacobs CA, Christensen CP, Greenwald AS, McKellop


    H: Clinical performance of highly cross-linked polyethylenes in total hip arthroplasty. J Bone Joint Surg Am
    2007;89(12):2779-2786.
    The authors present a review of the clinical performance
    of highly cross-linked polyethylene and summarize information on the manufacturing processes and other influences on clinical performance.

    41.

    McKellop H, Shen F, Lu B, Campbell P, Salovey R: Effect of sterilization method and other modifications on
    the wear resistance of acetabular cups made of ultrahigh molecular weight polyethylene. A hip-simulator
    study. J Bone Joint Surg Am 2000;82-A(12):1708-1725.

    42.

    McCalden RW, MacDonald SJ, Rorabeck CH, Bourne


    RB, Chess DG, Charron KD: Wear rate of highly crosslinked polyethylene in total hip arthroplasty. A randomized controlled trial. J Bone Joint Surg Am 2009;91(4):
    773-782.
    This prospective, randomized controlled study compared clinical outcomes and head penetration in 50 patients with highly cross-linked polyethylene prostheses
    and 50 patients with conventional polyethylene. Level
    of evidence: Therapeutic level I.

    43.

    Tower SS, Currier BH, Lyford KA, Van Citters DW,


    Mayor MB: Rim cracking of the cross-linked longevity

    2011 American Academy of Orthopaedic Surgeons

    Chapter 7: Bearing Surface Materials for Hip, Knee, and Spinal Disk Replacement

    polyethylene acetabular liner after total hip arthroplasty. J Bone Joint Surg Am 2007;89(10):2212-2217.

    Zeh A, Becker C, Planert M, Lattke P, Wohlrab D:


    Time-dependent release of cobalt and chromium ions
    into the serum following implantation of the metal-onmetal Maverick type artificial lumbar disc (Medtronic
    Sofamor Danek). Arch Orthop Trauma Surg 2009;
    129(6):741-746.
    The authors measured the serum cobalt and chromium
    concentrations in 15 patients after lumbar metal-onmetal TDA and reported concentrations similar to those
    seen with THA and TKA. First and second follow-ups
    occurred at an average of 14.8 and 36.7 months, respectively.

    50.

    Zigler J, Delamarter R, Spivak JM, et al: Results of the


    prospective, randomized, multicenter Food and Drug
    Administration investigational device exemption study
    of the ProDisc-L total disc replacement versus circumferential fusion for the treatment of 1-level degenerative
    disc disease. Spine (Phila Pa 1976) 2007;32(11):11551162, discussion 1163.
    This prospective, randomized, multicenter clinical trial
    evaluated 286 patients at 6 weeks and 3, 6, 12, 18, and
    24 months to compare lumbar disk replacement and circumferential spinal fusion for treating discogenic pain at
    one vertebral level between L3 and S1.

    51.

    Nunley P, Gordon C, Jawahar A, et al: Total disc arthroplasty affords quicker recovery in one-level degenerative disc disease of cervical spine: Preliminary results of
    a prospective randomized trial. Spine J 2008;8:17S.
    The authors present clinical data from a prospective,
    randomized, multicenter trial comparing cervical TDA
    with anterior cervical diskectomy and fusion for treating
    single-level degenerative disk disease. Fifty-one patients
    were evaluated at an average follow-up of 13 months.

    52.

    Devin CJ, Myers TG, Kang JD: Chronic failure of a


    lumbar total disc replacement with osteolysis. Report of
    a case with nineteen-year follow-up. J Bone Joint Surg
    Am 2008;90(10):2230-2234.
    This case report describes a patient treated in 1993 with
    an L3-L4 TDA that was determined to have good results. Revision was required 19 years later. Significant
    osteolysis led to biomechanical failure of the TDA.

    Four fractured highly cross-linked polyethylene acetabular liners were examined to determine the factors that
    played a role in their failure. The authors suggest that
    material properties of the acetabular liners were partly
    responsible for fractures.
    44.

    Williams S, Schepers A, Isaac G, et al: The 2007 Otto


    Aufranc Award: Ceramic-on-metal hip arthroplasties. A
    comparative in vitro and in vivo study. Clin Orthop
    Relat Res 2007;465:23-32.
    An in vitro and in vivo comparison of ceramic-on-metal
    bearing couples with metal-on-metal and ceramic-onceramic bearing couples is presented. Thirty-one patients were analyzed for metal ion levels at 6-month
    follow-up. Level of evidence: Therapeutic level II.

    45.

    Bourne RB, Barrack R, Rorabeck CH, Salehi A, Good


    V: Arthroplasty options for the young patient: Oxinium
    on cross-linked polyethylene. Clin Orthop Relat Res
    2005;441:159-167.

    46.

    Kop AM, Whitewood C, Johnston DJ: Damage of oxinium femoral heads subsequent to hip arthroplasty dislocation: Three retrieval case studies. J Arthroplasty 2007;
    22(5):775-779.
    The authors highlight the relative softness of the zirconium base beneath the oxidized zirconium femoral
    head. Significant damage after hip dislocation and subsequent reduction was reported in three retrieval case
    studies.

    47.

    48.

    Lin EL, Wang JC: Total disk arthroplasty. J Am Acad


    Orthop Surg 2006;14(13):705-714.
    Punt IM, Cleutjens JP, de Bruin T, et al: Periprosthetic
    tissue reactions observed at revision of total intervertebral disc arthroplasty. Biomaterials 2009;30(11):20792084.
    Periprosthetic tissue samples were obtained during revision of TDAs in 16 patients; osteolysis was observed in
    1 patient.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    49.

    83

    Chapter 8

    Musculoskeletal Imaging
    Kenjirou Ohashi, MD, PhD

    Georges Y. El-Khoury, MD

    Introduction

    Radiography

    Advances in Technology
    Since the discovery of x-rays in 1895, images have been
    captured and reviewed on silver halidebased hard
    films. Although digital image acquisition began in the
    mid 1980s, filmless methodology became available in
    the early 1990s with the advent of picture archiving
    and communication systems. Computed radiography, a
    cassette-based photostimulable phosphor and plate
    reading storage system, initially replaced the analog
    screen film system. Alternate (cassetteless) technologies
    for digital imaging, historically categorized as digital
    radiography, appeared in the mid 1990s. The digital radiography system reads the x-ray signal immediately after exposure with the detector in place.
    Currently, the term digital radiography is used to refer to all types of digital radiographic systems for both
    cassette and cassetteless operations. The efficiency of
    digital radiography has markedly improved; however,
    without constant quality control there is a potential
    risk of a gradual increase in patient radiation dose
    (dose creep). Digital radiography systems must provide
    quality imaging services and protect patients from unnecessary radiation.1,2

    Dr. Menda or an immediate family member has received


    research or institutional support from Siemens Medical
    Solutions. Neither of the following authors or a member
    of their immediate families has received anything of
    value from or owns stock in a commercial company or
    institution related directly or indirectly to the subject of
    this chapter: Dr. Ohashi and Dr. El-Khoury.

    2011 American Academy of Orthopaedic Surgeons

    Fracture Imaging
    Spine Fractures
    Although cervical spine radiography is limited in visualizing ligamentous injuries, quality radiographs can
    exclude unstable cervical spinal injuries in a high percentage of patients.
    Cervical spine radiography is no longer used to rule
    out injuries to the cervical spine in high-risk multitrauma patients when CT of the head or other body parts is
    performed. For patients with more than a 5% risk of a
    cervical spine fracture, CT of the cervical spine is more
    efficient than obtaining multiple radiographic views.3,4
    In patients with traumatic injuries, radiographic studies
    often require several exposures and may not detect up
    to 61% of cervical spine fractures.5 CT screening is also
    a cost-effective modality in patients at high or moderate
    risk for cervical spine fracture.6
    Patients 65 years or older with blunt trauma have
    characteristic injury patterns and require special diagnostic strategies. Approximately two thirds of the fractures involve the upper cervical spine (level C0-C2) and
    can be caused by low-energy mechanisms such as a fall
    from standing7 (Figure 1). A retrospective analysis of
    cervical spine injuries in elderly patients (age 65 to 75
    years compared with those older than 75 years) suggested that CT may be appropriate as the primary modality for all trauma patients older than 75 years because of increased incidence of injuries in low-energy
    mechanisms.7 For these patients, radiographic detection
    of cervical spine fractures is often difficult due to degenerative changes.
    AP, lateral, open-mouth, and swimmers views are
    often used in imaging of the cervical spine. The lateral
    view should include the C7-T1 junction (Figure 2).
    Quality radiography remains a valuable screening test
    for thoracic and lumbar spinal fractures. Because the
    shoulders overlap on lateral views, visualization of the
    upper thoracic spine is often limited. CT is increasingly
    being used to diagnose or exclude thoracic and lumbar
    spine fractures, especially in patients with multiple
    traumatic injuries.

    1: Principles of Orthopaedics

    Imaging studies are an integral part of orthopaedic


    practices. As the availability of imaging modalities increases, having a working knowledge and understanding of the indications of each modality is becoming increasingly important for orthopaedic surgeons. Recent
    advances in technology, indications for each imaging
    test, and imaging features of common pathologies will
    be discussed in this chapter.

    Yusuf Menda, MD

    Fractures of the Extremities


    The diagnosis and assessment of extremity fractures are
    the most common indications for radiography. At least
    two orthogonal views should be obtained because the
    fractures may not be seen on a single view. Additional
    and/or special views are commonly used for the wrist,
    elbow, shoulder, and ankle. The cross-table lateral view

    Orthopaedic Knowledge Update 10

    85

    Section 1: Principles of Orthopaedics

    fracture, is highly predictive of an occult intra-articular


    fracture (Figure 3).
    Proximal Femoral Fractures
    Nondisplaced fractures of the femoral neck or intertrochanteric region may be missed on standard radiographs
    in patients with osteopenia. Because of the serious consequences of a delayed diagnosis, limited MRI (coronal
    images through both hips) may be indicated for early
    diagnosis or to exclude the presence of a fracture.

    Arthritis

    1: Principles of Orthopaedics

    The diagnosis of arthritis is primarily based on radiographic findings. Radiography is not sensitive for detecting early soft-tissue changes; however, characteristic
    bony changes often lead to a specific diagnosis.8,9 Classic radiographic assessment for arthritis includes evaluation of joint alignment, bone mineral status (osteopenia), cartilage (joint space, erosion), and distribution of
    the affected joints. A weight-bearing study is necessary
    to assess joint-space narrowing in the hip, knee, and
    ankle joints.

    Figure 1

    Sagittal reformatted CT image of the cervical


    spine of a 71-year-old man injured in a fall
    shows a type II odontoid fracture (arrow) with
    posterior subluxation of C1 on C2.

    can be used to detect fluid-fluid levels (lipohemarthrosis) in the knee. Adjacent joints should be examined separately if there is a clinical suspicion of injury. Radiography can detect radiopaque foreign bodies; however,
    ultrasound has higher sensitivity for detecting foreign
    bodies. Radiographs are less sensitive for detecting fractures in severely osteopenic patients. Certain fractures,
    such as scaphoid, radial head and/or neck, and proximal femoral fractures are easily missed by radiography.
    Scaphoid Fractures
    The scaphoid is the most commonly fractured bone in
    the wrist. Early diagnosis is important because immediate treatment minimizes the risks of nonunion and osteonecrosis. Standard radiographic imaging includes
    PA, oblique, lateral, and scaphoid (ulnar flexion) views.
    Imaging protocols, including the indications for advanced techniques such as MRI, may vary from hospital to hospital.
    Radial Head and/or Neck Fractures
    The radial head capitellar view (oblique lateral) may be
    added to AP and lateral views of the elbow to detect
    subtle fractures of the radial head and/or neck. The fat
    pad sign (capsular distention), even without obvious
    86

    Orthopaedic Knowledge Update 10

    Rheumatoid Arthritis
    Proximal joints of the hand and foot are typically affected by rheumatoid arthritis. Periarticular soft-tissue
    swelling, osteopenia, marginal erosion, and uniform
    joint-space narrowing are characteristic radiographic
    findings. A semisupinated oblique view of the hand and
    wrist (so-called ball-catcher view) will better show
    metacarpophalangeal and pisotriquetral joint erosions.
    Osteoarthritis
    Osteoarthritis (OA) affects the cartilage in weightbearing joints of the hip and knee and is characterized
    by increased bone mineralization (subchondral sclerosis), osteophyte formation, and nonuniform joint-space
    narrowing. Identical radiographic findings in the distal
    joints of the hand and foot, which typically occur in
    women 50 years or older, are referred to as idiopathic
    OA. Radiographic findings of OA in the hands may be
    associated with central erosive changes and typically
    occur along the articular surfaces. This variant is called
    erosive OA. The erosive changes may be accompanied
    by osteopenia or proliferative changes.
    Pyrophosphate Arthropathy
    Calcium pyrophosphate dihydrate crystal deposition
    occurs in the soft tissues in and around a joint and may
    cause synovitis. Pyrophosphate arthropathy typically
    affects elderly patients but can affect relatively young
    adults.10 Chondrocalcinosis (calcification of cartilage)
    may be present. The knee (meniscus), symphysis pubis
    (disk), and wrist (triangular fibrocartilage) are common
    locations for chondrocalcinosis. Bone minerals are typically preserved. Large osteophytes and uniform jointspace narrowing can be observed. Findings of large osteophytes in nonweight-bearing joints, such as the
    glenohumeral and patellofemoral joints, should raise
    the possibility of pyrophosphate arthropathy.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 8: Musculoskeletal Imaging

    1: Principles of Orthopaedics

    Figure 2

    A cross-table lateral radiograph (A) of the cervical spine of a 53-year-old patient who was struck by a vehicle shows
    unremarkable alignment of the cervical spine. C7 is not shown. A swimmers view (B) shows anterior displacement
    of C6 on C7 (arrows). Unilateral facet dislocation was confirmed by CT (not shown).

    Seronegative Spondyloarthropathies
    Seronegative arthropathies include ankylosing spondylitis, sacroiliitis associated with inflammatory bowel
    disease, psoriatic arthritis, and reactive arthritis. The
    unifying radiographic manifestation is enthesitis
    chronic inflammation at the tendon/ligament insertion.
    Erosions initially occur at the capsular insertion followed by bony proliferation (sclerosis and bony outgrowth) (Figure 4). Ankylosis may eventually occur.
    Neuropathic Arthropathy
    Chronic repetitive trauma in a joint with poor sensibility may explain some of the radiographic changes of
    neuropathic arthropathy, but the exact pathogenesis is
    not clear. The radiographic changes include the wide
    spectrum of bony changes from total bony resorption
    (an atrophic neuropathic joint) to excessive repair (a
    hypertrophic neuropathic joint). The hypertrophic
    changes show the classic pattern of joint destruction,
    dislocation, debris, and excessive bone formation. In
    the foot and ankle, diabetes mellitus is the most common cause of neuropathic arthropathy, typically involv-

    2011 American Academy of Orthopaedic Surgeons

    ing the midfoot and forefoot. Septic joint and osteomyelitis are often difficult to exclude in patients with a
    neuropathic joint.

    Neoplasms
    Diagnosing bone tumors is primarily based on the patients history (age and symptoms) and the radiographic
    findings. The tumor location, border (for lytic lesions),
    periosteal reaction, and matrix calcifications should be
    evaluated. Cross-sectional imaging with CT and MRI
    may be used to confirm the radiographic findings and
    provide additional information such as the cystic nature of the lesion (fluid-fluid levels or peripheral enhancement after intravenous contrast) and the extent of
    the tumor. Clinically important distinctions between
    benign and malignant tumors rely mainly on radiographic findings. Without radiographic correlation,
    MRI findings alone can be misleading in diagnosing
    certain benign lesions such as osteoid osteoma,
    osteoblastoma, chondroblastoma, and eosinophilic
    granuloma. In such instances, the appearance of the lesion on MRI scans may suggest an aggressive tumor.

    Orthopaedic Knowledge Update 10

    87

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 3

    A, Lateral radiograph of the elbow of a 26-year-old man with an impacted posterior aspect of the elbow after a fall
    shows no acute fracture. Moderate capsular distention is noted with displaced fat pads (arrows). B, Sagittal T1weighted MRI scan shows a linear low signal (arrow) along the radial head-neck junction consistent with a nondisplaced fracture.

    structures. Additional advantages of cross-sectional images include evaluation of fat content and cystic or
    solid nature of the lesions.

    Infections

    Figure 4

    Ferguson radiographic view shows extensive


    bony erosion along the sacroiliac joint with proliferative sclerotic changes especially along the
    iliac side bilaterally (arrows) in a 29-year-old
    man with a stiff neck and back pain. The radiographic findings are consistent with sacroiliitis.
    The patient was diagnosed with ankylosing
    spondylitis.

    Radiography is generally not helpful in diagnosing


    soft-tissue tumors. Radiography may detect calcification (for example, in synovial cell sarcomas), phleboliths (for example, in hemangiomas), and hyperostosis
    at the adjacent bone (associated with benign soft-tissue
    lesions). Cross-sectional images provide information
    about the location and size of a lesion and its relationship to the adjacent structures, especially neurovascular
    88

    Orthopaedic Knowledge Update 10

    Radiography is less sensitive than other imaging modalities, such as bone scanning and MRI, for the early detection of acute osteomyelitis; however, radiography
    may show focal osteolysis and periosteal reaction in patients with acute osteomyelitis. A comparison with previous radiographs is important, especially for patients
    with diabetic foot infections in whom it can be difficult
    to differentiate between neuropathic osteoarthropathy
    and infection. Radiography is sensitive for detecting
    soft-tissue emphysema (Figure 5), which can be caused
    by a life-threatening infection.

    Metabolic Diseases
    Digital radiography automatically adjusts the amount
    of radiation in the field of view. Because a wide range
    of settings is available to review the digital images on
    the display monitor, the bone density, which is subjectively estimated by a digital system, can be misleading.
    Cortical thinning and accentuation of trabeculae can be
    assessed when considering the diagnosis of osteoporosis. Characteristic radiographic findings of rickets are
    often seen on a chest radiograph (Figure 6). Enlargement of the rib ends (rachitic rosary), widening of the
    proximal humeral physes, and subcortical bone resorption at the inferior scapular angles can be detected.
    Fragile osteopenic bones in patients with osteogenesis
    imperfecta usually lead to multiple fractures. Radio-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 8: Musculoskeletal Imaging

    Chest radiograph of a 13-month-old boy with failure to thrive shows enlargement of rib ends (rachitic rosary) (short arrows) and widening of the
    physis of the proximal humerus (long arrow)
    consistent with rickets.

    Figure 7

    Lateral radiograph of the elbow of a 6-year-old


    girl shows congenital posterior dislocation of
    the radial head, which is dome-shaped (arrow).
    The capitellum is hypoplastic. No capsular distention is seen.

    1: Principles of Orthopaedics

    Figure 5

    Figure 6

    AP radiograph of the tibia and fibula shows extensive air lucencies in the soft tissue (subcutaneous emphysema) consistent with gas
    gangrene.

    graphic features of rickets and osteogenesis imperfecta


    may overlap with those of child abuse.

    Congenital Anomalies
    Radiography can be used in the diagnosis of certain
    congenital bony anomalies. Congenital dislocation of
    the radial head may be an isolated abnormality or may
    be associated with other conditions such as scoliosis or
    Klippel-Feil and nail-patella syndromes. Radial head
    dislocation is associated with a small, dome-shaped radial head and hypoplastic capitellum (Figure 7). Congenital pseudarthrosis of the clavicle almost always occurs in the right clavicle. Radiographically, the middle
    segment is partially missing with tapering of the medial
    segment (Figure 8). These congenital anomalies can potentially be misdiagnosed as a posttraumatic condition.
    A standing PA view of the entire spine is obtained on a
    single image for the evaluation of scoliosis. The PA projection reduces radiation exposure to the breast and
    thyroid by threefold to sevenfold compared with the
    AP projection. Lateral radiographs may be obtained after scoliosis is diagnosed to assess sagittal alignment.

    Computed Tomography

    Recent Advances in Technology


    Substantial advances in CT technologies have occurred
    in the past two decades. Helical CT was commercially

    2011 American Academy of Orthopaedic Surgeons

    introduced in 1988 and multidetector CT (MDCT)


    technologies were introduced in 1992. In a singledetector helical CT, detectors are aligned along the patients axial plane (x-y plane). With MDCT, detectors
    are also stacked along the long axis (z-axis), enabling
    collection of large amounts of data per each x-ray tube
    rotation. Increasing the speed of the x-ray tube rotation
    (to 0.5 to 0.35 seconds/rotation) contributed to further
    reduction of total scanning time. CT scanners with 64

    Orthopaedic Knowledge Update 10

    89

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    detectors have been installed in many facilities, and


    scanners with 320 detectors became commercially
    available in 2008. With MDCT, the emitted x-ray beam
    is more efficiently used than before, thus contributing
    to a reduction in the radiation dose.
    MDCT is capable of generating multiple thin slice
    images (reconstructed images) from large volumetric
    data sets. With this technology, hundreds of axial images are usually generated with each study. The images
    are reviewed as a volume rather than as individual axial images. Three-dimensional workstations are necessary for viewing these large image data sets from which

    90

    multiplanar reformatted images can be interactively reviewed in any chosen plane and are not limited to sagittal or coronal planes (Figure 9). Internet-based threedimensional software can be easily accessed by multiple
    readers and may eventually replace three-dimensional
    workstations.

    Fracture Imaging
    Spine Fractures
    The increased availability of CT has contributed to the
    recent change in indications for CT of cervical spine
    fractures in the emergency department. Because the
    time required to reach a correct diagnosis is a critical
    factor for managing multitrauma patients, CT has become an essential tool for ruling out or diagnosing cervical spine fractures. A recent survey has shown that
    40% of emergency departments in the United States
    have CT scanners.11 Indications for cervical spine CT in
    high-risk patients were previously discussed in this
    chapter.
    CT is recommended to assess spine trauma in patients with ankylosing spondylitis or diffuse idiopathic
    skeletal hyperostosis whose spines are rigid because of
    bony fusion.12 In patients with advanced ankylosing
    spondylitis, severe osteoporosis makes radiographic detection of a fracture less reliable (Figure 10). Fractures
    in an ankylosed spine are typically oriented transversely
    and affect all three columns. Multiplanar reformatted
    images clearly delineate such fractures, which are difficult to detect on axial images.
    Because CT allows poor visualization of ligaments
    compared with MRI, it is debated whether CT alone

    Figure 8

    Chest radiograph of a 4-day-old girl shows pseudarthrosis of the right clavicle (arrow). Opposing
    midclavicular ends are corticated and no callus
    formation is seen.

    Figure 9

    A: Orthogonal three-plane (sagittal [upper left], coronal [upper right], and axial [bottom right]) CT images of the
    wrist of a 20-year-old man with a scaphoid fracture show screw placement. Color three-dimensional volumerendered CT image showing bone and tendon (lower left). The color lines represent the location and orientation
    of the slices seen in the other boxes. B, Double oblique CT images along the screw show the long axis of the scaphoid to a better advantage (upper right and left). Screw displacement and angular deformity of the scaphoid (arrow; upper left) is noted. The short axis (transverse plane) of the scaphoid is shown in the lower right image. The
    lower left image is a color three-dimensional volume-rendered CT image showing bone and tendon. The color
    lines represent the location and orientation of the slices seen in the other boxes.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 8: Musculoskeletal Imaging

    1: Principles of Orthopaedics

    Figure 10

    A, Cross-table lateral radiograph of the cervical spine of a 49-year-old man with known ankylosing spondylitis who
    was involved in a motor vehicle crash shows extensive bony fusion of the spine. No fracture is seen. B, Sagittal
    reformatted CT image shows a nondisplaced fracture at the C5-C6 level (arrow).

    can be used to exclude cervical spine injuries. However,


    studies have shown that pure ligamentous injuries without fractures are uncommon.13 Studies on ruling out
    cervical spinal injuries in obtunded patients have
    shown that CT, in comparison with a composite reference standard (subsequent imaging and clinical examinations) or with MRI, has a 99% negative predictive
    value for ruling out ligamentous injuries and a 100%
    negative predictive value for ruling out unstable cervical spine injuries.14,15
    In the thoracic and lumbar areas of the spine, most
    fractures occur at the fulcrum of motion between T11
    and L2. These fractures account for approximately
    50% of all spinal fractures. In multitrauma patients imaged with MDCT of the chest, abdomen, and pelvis,
    spine CT images can be reconstructed without additional scanning. CT body studies using a 2.5-mm detector collimation and reconstructed spinal CT images
    have shown high accuracy in depicting thoracic and
    lumbar spine fractures.16,17 Single-pass, whole-body
    scanning can be used to cover an extended area from
    the head to the pelvis. This method contrasts with the
    segmented approach in which each body region is
    scanned separately. The single-pass, whole-body approach exposes the patient to 17% less radiation than

    2011 American Academy of Orthopaedic Surgeons

    the segmented approach because there is no overlap between the irradiated fields.18,19
    Pelvic and Acetabular Fractures
    Because of the complex anatomy of the pelvis, conventional radiography often fails to show the full extent of
    a fracture, the spatial relationship of the major fracture
    fragments, and the intra-articular bony fragments. Specific indications for CT include acetabular fractures,
    sacroiliac joint involvement, and sacral and lumbosacral junction injuries.20
    Approximately 30% to 40% of pelvic injuries involve the acetabulum.21,22 The Letournel classification
    is based on AP and oblique (Judet) pelvic radiographs.
    CT is routinely performed to aid preoperative planning.
    Standard pelvic radiographs add little information to
    CT scans in classifying acetabular fractures;23 however,
    standard radiographs are still important for intraoperative assessment and follow-up evaluation.
    Fractures of the Extremities
    Wrist Fractures
    Traditionally, clinically suspected scaphoid fractures
    are treated with immobilization and followed clinically
    and radiographically regardless of the initial radio-

    Orthopaedic Knowledge Update 10

    91

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 11

    A, Lateral radiograph of the elbow of a 51-year-old man shows a right elbow fracture-dislocation. B, Sagittal CT
    image through the radius shows a radial head fracture (black arrow) and a coronally oriented lateral condyle
    fracture of the humerus (white arrow). C, Sagittal CT image through the ulna shows a comminuted coronoid fracture (black arrow) and a proximally displaced small avulsion fracture of the olecranon (white arrow). Displaced
    anterior and posterior fat pads are noted (arrowheads).

    graphic findings. To improve cost-effectiveness and


    speed a patients return to function, more sensitive imaging modalities such as bone scans, MRIs, and highspatial-resolution ultrasound studies are now commonly used.24-30 CT has been used to detect occult
    fractures of the wrist when radiographs are negative.25,31 There have been case reports of scaphoid fractures diagnosed by bone scanning and/or MRI but
    missed by CT.32,33
    Elbow Fractures
    Complex fractures or fracture-dislocations of the elbow
    can be difficult to characterize by radiography alone,
    especially after cast immobilization. CT can clearly
    show the relationship between multiple bony fragments
    when reviewed on multiplanar reformatted images
    along the humerus, radius, and ulna and on threedimensional images (Figure 11).
    Tibial Plateau Fractures
    Studies of CT using multiplanar reformatted or threedimensional imaging have shown that using CT scans in
    addition to radiographs changes an observers classification of a tibial plateau fracture in 12% to 55% of cases
    compared with using radiographs alone; the use of both
    imaging modalities also results in treatment modifications in 26% to 60% of patients.34-37 CT is an excellent
    modality for assessing comminution in a tibial plateau
    fracture and the amount of depression of the articular
    fragments, and is helpful in preoperative planning.
    Ankle Fractures
    Radiographic studies may underestimate the size and
    displacement of a posterior malleolar fracture. A report
    of 57 surgically treated patients with a posterior malleolar fracture showed a wide variation in fracture orientation and that approximately 20% of the fractures extended to the medial malleolus.38
    92

    Orthopaedic Knowledge Update 10

    Calcaneal Fractures
    In the mid 1990s, CT was shown to allow excellent visualization and evaluation of the pathoanatomy of
    intra-articular calcaneus fractures with direct axial and
    coronal scans.39 Since that time, CT with multiplanar
    reformatted imaging and three-dimensional imaging
    has become the standard investigative modality to
    guide the treatment of intra-articular fractures of the
    calcaneus.40 Using isotropic imaging, single scanning
    through the calcaneus is sufficient to evaluate the integrity of subtalar and calcaneocuboid joints. Volume rendering to visualize tendon-bone relationships has been
    introduced and clinically applied to evaluate the tendons in the ankle and foot41 (Figure 12).

    Postoperative Complications
    The use of CT in patients with orthopaedic hardware
    can be hampered by severe metal artifacts. Metal artifacts are displayed on CT scans as streak or sunburst
    artifacts, which degrade the image quality. With proper
    data acquisition, image reconstruction, and image reformatting, diagnostic CT scans can be obtained for
    most patients. Prostheses made of a cobalt-chromium
    alloy cause substantial artifacts, whereas titanium implants produce less significant metal artifacts. The use
    of multiplanar reformatted imaging helps to decrease
    the adverse effects of metal artifacts on image quality.
    Three-dimensional volume rendering is also helpful in
    reducing streak artifacts associated with hardware.42,43
    Postoperative CT may be performed to evaluate
    intra-articular fracture reduction and hardware placement. In the spine, pedicle screw misplacement can be
    associated with neurologic complications. CT has been
    reported to be 10 times more sensitive than radiography for detecting medial pedicle cortex violations.44 Recently developed three-dimensional C-arm CT scanning
    with flat-panel detectors has been introduced into orthopaedic practices.45 C-arm CT has been used to intra-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 8: Musculoskeletal Imaging

    1: Principles of Orthopaedics

    Figure 12

    Three-dimensional color volume-rendered CT


    image of the ankle (tendon and bone) of a
    35-year-old man with a closed calcaneal fracture shows dislocation of the peroneal tendons
    (arrow) and a comminuted fracture of the
    calcaneus.
    Figure 13

    operatively assess spinal fusion and pedicle screw placement.


    Failure of Bony Fusion
    Radiography is inaccurate in assessing bony fusion
    when compared with CT.46 Radiography may underestimate or overestimate bony fusion in patients with
    fracture fixation or arthrodesis.46 In a recent investigation, CT was reported to be useful in predicting stability for patients with ankle or subtalar arthrodesis.47
    Following surgery for spinal fusion, the assessment
    of the bony fusion with flexion and extension lateral
    radiographic views may be useful for the gross evaluation of instability. Sagittal and coronal reformatted
    CT images through the fusion site are best for evaluating bone bridging and the integrity of the fusion
    mass.48
    Osteolysis
    Radiographic detection of osteolysis can be influenced
    by the patients body habitus, the position of the hardware, and the location of the lesion. Radiography can
    provide limited information, even with multiple projections, on the location and amount of osteolysis. Fluoroscopically guided radiographs may be indicated to obtain true tangential views of components in total knee
    replacements.49 CT may be indicated not only for the
    detection of osteolysis but also for the evaluation of
    bone loss before surgery.50-52
    Hardware Problems
    Hardware fractures may be detected on CT scans and
    are usually associated with other complications such as

    2011 American Academy of Orthopaedic Surgeons

    Sagittal reformatted CT image of the lumbar


    spine of a 61-year-old woman shows fracture
    of S1 pedicle screw (arrow) associated with
    marginal lucency around the screw and sagging of L5 inferior end plate (arrowheads) at
    the bone graft.

    nonunion and osteolysis (Figure 13). The position of


    the component, subsidence of the component, and
    polyethylene wear following hip or knee arthroplasty
    are usually assessed on radiographs. CT can be used to
    detect polyethylene liner dislocations. Patellofemoral
    symptoms may be associated with component malrotation. CT is the study of choice to evaluate rotational
    malalignment of the femoral and tibial components in
    total knee arthroplasty.53,54
    The efficacy of CT in detecting hardware complications has not been well investigated. One study of 114
    CT imaging studies from 109 patients used clinical or
    surgical outcomes as the reference standard and measured sensitivity, specificity, and positive and negative
    predictive values of CT (74%, 95%, 88%, and 88%,
    respectively).55 Radiography alone was less sensitive in
    detecting hardware complications such as nonunion
    and osteolysis than was CT alone.

    Magnetic Resonance Imaging

    Advantages and Limitations


    Because of its excellent soft-tissue contrast, MRI has
    become the diagnostic modality of choice for evaluating bone marrow, cartilage, and soft tissues; the absence of ionizing radiation also makes it an ideal mo-

    Orthopaedic Knowledge Update 10

    93

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 14

    A lung tumor in a 66-year-old man metastasized to the thoracic spine. A, Lateral radiograph of the thoracic spine
    is unremarkable except for some degenerative changes. B, Sagittal T1-weighted MRI of the thoracic spine shows
    an infiltrative process involving the entire vertebral body of T10 with extension into the body of T9 (long arrow).
    Early involvement of the body of T3 was also suspected (short arrow).

    dality for imaging in children. Limitations of MRI


    include the relatively long scanning time, which necessitates the use of sedation or general anesthesia in
    young children and uncooperative adults. MRI cannot
    be used in patients with cochlear implants or a pacemaker, and may not be useable in some patients with
    certain orthopaedic metal implants that are located in
    close proximity to the area being scanned. Fortunately,
    most modern orthopaedic implants are nonferromagnetic and will not displace when the patient is within a
    strong magnetic field. When an implant is suspected of
    being ferromagnetic, an identical implant can be tested
    with a horseshoe magnet before MRI. In practice, most
    radiology departments try to obtain the specific manufacturers part number and check for magnetic resonance compatibility. Specific absorption rate (SAR) is
    related to the amount of tissue heating resulting from
    radiofrequency pulses. Modern scanners typically esti94

    Orthopaedic Knowledge Update 10

    mate the SAR values and will suggest protocol changes


    to reduce SAR values to safe levels. SAR increases at
    higher field strengths, which may require adjustments
    to the imaging protocol such as increasing the repetition time or reducing the number of slices. Most metal
    implants produce susceptibility artifacts, rendering the
    images nondiagnostic for abnormalities close to the
    metal implants. Ideally, the radiologist should be notified in advance about the presence of a metal implant
    in the area of interest; a special MRI sequence can then
    be prescribed that can reduce, but not completely eliminate, metal artifacts.56

    MRI Sequences
    Orthopaedic surgeons should be familiar with the capabilities of commonly used MRI sequences. T1-weighted
    sequences take a short time to acquire and are excellent
    for the initial investigation of any disease process in

    2011 American Academy of Orthopaedic Surgeons

    Chapter 8: Musculoskeletal Imaging

    1: Principles of Orthopaedics

    Figure 15

    A 73-year-old man presented to the emergency department with right hip pain and inability to bear weight on
    the right hip. A, AP radiograph of the right hip was unremarkable. B, Coronal T1-weighted MRI of the pelvis
    shows a fracture line in the right femoral neck (arrow) surrounded by an area of low signal, which represents
    marrow edema. C, Coronal fat-suppressed T2-weighted image of the pelvis shows the fracture in the right femoral neck (arrow) surrounded by bright signals, which represent marrow edema.

    bones, joints, or soft tissues. T1-weighted sequences


    show good anatomic detail and are highly sensitive for
    detecting marrow abnormalities such as infiltrative processes, metastases, or infections57 (Figure 14). A T1weighted sequence is often the only sequence needed to
    diagnose an occult fracture of the hip in elderly patients
    or metastases in the spine. Most abnormalities have
    low signal intensity on a T1-weighted sequence.58
    T2-weighted sequences are ideally suited for diagnosing pathologic processes. When fat suppression is
    added to T2-weighted sequences, all fat-containing tissues appear black. Fat suppression is useful in accentuating the difference in contrast between normal and abnormal tissues. T2-weighted sequences are water
    sensitive; therefore, a bright signal is displayed for lesions containing water, such as bone marrow edema
    (Figure 15), soft-tissue edema, tumors, infections, abscesses, and acute fractures.
    Proton density-weighted sequences (also known as
    intermediate-weighted sequences) have a high signal-tonoise ratio and reveal exquisite anatomic detail. Fatsuppressed proton density sequences have been used,
    with excellent results, for imaging articular cartilage.
    A short-tau inversion recovery (STIR) sequence is
    also a water-sensitive sequence. This sequence suppresses the signals from fat much like the fatsuppressed T2-weighted sequences; however, it has two
    advantages over the fat-suppressed T2-weighted sequences. STIR sequences uniformly suppress fat over a
    large field of view, which is often not the case with fatsuppressed T2-weighted sequences. Metal artifacts are
    significantly less pronounced with a STIR sequence
    than with other sequences, although STIR imaging has

    2011 American Academy of Orthopaedic Surgeons

    a lower signal-to-noise ratio than the fat-suppressed sequences.


    Gradient-echo sequences also have advantages for
    some applications, and typically a short acquisition time.
    Some gradient-echo sequences are good for imaging articular cartilage because articular cartilage can be distinguished from intra-articular fluid by assigning slightly
    different signal intensity to each. Gradient-echo sequences also are useful when scanning for hemosiderin
    in lesions such as pigmented villonodular synovitis. The
    three-dimensional fat-suppressed spoiled gradient-echo
    sequence in the steady state and the three-dimensional
    gradient-echo double excitation sequence in the steady
    state have been successfully used for cartilage imaging59
    (Figure 16).

    Contrast Agents for MRI


    Gadolinium compounds have been used in musculoskeletal imaging for approximately 20 years and can be
    used intravenously to evaluate synovial inflammation,
    vascular lesions, neoplasms, and abscesses. Gadolinium
    is useful in differentiating a neoplasm from a cyst because the neoplasm enhances after an intravenous injection of gadolinium, whereas the cyst does not enhance.
    This contrast agent can be used to differentiate a drainable abscess from a phlegmon because pus within the
    abscess will not enhance, whereas the entire phlegmon
    will enhance (Figure 17). It also can be used to assess
    the extent of necrosis within a tumor. Such information
    is helpful in planning a biopsy because the necrotic tissue can be avoided and the biopsy needle can be directed at the enhancing tissue. The recommended dose
    for gadolinium is 0.1 mmol per kg of body weight. Re-

    Orthopaedic Knowledge Update 10

    95

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    noise ratio, which provides the potential for improved


    diagnostic confidence. There is little evidence, however,
    to show that 3-T MRI provides better diagnostic accuracy compared with 1.5-T MRI in diagnosing anterior
    cruciate ligament tears, meniscal tears, or shoulder abnormalities. Current clinical experience suggests that
    the higher signal-to-noise ratio enhances the visualization of ligaments and articular cartilage in small structures such as the hand and wrist.61
    Isotropic data sets on 100 consecutive shoulder examinations were acquired after the injection of diluted
    gadolinium into the joint.62 An isotropic gradient-echo
    sequence and thin sections (0.4 mm) were used. With
    arthroscopy as the reference standard, 3-T MRI was reported to be accurate in assessing rotator cuff tears and
    labral tears.62 The authors of another study used isotropic MRI to study internal derangement of the knee
    with a three-dimensional fast spin-echo sequence.63 Initial results from this study on knees of healthy volunteers were promising.

    Occult Fractures

    Figure 16

    Coronal fat-suppressed gradient-echo MRI sequence of the knee on a normal individual


    shows normal articular cartilage, which appears bright on this sequence (arrows).

    cently, gadolinium was shown to cause serious adverse


    effects in patients with impaired renal function; a potentially lethal disease known as nephrogenic systemic
    fibrosis developed in some patients.60
    Diluted gadolinium (1:100) is frequently used as an
    intra-articular contrast agent before magnetic resonance arthrography. It clearly delineates intra-articular
    abnormalities such as labral tears, recurrent meniscal
    tears, and cartilage defects. Despite the widespread use
    of gadolinium as an intra-articular contrast agent, the
    FDA has not approved its use for this purpose.

    Recent Advances in Technology


    In 2003, 3-Tesla (3-T) MRI began to achieve more
    widespread use as a clinical tool for musculoskeletal
    imaging. Because of the delay in creating dedicated
    coils for the different joints, the impact of the 3-T magnet on musculoskeletal imaging has been less dramatic
    than in other systems, such as the nervous system. The
    advantage of the 3-T magnet is in its high signal-to96

    Orthopaedic Knowledge Update 10

    The most common lawsuit filed against emergency department physicians involves missed orthopaedic injuries. In the past two decades, MRI has become an important tool for diagnosing injury in trauma patients in
    the emergency department. MRI is particularly useful
    in evaluating suspected occult fractures (those not initially seen on radiographs) and for ruling out ligamentous injuries in the cervical spine of obtunded patients.
    Common sites for occult fractures are the femoral neck,
    scaphoid bone, tibial plateau, and talar neck.
    Hip radiography has more than a 90% sensitivity
    for detecting fractures; however, approximately 3% to
    4% of patients present with occult hip fractures. Current evidence favors MRI as the best modality for detecting these occult fractures. Coronal T1-weighted images of the hip typically show a dark line at the fracture
    site (Figure 15). Studies have reported that a T1weighted sequence is sufficient for diagnosing occult
    hip fractures.64
    Occult scaphoid fractures can be challenging to diagnose, and delayed treatment increases the risk of
    complications. There is mounting evidence to suggest
    that MRI is the modality of choice for detecting occult
    scaphoid fractures.65

    Cervical Spine Injuries


    Cervical spine injuries occur in approximately 2% to
    6% of patients with blunt trauma; there is a real potential for a catastrophic neurologic deficit if such injuries
    are undiagnosed. In an alert trauma patient without a
    distracting injury, the cervical spine can be clinically
    cleared provided the neurologic examination is negative
    and the cervical spine has full range of motion and is
    without pain or tenderness. In the obtunded or unreliable patient, the optimal approach for ruling out cervical spinal injury has not yet been determined. The possibility of an unstable ligamentous injury is a troubling
    consideration in the obtunded patient and is the reason

    2011 American Academy of Orthopaedic Surgeons

    Chapter 8: Musculoskeletal Imaging

    1: Principles of Orthopaedics

    Figure 17

    A 57-year-old man with type II diabetes mellitus presented with pain and soft-tissue swelling on the dorsum of the
    left forefoot. A, Lateral radiograph shows significant soft-tissue swelling on the dorsum of the forefoot (arrows).
    B, Axial T1-weighted MRI shows an area of low signal in the subcutaneous fat on the dorsum of the foot (arrows). C, Sagittal fat-suppressed T2-weighted image shows bright signals (arrows) corresponding to the dark area
    in B. D, Sagittal fat-suppressed T1-weighted image after an intravenous gadolinium injection shows a central dark
    area (arrows) surrounded by a bright zone. This appearance is characteristic of a soft-tissue abscess.

    for further imaging after a negative CT examination to


    confirm intact ligamentous structures. The use of lateral flexion and extension views with fluoroscopy was
    briefly advocated, but was judged too hazardous and
    has been replaced with MRI. Recently, several investigators have reported that MDCT alone is sufficient for
    clearing the cervical spine.14 Because MDCT cannot be
    used to image spinal ligaments or the spinal cord, MRI
    continues to be recommended by some authors to rule
    out unstable ligamentous injuries of the cervical spine
    in obtunded patients.66 However, transporting an obtunded patient from the intensive care unit to the MRI
    suite is a difficult task and involves risks for the patient.
    A retrospective review of 366 obtunded patients
    whose cervical spines were evaluated with both CT and
    MRI showed that 12 patients (3.3%) had cervical spine
    injuries that were not detected by MDCT; however,
    none of the injuries were unstable and none of the patients required surgery. It was concluded that MDCT
    has negative predictive values of 98.9% for detecting
    ligamentous injuries and 100% for detecting unstable
    injuries.14 Another review of 202 patients initially eval-

    2011 American Academy of Orthopaedic Surgeons

    uated with CT followed by MRI showed that MDCT


    continues to miss both stable and unstable cervical spinal injuries.66 Of 18 patients (8.9%) who had abnormal
    MRI examinations, 2 required surgical spinal repairs,
    14 required extended use of a cervical collar, and the
    cervical collar was removed in 2 patients at the discretion of the attending surgeon. It was concluded that
    MRI changed treatment management in 7.9% of patients with negative MDCT examinations. The continued use of MRI for cervical spine clearance in the obtunded or unreliable patient was recommended by the
    study authors. However, recent evidence supports the
    belief that MRI is unlikely to uncover unstable cervical
    spine injuries in obtunded patients when a lategeneration MDCT examination is negative.67
    Spinal Cord Injury Without Radiographic Abnormalities
    The acronym SCIWORA was coined in 1982 for describing the presence of spinal cord injury without radiographic abnormality in children. After MRI became
    widely available for assessing spinal cord injuries, the
    term SCIWORA became somewhat ambiguous.68 In a

    Orthopaedic Knowledge Update 10

    97

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 18

    Imaging showing a stress fracture. A and B, Blood pool images of the bone scan show focal hyperemia (arrows) in
    the right distal tibia. C and D, Delayed bone scan images show intense uptake of the bone tracer involving the
    entire cortical thickness of the right distal tibia (arrow in C), consistent with an advanced stress fracture. There is
    also mild superficial uptake in the right proximal and left midfemur (arrows in D), consistent with early stress
    fractures.

    2008 literature review performed to clarify this ambiguity, it was recommended that if any pathology is detected on MRI, with or without radiographic abnormality, the classification of SCIWORA should not be
    used for the patient.68 It was also recommended that
    the label and meaning of SCIWORA be changed to reflect the concept of spinal cord injury without neuroimaging abnormality. A 2004 study also recommended
    the importance of considering MRI findings before using the SCIWORA classification for a patient.69

    Nuclear Medicine
    The most common radionuclide studies in musculoskeletal imaging are bone scans and positron emission tomography (PET) scans. Bone scans are performed using
    technetium-Tc 99m-labeled phosphonates (Tc-99m
    methylene diphosphonate [MDP], Tc-99m hydroxyethylidene diphosphonate). After intravenous injection, approximately one third of the injected dose of Tc-99m
    MDP localizes in the bone within 2 to 4 hours. Tc-99m
    emits gamma photons with a half-life of 6 hours. The
    gamma photons are detected by a gamma camera to produce images reflecting the distribution of the radiopharmaceutical. Tc-99mlabeled phosphonates accumulate
    preferentially in areas of active bone formation. As a result, areas of increased bone remodeling caused by tumor, infection, trauma, or metabolic bone disease appear
    hot on a bone scan. Therefore, bone scan abnormalities may not be specific for a disease process and should
    be interpreted in conjunction with the clinical history
    and other imaging modalities. Bone scans are routinely
    done 2 to 4 hours after injection of the radiopharmaceutical. Whole-body bone scans are used for screening the
    entire skeleton for metastatic bone disease. Single photon emission CT (SPECT) provides imaging in transaxial, coronal, and sagittal tomographic scans and is particularly helpful for evaluating the spine.
    98

    Orthopaedic Knowledge Update 10

    PET uses radiopharmaceuticals that are labeled with


    positron emitters. The most commonly used radiopharmaceutical in clinical PET is fluorine-18 deoxyglucose
    (FDG), which is a glucose analog labeled with fluoride18, with a half-life of 110 minutes. FDG-PET is primarily used in staging and restaging of malignancies. FDG
    shows increased accumulation in cancer cells because
    of enhanced transport of glucose and an increased rate
    of glycolysis in tumors. Most PET imaging currently is
    done on integrated PET-CT scanners. The CT portion
    of PET-CT is used for localization of metabolically active lesions but also may be used to obtain diagnosticquality CT scans. FDG-PET scans are performed 60 to
    90 minutes after injection of the radiopharmaceutical.
    FDG-PET scans should not be obtained in patients with
    uncontrolled diabetes because high glucose levels reduce the uptake of FDG in tumors.

    Occult Fractures and Stress Fractures


    Bone scans are highly sensitive for diagnosing occult
    fractures in symptomatic patients with negative radiographs. Bone scans are most often done to evaluate
    fractures in the wrist, hips, and spine; the scans are positive in 90% to 95% of fractures within 24 hours of the
    traumatic event. In elderly patients, bone scans may be
    negative in the initial 24 hours; therefore, repeated imaging at 72 hours is recommended if the initial bone
    scan is negative.70 Bone scans may remain positive for
    up to 3 years after a fracture because of persistent bone
    remodeling.71
    Bone scans also can be helpful in diagnosing stress
    fractures. These fractures may not be initially identified
    on plain radiographs. A negative bone scan excludes
    the presence of a stress fracture.72 A long-bone stress
    fracture on a bone scan shows focal fusiform increased
    uptake at the site of injury (Figure 18). Bone scintigraphy also is useful in differentiating stress fractures from
    shin splints. Shin splints typically refer to tibial perios-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 8: Musculoskeletal Imaging

    1: Principles of Orthopaedics

    Figure 19

    Imaging showing spondylolysis. A, Planar posterior bone scan image shows subtle uptake at L5 vertebra (arrow).
    Tracer uptake is clearly visualized on SPECT coronal (B), sagittal (C), and transaxial (D) bone scans, which localize
    the focus in the right pars region (arrows) of the L5 vertebra, consistent with a pars fracture.

    titis and usually require a shorter recovery period than


    stress fractures.73 The typical appearance of shin splints
    is linear uptake along the posteromedial aspect of the
    middle third of the involved tibia.
    Spondylolysis refers to a bone defect in the pars interarticularis of a vertebra, most commonly at L4 or L5,
    and is believed to occur as a result of a stress fracture.
    Patients with spondylolysis may be asymptomatic; in
    such instances, the condition may be diagnosed as an incidental imaging finding. However, in some patients,
    spondylolysis causes severe low back pain. A positive
    bone scan with focal uptake in the pars region indicates
    that the spondylolysis may be the cause of low back pain
    and correlates with a good outcome after fusion surgery.74 SPECT images of the lumbar spine always should
    be obtained because more than 50% of active spondylolysis may not be detected with routine planar bone scans75
    (Figure 19). Bone scans should be interpreted in correlation with radiographs and/or CT scans because other
    conditions such as infections, osteoid osteomas, and tumors may also be positive on bone scintigraphy.

    Infection
    After a negative radiograph, a three-phase bone scan is
    considered a good choice for diagnosing osteomyelitis.
    The typical findings of acute osteomyelitis on a bone
    scan are focal increased flow and focal increased uptake of the tracer on the delayed bone scan phase. In
    patients with no prior fracture or hardware, a threephase bone scan is highly accurate for diagnosing osteomyelitis, with a sensitivity and specificity of more
    than 90%.76 Increased bone tracer uptake may be seen
    after a fracture, surgery, or hardware placement. In
    these patients, labeled white blood cell (WBC) scans are
    needed to complement the bone scans for diagnosis of
    osteomyelitis.
    Labeled WBC scans are considered the primary imaging modality for assessing osteomyelitis in trauma
    patients with metallic implants or in patients with pros-

    2011 American Academy of Orthopaedic Surgeons

    thetic joints. WBC scans can be labeled with indium111 (In-111) or Tc-99m. Labeled WBCs do not show
    significant accumulation at surgical sites or fractures in
    the absence of infection. Labeled WBCs, however, accumulate in the bone marrow. Therefore, WBC scans
    need to be complemented with bone marrow scans if
    active marrow distribution is altered as a result of surgery, hardware, or diabetic osteoarthropathy. In osteomyelitis, there is an increased accumulation of labeled
    WBCs, which is incongruent with the bone marrow distribution delineated on Tc-99m sulfur colloid bone
    marrow scans77(Figure 20). The sensitivity and specificity of labeled WBC scans for osteomyelitis in the peripheral skeleton and prosthetic joints is between 83%
    and 89%.78
    Labeled WBC scans are less accurate for diagnosing
    spinal osteomyelitis because of intense uptake of labeled WBCs in normal bone marrow, and possibly because of the reduced delivery of labeled WBCs. Vertebral osteomyelitis may show decreased uptake of
    labeled WBCs (cold vertebra); however, this pattern is
    nonspecific and may also be seen with tumors, infarcts,
    compression fractures, and in Paget disease.77 MRI is
    the modality of choice for imaging spinal infections. If
    MRI cannot be used or is inconclusive, radionuclide
    studies, including gallium-67 and FDG-PET scans, may
    be helpful. The exact mechanism of gallium-67 accumulation in inflammation is not known but appears to
    be related to the increased vascular permeability and
    presence of iron-binding proteins such as lactoferrin
    and siderophores in inflammatory lesions.79 Gallium-67
    is taken up in areas of both bone remodeling and inflammation and may be inconclusive in a substantial
    group of patients.80 Although FDG-PET is primarily
    used in malignancy workup, substantial accumulation
    of FDG is also observed in infections because of increased glucose metabolism in activated neutrophils
    and macrophages.81 Experience using FDG-PET to diagnose infections is limited; however, the available data
    are encouraging, particularly as an alternative imaging

    Orthopaedic Knowledge Update 10

    99

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 20

    Osteomyelitis in a patient with screw fixation for a tibial fracture. A, Bone scan of the ankle shows intense uptake
    in the left distal tibia (arrow). B, Labeled WBC scan shows increased accumulation of labeled WBCs in the left distal tibia (bold arrow) and in the soft tissue superficially (dashed arrow). C, Bone marrow scan of the ankles shows
    symmetric uptake. The radioactive marker (M) indicates the right side. The WBC accumulation in the bone is incongruent with the marrow distribution, which is consistent with osteomyelitis.

    modality in chronic osteomyelitis. In a recent metaanalysis that included four studies with FDG-PET, the
    sensitivity and specificity for diagnosing osteomyelitis
    was 96% and 91%, respectively.82 FDG-PET is promising in diagnosing spinal infections, with a reported sensitivity of 100% and specificity of 88%.78

    Tumors
    Whole-body bone scans are routinely used for surveillance of metastatic bone disease. The typical pattern of
    osseous metastasis is the presence of multiple focal areas of increased tracer uptake predominantly in the axial skeleton. Bone scanning is more sensitive than radiography for detecting metastatic bone disease. A
    notable exception is multiple myeloma, which does not
    induce a significant osteoblastic response and is better
    detected on radiographs. Osteosarcomas and Ewing
    sarcomas show intense tracer uptake on bone scans.
    The primary use of bone scans in osteosarcoma and
    Ewing sarcoma is for initial staging and follow-up of
    the disease. Many benign bone tumors and tumor-like
    lesions may also show intense tracer uptake on bone
    scans. Therefore, bone scans cannot be used to differentiate between benign and malignant lesions. Bone
    scans can be used to screen for polyostotic disease in fibrous dysplasia, enchondroma, and Paget disease. Bone
    scans are also highly sensitive for diagnosing osteoid
    osteoma in patients with chronic pain and negative radiographic results.83
    FDG-PET is increasingly being used in sarcoma
    workups. In a recent study that included 160 soft-tissue
    sarcomas and 52 osseous sarcomas, the sensitivity of
    FDG PET was 94% for detecting soft-tissue sarcomas
    and 95% for osseous sarcomas.84 The sensitivity was
    80% or greater for all histologic types, with false negative lesions seen in synovial sarcoma, liposarcoma,
    chondrosarcoma, and osteosarcomas. High-grade sar100

    Orthopaedic Knowledge Update 10

    Figure 21

    Imaging studies of a patient with gluteal metastatic sarcoma. A, Maximum-projection wholebody image shows normal distribution of FDG
    in the brain, myocardium, liver, spleen, kidneys, bone marrow, and neck muscles. B and C,
    Representative transaxial PET CT images of the
    sarcoma. There is intense uptake of FDG in the
    high-grade left gluteal sarcoma (orange arrow
    in A and B), which also includes areas of decreased uptake in the center of the tumor,
    consistent with central necrosis. There is also a
    focus of increased uptake at the L5 vertebra
    (black arrow in A and C) with an underlying
    small lytic lesion on CT, which is consistent
    with metastasis.

    comas generally have more intense FDG uptake than


    low-grade lesions; however, because of significant overlap, FDG-PET cannot be used to reliably grade sarcomas.85 False-positive PET scans can occur in several benign bone lesions, including giant cell tumors, fibrous

    2011 American Academy of Orthopaedic Surgeons

    Chapter 8: Musculoskeletal Imaging

    1: Principles of Orthopaedics

    Figure 22

    A 10-year-old boy presented with left hip pain of 4 months duration. A, AP radiograph of the pelvis shows sclerosis and thickening of the medial cortex in the left femoral neck (arrow). B, Bone scan with Tc-99m MDP shows
    focal increase in uptake of the radiotracer at the medial aspect of the left femoral neck (arrow). C, Axial CT section through the left femoral neck shows a small lucent nidus surrounded by a sclerotic reaction (arrow). The appearance is characteristic of an osteoid osteoma. D, Axial CT section shows the tip of the RFA needle within the
    nidus.

    dysplasias, eosinophilic granulomas, chondroblastomas, aneurysmal bone cysts, and nonossifying fibromas.86 FDG-PET can be helpful in guiding the biopsy to
    sample the metabolically active part of the tumor.
    FDG-PET CT is highly accurate in staging sarcomas
    (Figure 21). An 88% sensitivity was reported for PET
    CT in nodal staging of 117 patients with sarcoma compared with a 53% sensitivity for conventional imaging,
    which included MRI, chest radiographs, whole-body
    contrast-enhanced CT, and bone scans.87 PET CT was
    also more sensitive for detecting distant metastases,
    with a sensitivity of 92% compared with 65% for conventional imaging.87 These findings were confirmed in a
    multicenter prospective study, which included 46 pediatric patients with osteosarcoma, Ewing sarcoma, or

    2011 American Academy of Orthopaedic Surgeons

    rhabdomyosarcoma.88 The sensitivity of PET is limited


    in diagnosing lung metastases, particularly for lesions
    smaller than 1 cm;89 however, those lesions can be diagnosed on the CT component of the PET CT scan. FDGPET CT was also found to be useful in detecting recurrent metastatic disease after therapy.90
    The use of FDG-PET CT also has been investigated as
    a tool in evaluating the chemotherapy response in patients with sarcomas. In one study, the change in FDG
    uptake between baseline and post therapy PET scans was
    found to be a significantly better predictor for evaluating the response to neoadjuvant therapy than the change
    in lesion size.91 Large multicenter trials are needed to further define the role and criteria for PET in assessing responses to chemotherapy in sarcoma patients.

    Orthopaedic Knowledge Update 10

    101

    Section 1: Principles of Orthopaedics

    Interventional Procedures

    Needle Biopsy

    1: Principles of Orthopaedics

    Percutaneous needle biopsies have been a safe and accurate procedure for more than 70 years. For primary
    bone tumors and soft-tissue sarcomas, a core needle biopsy is preferred over fine-needle aspiration. Core needle biopsy is better for determining the cell type and tumor grade.92 For metastatic lesions and round cell
    sarcomas, fine-needle aspiration can suffice. Currently,
    most bone biopsies are performed with CT guidance,
    whereas soft-tissue tumors are biopsied with ultrasound guidance. In the past decade, CT fluoroscopy
    was introduced to assist in real-time positioning of the
    needle; its value has been documented in thoracic and
    abdominal lesions. Using CT fluoroscopy in the biopsy
    of musculoskeletal lesions achieved similar or better results than conventional CT. However, the high ionizing
    radiation exposure to both the patient and operator are
    an important risk factor in using this technique.
    Recently, MRI-guided percutaneous biopsies for
    musculoskeletal lesions have been attempted.93 Indications include the need to improve the lesion conspicuity
    when it is not well seen by other imaging techniques or
    when the lesion is adjacent to critical structures that are
    better visualized with MRI. The open-configuration
    magnet has been recommended for interventional procedures because it provides better access to the patient.
    Results in one study ranged from very good for bone lesions to moderate and fair for soft-tissue lesions.93
    Three to four biopsy cores are usually sufficient for
    arriving at a pathologic diagnosis. Most biopsies are
    performed under local anesthesia. Less than one third
    of adult patients require conscious sedation. General
    anesthesia is reserved for young children and uncooperative adults. For primary bone tumors, it is recommended that the approach and needle route be discussed with the orthopaedic tumor surgeon. If the
    tumor has a necrotic center, it should be avoided and
    the biopsy cores should be cut from the periphery of
    the lesion. The main drawback of a needle biopsy is the
    possibility of a false-negative result because the accuracy of a negative result can be established only by
    follow-up or by open biopsy. The diagnostic yield is
    higher in lytic than in sclerotic lesions, in larger lesions,
    and in those with increased core length. Nondiagnostic
    cores tend to occur with benign lesion.

    Percutaneous Radiofrequency Ablation for


    Osteoid Osteoma
    Osteoid osteoma accounts for about 12% of all benign
    bone tumors. Although spontaneous resolution has
    been reported, pain may persist for years and patients
    often seek definitive treatment. Over the past decade,
    radiofrequency ablation (RFA) has become the treatment of choice for osteoid osteomas. The technique involves the introduction of an electrode through a biopsy needle into the lesion to heat the abnormal tissue
    and produce cell death. The tip of the electrode is
    heated to approximately 90C for 4 minutes. Most of
    102

    Orthopaedic Knowledge Update 10

    the experience with RFA is in the lower extremity


    where most osteoid osteomas occur (Figure 22). Lesions that do not allow a safe distance between the electrode tip and a major neurovascular structure may require surgical excision. This is true for the spine, hand,
    and carpus. However, some investigators have found
    RFA for spinal lesions to be safe and effective.94 The
    cost of RFA is estimated to be approximately 25% of
    the cost of open surgery.

    Summary
    Current imaging techniques and the indications for various orthopaedic conditions have been discussed along
    with characteristic imaging features. Working knowledge of imaging studies is important for orthopaedic
    surgeons to provide quality patient care.

    Annotated References
    1.

    Williams MB, Krupinski EA, Strauss KJ, et al: Digital


    radiography image quality: Image acquisition. J Am
    Coll Radiol 2007;4(6):371-388.
    The authors describe current technologies of digital radiography compared with conventional screen-film systems. Image acquisition to establish image quality standards is discussed.

    2.

    Krupinski EA, Williams MB, Andriole K, et al; ACR;


    AAPM; Society for Imaging Informatics in Medicine:
    Digital radiography image quality: Image processing
    and display. J Am Coll Radiol 2007;4(6):389-400.
    The authors describe current technologies of digital radiography to provide high-quality radiologic care. Image processing and display are discussed. The management of data may have a great impact on the quality of
    patient care.

    3.

    Hanson JA, Blackmore CC, Mann FA, Wilson AJ: Cervical spine injury: A clinical decision rule to identify
    high-risk patients for helical CT screening. AJR Am J
    Roentgenol 2000;174(3):713-717.

    4.

    Daffner RH: Helical CT of the cervical spine for trauma


    patients: A time study. AJR Am J Roentgenol 2001;
    177(3):677-679.

    5.

    Woodring JH, Lee C: Limitations of cervical radiography in the evaluation of acute cervical trauma.
    J Trauma 1993;34(1):32-39.

    6.

    Blackmore CC, Ramsey SD, Mann FA, Deyo RA: Cervical spine screening with CT in trauma patients: A
    cost-effectiveness analysis. Radiology 1999;212(1):117125.

    7.

    Lomoschitz FM, Blackmore CC, Mirza SK, Mann FA:


    Cervical spine injuries in patients 65 years old and older: Epidemiologic analysis regarding the effects of age

    2011 American Academy of Orthopaedic Surgeons

    Chapter 8: Musculoskeletal Imaging

    tional injuries for all study patients. Level of evidence:


    II.

    and injury mechanism on distribution, type, and stability of injuries. AJR Am J Roentgenol 2002;178(3):573577.
    8.

    9.

    Wintermark M, Mouhsine E, Theumann N, et al: Thoracolumbar spine fractures in patients who have sustained severe trauma: Depiction with multi-detector row
    CT. Radiology 2003;227(3):681-689.

    17.

    Jacobson JA, Girish G, Jiang Y, Resnick D: Radiographic evaluation of arthritis: Inflammatory conditions. Radiology 2008;248(2):378-389.
    The authors review the radiographic features of several
    types of arthritis emphasizing the radiographic differentials in inflammatory conditions.

    Roos JE, Hilfiker P, Platz A, et al: MDCT in emergency


    radiology: Is a standardized chest or abdominal protocol sufficient for evaluation of thoracic and lumbar
    spine trauma? AJR Am J Roentgenol 2004;183(4):959968.

    18.

    Hayashi M, Matsunaga T, Tanikawa H: Idiopathic


    widespread calcium pyrophosphate dihydrate crystal deposition disease in a young patient. Skeletal Radiol
    2002;31(4):246-250.

    Ptak T, Rhea JT, Novelline RA: Radiation dose is reduced with a single-pass whole-body multi-detector row
    CT trauma protocol compared with a conventional segmented method: Initial experience. Radiology 2003;
    229(3):902-905.

    19.

    Fanucci E, Fiaschetti V, Rotili A, Floris R, Simonetti G:


    Whole body 16-row multislice CT in emergency room:
    Effects of different protocols on scanning time, image
    quality and radiation exposure. Emerg Radiol 2007;
    13(5):251-257.
    For multitrauma patients, whole-body, single-pass CT
    protocol in 26 patients was compared with conventional
    segmented protocol in 20 patients to define scanning
    time, image quality, and radiation dose. The whole-body
    protocol showed a reduced total radiation dose with no
    relevant loss of diagnostic image quality.

    20.

    Leone A, Cerase A, Priolo F, Marano P: Lumbosacral


    junction injury associated with unstable pelvic fracture:
    Classification and diagnosis. Radiology 1997;205(1):
    253-259.

    21.

    Gansslen A, Pohlemann T, Paul C, Lobenhoffer P, Tscherne H: Epidemiology of pelvic ring injuries. Injury
    1996;27(suppl 1):S-A13-S-A20.

    22.

    Tibbs BM, Kopar P, Dente CJ, Rozycki GS, Feliciano


    DV: Acetabular and isolated pelvic ring fractures: A
    comparison of initial assessment and outcome. Am Surg
    2008;74(6):538-541.
    The authors retrospectively reviewed and compared the
    outcomes among the patients with acetabular and pelvic
    ring fractures (1,334 patients with 320 acetabular, 826
    pelvic ring, and 188 combination fractures). Level of evidence: II.

    23.

    Ohashi K, El-Khoury GY, Abu-Zahra KW, Berbaum


    KS: Interobserver agreement for Letournel acetabular
    fracture classification with multidetector CT: Are standard Judet radiographs necessary? Radiology 2006;
    241(2):386-391.

    24.

    Dorsay TA, Major NM, Helms CA: Cost-effectiveness


    of immediate MR imaging versus traditional follow-up
    for revealing radiographically occult scaphoid fractures.
    AJR Am J Roentgenol 2001;177(6):1257-1263.

    11.

    Thomas J, Rideau AM, Paulson EK, Bisset GS III: Emergency department imaging: Current practice. J Am Coll
    Radiol 2008;5(7):811-816, e2.
    A snapshot of the demographics of current imaging
    practices in emergency departments in the United States
    is presented. The study is based on the responses to an
    e-mail survey from 192 (28%) of contacted radiology
    groups.

    12.

    Whang PG, Goldberg G, Lawrence JP, et al: The management of spinal injuries in patients with ankylosing
    spondylitis or diffuse idiopathic skeletal hyperostosis: A
    comparison of treatment methods and clinical outcomes. J Spinal Disord Tech 2009;22(2):77-85.
    A retrospective review of 12 patients with ankylosing
    spondylitis and 18 patients with diffuse idiopathic skeletal hyperostosis reported complete neurologic deficits
    in 41% of patients with ankylosing spondylitis and
    28% of those with hyperostosis. Level of evidence: III.

    13.

    Chiu WC, Haan JM, Cushing BM, Kramer ME, Scalea


    TM: Ligamentous injuries of the cervical spine in unreliable blunt trauma patients: Incidence, evaluation, and
    outcome. J Trauma 2001;50(3):457-463, discussion
    464.

    14.

    Hogan GJ, Mirvis SE, Shanmuganathan K, Scalea TM:


    Exclusion of unstable cervical spine injury in obtunded
    patients with blunt trauma: Is MR imaging needed
    when multi-detector row CT findings are normal? Radiology 2005;237(1):106-113.

    15.

    Harris TJ, Blackmore CC, Mirza SK, Jurkovich GJ:


    Clearing the cervical spine in obtunded patients. Spine
    (Phila Pa 1976) 2008;33(14):1547-1553.
    Based on this retrospective cohort study of 367 obtunded patients, initial cervical CT failed to identify an
    injury in one patient, resulting in a false-negative rate of
    0.3%. The upright radiographs did not show any addi-

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    10.

    16.
    Jacobson JA, Girish G, Jiang Y, Sabb BJ: Radiographic
    evaluation of arthritis: Degenerative joint disease and
    variations. Radiology 2008;248(3):737-747.
    The authors review radiographic features of several
    types of arthritis emphasizing the radiographic differentials in degenerative joint disease and its variations.

    25. Groves AM, Kayani I, Syed R, et al: An international

    Orthopaedic Knowledge Update 10

    103

    Section 1: Principles of Orthopaedics

    26.

    27.

    1: Principles of Orthopaedics

    28.

    37.

    Macarini L, Murrone M, Marini S, Calbi R, Solarino


    M, Moretti B: Tibial plateau fractures: Evaluation with
    multidetector-CT. Radiol Med 2004;108(5-6):503-514.

    Tiel-van Buul MM, van Beek EJ, Broekhuizen AH, Bakker AJ, Bos KE, van Royen EA: Radiography and scintigraphy of suspected scaphoid fracture: A long-term
    study in 160 patients. J Bone Joint Surg Br 1993;75(1):
    61-65.

    38.

    Haraguchi N, Haruyama H, Toga H, Kato F: Pathoanatomy of posterior malleolar fractures of the ankle.
    J Bone Joint Surg Am 2006;88(5):1085-1092.

    39.

    Sanders R, Gregory P: Operative treatment of intraarticular fractures of the calcaneus. Orthop Clin North
    Am 1995;26(2):203-214.

    40.

    Prasartritha T, Sethavanitch C: Three-dimensional and


    two-dimensional computerized tomographic demonstration of calcaneus fractures. Foot Ankle Int 2004;25(4):
    262-273.

    41.

    Ohashi K, Restrepo JM, El-Khoury GY, Berbaum KS:


    Peroneal tendon subluxation and dislocation: Detection
    on volume-rendered images. Initial experience. Radiology 2007;242(1):252-257.
    A preliminary study consisting of 32 patients with acute
    calcaneal fractures showed that viewing threedimensional volume-rendered images is more timeefficient compared with reviewing multiplanar reformatted images for detecting peroneal tendon dislocation.
    Level of evidence: III.

    42.

    Calhoun PS, Kuszyk BS, Heath DG, Carley JC, Fishman


    EK: Three-dimensional volume rendering of spiral CT
    data: Theory and method. Radiographics 1999;19(3):
    745-764.

    43.

    White LM, Buckwalter KA: Technical considerations:


    CT and MR imaging in the postoperative orthopedic
    patient. Semin Musculoskelet Radiol 2002;6(1):5-17.

    44.

    Farber GL, Place HM, Mazur RA, Jones DE, Damiano


    TR: Accuracy of pedicle screw placement in lumbar fusions by plain radiographs and computed tomography.
    Spine (Phila Pa 1976) 1995;20(13):1494-1499.

    Tiel-van Buul MM, Broekhuizen TH, van Beek EJ,


    Bossuyt PM: Choosing a strategy for the diagnostic
    management of suspected scaphoid fracture: A costeffectiveness analysis. J Nucl Med 1995;36(1):45-48.
    Gaebler C, Kukla C, Breitenseher M, Trattnig S, Mittlboeck M, Vcsei V: Magnetic resonance imaging of occult scaphoid fractures. J Trauma 1996;41(1):73-76.

    29.

    Breitenseher MJ, Metz VM, Gilula LA, et al: Radiographically occult scaphoid fractures: Value of MR imaging in detection. Radiology 1997;203(1):245-250.

    30.

    Herneth AM, Siegmeth A, Bader TR, et al: Scaphoid


    fractures: Evaluation with high-spatial-resolution US
    initial results. Radiology 2001;220(1):231-235.

    31.

    Welling RD, Jacobson JA, Jamadar DA, Chong S, Caoili


    EM, Jebson PJ: MDCT and radiography of wrist fractures: Radiographic sensitivity and fracture patterns.
    AJR Am J Roentgenol 2008;190(1):10-16.
    Radiographic and CT studies of 103 consecutive patients who were suspected of having wrist fractures were
    reviewed in this retrospective study. Thirty percent of
    wrist fractures were not prospectively diagnosed on radiography. Level of evidence: II.

    32.

    Tiel-van Buul MM, van Beek EJ, Dijkstra PF, Bakker


    AJ, Broekhuizen TH, van Royen EA: Significance of a
    hot spot on the bone scan after carpal injury: Evaluation by computed tomography. Eur J Nucl Med 1993;
    20(2):159-164.

    45.
    33.

    Groves AM, Cheow H, Balan K, Courtney H, Bearcroft


    P, Dixon A: 16-MDCT in the detection of occult wrist
    fractures: A comparison with skeletal scintigraphy. AJR
    Am J Roentgenol 2005;184(5):1470-1474.

    Linsenmaier U, Rock C, Euler E, et al: Threedimensional CT with a modified C-arm image intensifier: Feasibility. Radiology 2002;224(1):286-292.

    46.

    Chan PS, Klimkiewicz JJ, Luchetti WT, et al: Impact of


    CT scan on treatment plan and fracture classification of
    tibial plateau fractures. J Orthop Trauma 1997;11(7):
    484-489.

    Krestan CR, Noske H, Vasilevska V, et al: MDCT versus digital radiography in the evaluation of bone healing
    in orthopedic patients. AJR Am J Roentgenol 2006;
    186(6):1754-1760.

    47.

    Dorsey ML, Liu PT, Roberts CC, Kile TA: Correlation


    of arthrodesis stability with degree of joint fusion on
    MDCT. AJR Am J Roentgenol 2009;192(2):496-499.
    The authors of this study, based on the retrospective review of 42 consecutive CT studies from 29 patients, reported that ankle or subtalar fusion is likely stable if
    more than 33% of the joint has bone fusion on sagittal
    CT images. Level of evidence: III.

    48.

    Shah RR, Mohammed S, Saifuddin A, Taylor BA: Comparison of plain radiographs with CT scan to evaluate
    interbody fusion following the use of titanium interbody

    34.

    104

    survey of hospital practice in the imaging of acute scaphoid trauma. AJR Am J Roentgenol 2006;187(6):
    1453-1456.

    35.

    Liow RY, Birdsall PD, Mucci B, Greiss ME: Spiral computed tomography with two- and three-dimensional reconstruction in the management of tibial plateau fractures. Orthopedics 1999;22(10):929-932.

    36.

    Wicky S, Blaser PF, Blanc CH, Leyvraz PF, Schnyder P,


    Meuli RA: Comparison between standard radiography
    and spiral CT with 3D reconstruction in the evaluation,
    classification and management of tibial plateau fractures. Eur Radiol 2000;10(8):1227-1232.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 8: Musculoskeletal Imaging

    with renal failure and the development of nephrogenic


    systemic fibrosis.

    cages and transpedicular instrumentation. Eur Spine J


    2003;12(4):378-385.
    Fehring TK, McAvoy G: Fluoroscopic evaluation of the
    painful total knee arthroplasty. Clin Orthop Relat Res
    1996;331:226-233.

    50.

    Chiang PP, Burke DW, Freiberg AA, Rubash HE: Osteolysis of the pelvis: Evaluation and treatment. Clin
    Orthop Relat Res 2003;417:164-174.

    51.

    Berry DJ: Recognizing and identifying osteolysis around


    total knee arthroplasty. Instr Course Lect 2004;53:261264.

    52.

    Claus AM, Totterman SM, Sychterz CJ, Tamez-Pea JG,


    Looney RJ, Engh CA Sr: Computed tomography to assess pelvic lysis after total hip replacement. Clin Orthop
    Relat Res 2004;422:167-174.

    53.

    Jazrawi LM, Birdzell L, Kummer FJ, Di Cesare PE: The


    accuracy of computed tomography for determining femoral and tibial total knee arthroplasty component rotation. J Arthroplasty 2000;15(6):761-766.

    54.

    Scuderi GR, Komistek RD, Dennis DA, Insall JN: The


    impact of femoral component rotational alignment on
    condylar lift-off. Clin Orthop Relat Res 2003;410:148154.

    55.

    Ohashi K, El-Khoury GY, Bennett DL, Restrepo JM,


    Berbaum KS: Orthopedic hardware complications diagnosed with multi-detector row CT. Radiology 2005;
    237(2):570-577.

    56.

    Olsen RV, Munk PL, Lee MJ, et al: Metal artifact reduction sequence: Early clinical applications. Radiographics 2000;20(3):699-712.

    57.

    Ruzal-Shapiro C, Berdon WE, Cohen MD, Abramson


    SJ: MR imaging of diffuse bone marrow replacement in
    pediatric patients with cancer. Radiology 1991;181(2):
    587-589.

    58.

    59.

    60.

    Carmody RF, Yang PJ, Seeley GW, Seeger JF, Unger EC,
    Johnson JE: Spinal cord compression due to metastatic
    disease: Diagnosis with MR imaging versus myelography. Radiology 1989;173(1):225-229.
    Murphy BJ: Evaluation of grades 3 and 4 chondromalacia of the knee using T2-weighted 3D gradient-echo articular cartilage imaging. Skeletal Radiol 2001;30(6):
    305-311.
    Wiginton CD, Kelly B, Oto A, et al: Gadolinium-based
    contrast exposure, nephrogenic systemic fibrosis, and
    gadolinium detection in tissue. AJR Am J Roentgenol
    2008;190(4):1060-1068.
    A retrospective review of seven patients with nephrogenic systemic fibrosis showed that symptoms of the
    condition developed in all of the patients after receiving
    gadolinium and all had renal failure. The authors found
    an association between the use of gadolinium in patients

    2011 American Academy of Orthopaedic Surgeons

    61.

    Goncalves-Matoso V, Guntern D, Gray A, Schnyder P,


    Picht C, Theumann N: Optimal 3-T MRI for depiction
    of the finger A2 pulley: Comparison between T1weighted, fat-saturated T2-weighted and gadoliniumenhanced fat-saturated T1-weighted sequences. Skeletal
    Radiol 2008;37(4):307-312.
    The authors used a 3.0-T magnet with three different
    spin-echo sequences to study the visualization of normal
    and abnormal finger A2 pulley. They found that transverse
    fat-saturated
    T1-weighted
    gadoliniumenhancement sequences are best for depicting an abnormal A2 pulley.

    62.

    Magee T: Can isotropic fast gradient echo imaging be


    substituted for conventional T1 weighted sequences in
    shoulder MR arthrography at 3 Tesla? J Magn Reson
    Imaging 2007;26(1):118-122.
    The author presents the results of a retrospective review
    of 100 consecutive shoulder MR arthrograms studied by
    standard T1-weighted spin-echo sequences and by isotropic gradient-echo imaging using 0.4-mm thin sections. The author found that isotropic imaging provides
    the same clinical information as conventional imaging
    and can be acquired in less than 3 minutes.

    63.

    Gold GE, Busse RF, Beehler C, et al: Isotropic MRI of


    the knee with 3D fast spin-echo extended echo-train acquisition (XETA): Initial experience. AJR Am J Roentgenol 2007;188(5):1287-1293.
    In this prospective study, the authors compared isotropic three-dimensional fast spin-echo extended echo-train
    acquisition with two-dimensional fast spin-echo and
    two-dimensional fast recovery fast spin-echo for MRI of
    the knee. The authors reported that the threedimensional fast spin-echo extended echo-train acquisition method acquires high-resolution isotropic data with
    intermediate- and T2-weighting that may be reformatted in arbitrary planes.

    64.

    Haramati N, Staron RB, Barax C, Feldman F: Magnetic


    resonance imaging of occult fractures of the proximal
    femur. Skeletal Radiol 1994;23(1):19-22.

    65.

    Nikken JJ, Oei EH, Ginai AZ, et al: Acute wrist trauma:
    Value of a short dedicated extremity MR imaging examination in prediction of need for treatment. Radiology
    2005;234(1):116-124.

    66.

    Menaker J, Philp A, Boswell S, Scalea TM: Computed


    tomography alone for cervical spine clearance in the unreliable patient: Are we there yet? J Trauma 2008;64(4):
    898-903, discussion 903-904.
    The authors report on a retrospective review of patients
    with blunt trauma who had cervical spine imaging with
    CT and MRI in the acute phase. Newer generation CT
    missed cervical spine injuries in unreliable patients. MRI
    findings changed treatment in 7.9% of patients. Two
    patients required surgical repair. The authors recommend using MRI for clearing the cervical spine in unreliable patients.

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    49.

    105

    Section 1: Principles of Orthopaedics

    67.

    1: Principles of Orthopaedics

    68.

    69.

    106

    Tomycz ND, Chew BG, Chang YF, et al: MRI is unnecessary to clear the cervical spine in obtunded/comatose
    trauma patients: The four-year experience of a level I
    trauma center. J Trauma 2008;64(5):1258-1263.
    The authors report on a retrospective review of 180
    trauma patients who had a normal CT examination on
    admission along with a cervical spine MRI. In 38 patients (21.1%), the MRI showed acute traumatic findings; however, surgery was not needed and delayed instability did not develop. The authors concluded that
    MRI is unlikely to detect unstable cervical spine injuries
    when the CT examination is normal.
    Yucesoy K, Yuksel KZ: SCIWORA in MRI era. Clin
    Neurol Neurosurg 2008;110(5):429-433.
    A literature review was undertaken to investigate
    whether the meaning of SCIWORA had changed after
    the advent of MRI. The authors found that SCIWORA
    had an ambiguous meaning in the literature. They recommended that spines with MRI abnormalities, with or
    without radiographic abnormalities, should not be classified as SCIWORA.
    Pang D: Spinal cord injury without radiographic abnormality in children, 2 decades later. Neurosurgery 2004;
    55(6):1325-1342, discussion 1342-1343.

    70.

    Holder LE, Schwarz C, Wernicke PG, Michael RH: Radionuclide bone imaging in the early detection of fractures of the proximal femur (hip): Multifactorial analysis. Radiology 1990;174(2):509-515.

    71.

    Matin P: The appearance of bone scans following fractures, including immediate and long-term studies.
    J Nucl Med 1979;20(12):1227-1231.

    Nucl Med Commun 2006;27(8):633-644.


    79.

    Love C, Palestro CJ: Radionuclide imaging of infection.


    J Nucl Med Technol 2004;32(2):47-57, quiz 58-59.

    80.

    Schauwecker DS, Park HM, Mock BH, et al: Evaluation


    of complicating osteomyelitis with Tc-99m MDP, In111 granulocytes, and Ga-67 citrate. J Nucl Med 1984;
    25(8):849-853.

    81.

    Kaim AH, Weber B, Kurrer MO, Gottschalk J, Von


    Schulthess GK, Buck A: Autoradiographic quantification of 18F-FDG uptake in experimental soft-tissue abscesses in rats. Radiology 2002;223(2):446-451.

    82.

    Termaat MF, Raijmakers PG, Scholten HJ, Bakker FC,


    Patka P, Haarman HJ: The accuracy of diagnostic imaging for the assessment of chronic osteomyelitis: A systematic review and meta-analysis. J Bone Joint Surg Am
    2005;87(11):2464-2471.

    83.

    Lisbona R, Rosenthall L: Role of radionuclide imaging


    in osteoid osteoma. AJR Am J Roentgenol 1979;132(1):
    77-80.

    84.

    Charest M, Hickeson M, Lisbona R, Novales-Diaz JA,


    Derbekyan V, Turcotte RE: FDG PET/CT imaging in
    primary osseous and soft tissue sarcomas: A retrospective review of 212 cases. Eur J Nucl Med Mol Imaging
    2009;Jul 11:[Epub ahead of print].
    This large study evaluates the sensitivity of FDG-PET
    for detecting osseous and soft-tissue sarcomas with different histologies.

    85.

    Folpe AL, Lyles RH, Sprouse JT, Conrad EU III, Eary


    JF: (F-18) fluorodeoxyglucose positron emission tomography as a predictor of pathologic grade and other
    prognostic variables in bone and soft tissue sarcoma.
    Clin Cancer Res 2000;6(4):1279-1287.

    72.

    Zwas ST, Elkanovitch R, Frank G: Interpretation and


    classification of bone scintigraphic findings in stress
    fractures. J Nucl Med 1987;28(4):452-457.

    73.

    Minoves M: Bone and joint sports injuries: The role of


    bone scintigraphy. Nucl Med Commun 2003;24(1):310.

    86.

    Schulte M, Brecht-Krauss D, Heymer B, et al: Grading


    of tumors and tumorlike lesions of bone: Evaluation by
    FDG PET. J Nucl Med 2000;41(10):1695-1701.

    74.

    Raby N, Mathews S: Symptomatic spondylolysis: Correlation of CT and SPECT with clinical outcome. Clin
    Radiol 1993;48(2):97-99.

    87.

    75.

    Bellah RD, Summerville DA, Treves ST, Micheli LJ:


    Low-back pain in adolescent athletes: Detection of
    stress injury to the pars interarticularis with SPECT. Radiology 1991;180(2):509-512.

    Tateishi U, Yamaguchi U, Seki K, Terauchi T, Arai Y,


    Kim EE: Bone and soft-tissue sarcoma: Preoperative
    staging with fluorine 18 fluorodeoxyglucose PET/CT
    and conventional imaging. Radiology 2007;245(3):839847.
    This retrospective study compares PET-CT with CT,
    MRI, and bone scans in staging osseous and soft-tissue
    sarcomas.

    76.

    Maurer AH, Chen DC, Camargo EE, Wong DF, Wagner


    HN Jr, Alderson PO: Utility of three-phase skeletal scintigraphy in suspected osteomyelitis: Concise communication. J Nucl Med 1981;22(11):941-949.

    88.

    Vlker T, Denecke T, Steffen I, et al: Positron emission


    tomography for staging of pediatric sarcoma patients:
    Results of a prospective multicenter trial. J Clin Oncol
    2007;25(34):5435-5441.
    This prospective study evaluates the role of FDG-PET
    CT and its added value to conventional imaging in staging pediatric sarcomas.

    89.

    Franzius C, Daldrup-Link HE, Sciuk J, et al: FDG-PET

    77.

    Palestro CJ, Torres MA: Radionuclide imaging in orthopedic infections. Semin Nucl Med 1997;27(4):334-345.

    78.

    Prandini N, Lazzeri E, Rossi B, Erba P, Parisella MG,


    Signore A: Nuclear medicine imaging of bone infections.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 8: Musculoskeletal Imaging

    The authors present an overview of approaches to bone


    biopsies intended to minimize potential tumor seeding
    into the soft tissues. They also discuss safe approaches
    related to specific anatomic parts.

    for detection of pulmonary metastases from malignant


    primary bone tumors: Comparison with spiral CT. Ann
    Oncol 2001;12(4):479-486.
    90.

    91.

    Evilevitch V, Weber WA, Tap WD, et al: Reduction of


    glucose metabolic activity is more accurate than change
    in size at predicting histopathologic response to neoadjuvant therapy in high-grade soft-tissue sarcomas. Clin
    Cancer Res 2008;14(3):715-720.
    The authors compare the change of FDG uptake (measured in standarized uptake value) with the change in
    tumor size in predicting the response of sarcomas to
    chemotherapy.
    Espinosa LA, Jamadar DA, Jacobson JA, et al: CTguided biopsy of bone: A radiologists perspective. AJR
    Am J Roentgenol 2008;190(5):W283-W289.

    2011 American Academy of Orthopaedic Surgeons

    93.

    Carrino JA, Khurana B, Ready JE, Silverman SG, Winalski CS: Magnetic resonance imaging-guided percutaneous biopsy of musculoskeletal lesions. J Bone Joint
    Surg Am 2007;89(10):2179-2187.
    In a retrospective case series of 45 biopsies performed
    with magnetic resonance guidance, the authors reported
    very good results for bone lesions, moderate results for
    extra-articular soft-tissue lesions, and fair results for
    intra-articular soft-tissue lesions.

    94.

    Vanderschueren GM, Obermann WR, Dijkstra SP,


    Taminiau AH, Bloem JL, van Erkel AR: Radiofrequency
    ablation of spinal osteoid osteoma: Clinical outcome.
    Spine (Phila Pa 1976) 2009;34(9):901-904.
    The authors present the findings of a prospective study
    of 24 patients with spinal osteoid osteoma treated with
    RFA. The authors concluded that RFA is a safe and effective treatment for spinal osteoid osteoma. Surgery
    should be reserved for lesions causing nerve root compression.

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    92.

    Arush MW, Israel O, Postovsky S, et al: Positron emission tomography/computed tomography with 18fluorodeoxyglucose in the detection of local recurrence and
    distant metastases of pediatric sarcoma. Pediatr Blood
    Cancer 2007;49(7):901-905.
    The authors report on the role of FDG-PET CT in evaluating local recurrence at the primary site and distant
    disease in children with sarcoma.

    107

    Chapter 9

    Patient-Centered Care:
    Communication Skills and Cultural
    Competence
    John R. Tongue, MD

    Norman Y. Otsuka, MD

    The concept of patient-centered care compels physicians to treat patients as partners, involving them in decision making and enlisting a sense of self-responsibility
    for their care, while respecting their individual values
    and concerns.1 Specifically, this process includes striving to maintain eye contact; leaning forward; remaining
    physically calm; avoiding jargon and interruptions; validating the patients emotions; learning about the patients lifestyle; checking for understanding; and offering support.2 Effective communication skills allow for
    more accurate diagnoses, better adherence to treatment
    plans, decreased medical liability, and better patient
    outcomes.1
    Orthopaedic surgeons have tended to focus primarily on the technical aspects of caregiving;3,4 however,
    there is a need to improve communication skills as well
    as surgical skills. Good interviewing skills allow a surgeon to assess the level of a patients understanding and
    permit successful engagement to meet the patients expectations. The challenges of effective communication
    are driven by the increasing complexity of health care,
    the shifting demands of health care reform, and the
    progressively diversifying patient language and cultural
    barriers. To provide culturally competent care, orthopaedic surgeons must do their best to understand each
    patients cultural background, belief systems, and perception of their illness.
    Patient-centered care also requires knowledge of the

    Dr. Tongue or an immediate family member serves as a


    board member, owner, officer, or committee member of
    the Western Orthopaedic Association. Dr. Otsuka or an
    immediate family member serves as a board member,
    owner, officer, or committee member of the American
    Academy of Orthopaedic Surgeons, California Orthopaedic Association, and Pediatric Orthopaedic Society of
    North America; and has received research or institutional support from the National Institutes of Health
    and Shriners Hospitals for Children.

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    Introduction

    patients experiences and lifestyle, which then allows


    blending of these factors with the biomedical elements
    of patient care. This psychosocial information is best
    obtained with an interviewing style that actively seeks
    the patients input, and is facilitated through openended questions, expressions of concern, checks for understanding, and requests for opinions and expectations. The result is a more effective medical
    intervention, resulting in both increased patient and
    physician satisfaction.5 Nearly 70% of the variance in
    patient satisfaction scores has been attributed to communication, including nonverbal communication, attitude, information giving, and the style of decision making.6
    There is increasing interest and regard for the process of informed consent. Physicians are concerned
    about their ability to effectively complete the requirements of informed consent while efficiently managing
    their time. Surgeons who do well at fostering informed
    consent do not have substantially longer patient interviews than their colleagues.7 Recent court rulings set a
    high standard for achieving informed consent, and have
    stated that it ... is a health care providers duty to
    communicate information to enable a patient to make
    an intelligent and informed choice and that the law
    does not allow a physician to substitute his judgment
    for that of the patient.8 An open, patient-centered, interview approach can achieve timely informed patient
    consent, meeting both medical and legal standards,
    while uncovering relevant information that may otherwise be withheld by the patient.9
    Medical students are often drawn to careers in orthopaedic surgery because of their attraction to biomedical technology and scientific method. Medical
    school studies of the doctor-patient relationship are
    sometimes dismissed as an unscientific and low priority.
    There is often a striking decline in the attitudes of medical students toward the emotional and interpersonal
    dimensions of patient care as they seek to apply an
    overwhelming array of hard science. In this stressful
    environment, avoiding emotional situations with patients and the need to comfort them are common coping mechanisms. Emotional encounters with patients

    Orthopaedic Knowledge Update 10

    109

    Section 1: Principles of Orthopaedics

    Table 1

    Interpersonal Skills Evaluation by Consumers and Orthopaedic Surgeonsa

    1: Principles of Orthopaedics

    Highly trained

    Skills Important to Consumers


    (2008)

    Skills That Orthopaedic Surgeons


    Believe Are Important to Patients (2008)

    82%

    71%

    Listens

    83%

    53%

    Successful results

    84%

    89%

    Caring/compassionate

    74%

    55%

    Spends time with patient

    74%

    39%

    Value/cost

    73%

    44%

    Easy appointment scheduling

    65%

    24%

    Orthopaedic surgeons undervalue the interpersonal skills of listening, demonstrating compassion, and spending time with patients compared with patients ratings of these
    characteristics. Questions were developed on a scale from 1 to 5, with a higher number representing an increasing level of favorability. In analyzing this type of question, it
    is customary to combine 4 and 5 rating responses as a strong measure of agreement or performance and are valid at approximately 3.5% at a 95% confidence level. The
    table information is based on an AAOS 2008 Tracking Survey.12

    are often viewed as onerous and time consuming.


    When teachers exhibit dehumanizing patterns of communication, students imitate these patterns of dealing
    with patients.10 This hidden curriculum may also be evident as attending surgeons and senior residents are observed dealing with patients from multicultural backgrounds, with those observed interactions having a
    significant impact on how younger residents will relate
    to patients when they have their own practices.11

    Background
    Most practicing orthopaedic surgeons receive limited
    formal education in the communication skills necessary
    for patient-centered care; however, a substantial
    amount of time is spent talking with patients (approximately 160,000 interviews during a typical career).1
    Comparable surveys in 1998 and 2008 by the American Academy of Orthopaedic Surgeons (AAOS)
    showed that surgeons continue to believe that they
    have high technical and high interpersonal skills. However, orthopaedic surgeons also continue to view their
    colleagues as having much lower communication skills.
    The public believes that orthopaedic surgeons have low
    communication skills.12 Also, both surveys strongly indicate that orthopaedic surgeons do not value interpersonal skills as strongly as the public views such skills
    (Table 1).
    The AAOS 2008 Tracking Survey highlights the variance among the consumers stated beliefs on the importance of physician rating factors and the surgeons selfperceptions of their performance.12 Consumers
    favorably rate orthopaedic surgeons on successful medical results, which is the most important factor. However, the interpersonal skills of listening, demonstrating
    compassion, and spending time with patients also rank
    very high with patients but much lower with orthopaedic surgeons.
    110

    Orthopaedic Knowledge Update 10

    The most common deficiency in daily interviews


    with patients is the consistent failure of the orthopaedic
    surgeons to offer empathic responses.13 Social science
    research clearly indicates that doctors trained in empathy can improve their ability to make eye contact, appear more attentive, reflect understanding, and express
    feelings that encourage patients to talk openly.14
    Another challenge for surgeons is to complete effective, informed decision-making interviews within the
    time constraints of a busy office practice. A concern,
    which is often raised, is that proposed models of excellent communication may not be feasible in the timepressured setting of an orthopaedic surgeons practice.
    Research, however, indicates that a few additional minutes during an initial patient visit saves time later, while
    developing mutual trust, understanding, and satisfaction.14
    Among surgical specialty physician groups, orthopaedic surgeons have been reported to be both more
    satisfied and more dissatisfied than any other specialty
    groups, indicating a divided workforce.15 Possible explanations include variance in the ability to cope with
    losses in income and autonomy, the constraints of managed care, and differing communication skill sets for
    both residents and practicing orthopaedic surgeons. A
    recent report by the American Orthopaedic Association
    states, Residents reported a significant burnout, showing a high level of emotional exhaustion and depersonalization. The report adds, ... excellent communication skills contribute to effective prevention stress
    management, and that ... preventive stress management skills help avert burnout, emotional exhaustion,
    and even surgical errors.16
    Skilled medical interviews also reduce the risk of
    lawsuits. The burden of the protracted legal process involved in defending a malpractice suit adds considerable stress to the day-to-day practice of orthopaedic
    surgery. Malpractice lawsuits are frequently initiated
    because of a difference in expectations between the

    2011 American Academy of Orthopaedic Surgeons

    Chapter 9: Patient-Centered Care: Communication Skills and Cultural Competence

    Figure 2

    Most medical liability lawsuits result from communication problems in the doctor-patient relationship. A 1994 study showed that 71% of patients sue because of communication problems.
    The number at the top of the bars represents
    the percentage of patients who answered questions affirmatively. The numbers on the Y axis
    represent the percentage of patients in the
    study who sued. (Reproduced with permission
    from Beckman HB, Markakis KM, Suchman AL,
    Frankel RM: The doctor-patient relationship and
    malpractice: Lessons from plaintiff depositions.
    Arch Intern Med 1994;154(12):1365-1370.)

    physician and the patient. The tipping point for most


    medical liability suits in the United States has been attributed primarily to breakdowns in communication.
    Better communication reduces potential misunderstandings and unmet expectations17 (Figure 1).
    Good patient interviews have been shown to foster
    stronger patient-physician relationships while gathering
    superior qualitative and quantitative information that
    improves diagnostic accuracy, reduces medical errors,
    improves patient outcomes, and makes the practice of
    orthopaedic surgery less stressful and more enjoyable.1

    1: Principles of Orthopaedics

    Figure 1

    Illustration of the 4Es of complete clinical care,


    which represent a model for physician-patient
    communication. (Reproduced with permission
    from Tongue JR, Epps HR, Forese LL: Communication skills for patient-centered care: Researchbased, easily learned techniques for medical interviews that benefit orthopaedic surgeons and
    their patients. J Bone Joint Surg Am
    2005;87:652-658.)

    doctor who smiles; maintains eye contact; has a relaxed


    body posture; speaks with a calm consistent tone of
    voice; and sits, leaning forward with arms opened.
    Open-ended questions allow patients to tell their story
    and avoid possible false assumptions regarding the patients agenda.19,20 For example, the physician can begin
    with, How can I help you today? The question
    should be spoken with a combination of a smile, calm
    voice, handshake, and eye contact. By contrast, asking
    a vulnerable patient, How ya doing today? can create conflict for patients who feel compelled to answer
    fine to this typical American greeting, just before explaining why they have come to see a doctor. Unfortunately, doctors interrupt patients in most interviews
    within 23 seconds, and once interrupted, patients finish
    their comments in only 8% of interviews.21 Older patients report higher satisfaction rates when accompanied by a family member, friend, or advocate.22

    Empathy
    Communication Skills Techniques
    The 4Es educational model for communication is
    particularly useful for orthopaedic practices. Excellent
    orthopaedic care requires a high level of patient cooperation and adherence to treatment protocols to
    achieve the best possible outcomes. The 4Es of critical communication tasks, to engage, empathize, educate, and enlist patients have been proposed.18 These
    communication tasks are considered to be of equal importance to the biomedical tasks, or the 2Fs, of finding the problem (diagnosis) and fixing the problem
    (treatment) (Figure 2).

    Engagement
    Engagement establishes an interpersonal connection
    that sets the stage for the patient-physician interaction,
    drawing the patient in. The patient will respond to the

    2011 American Academy of Orthopaedic Surgeons

    Empathy allows physicians to demonstrate an understanding of and concern for the patients thoughts and
    feelings. The patient is seen, heard, and understood.
    Audiotaped interviews have shown that expressions of
    empathy by orthopaedic surgeons are rare.9,11 It is possible that surgeons feel uncomfortable showing empathy, fearing that statements of compassion will lead to
    time-consuming conversation, unpleasant emotional
    scenes, and the need to comfort patients.23 Empathy is
    the surgeons most powerful and underused tool. A true
    expression of empathy, such as that must have been
    painful/frustrating/frightening, spoken with a concerned tone and facial expression that models that of
    the patient can quickly establish a trusting relationship.
    Empathy, contrary to popular belief, actually saves
    time. Showing compassion with empathic comments
    encourages patients to express their true agenda and
    hidden concerns.24 Time-saving techniques include pri-

    Orthopaedic Knowledge Update 10

    111

    Section 1: Principles of Orthopaedics

    oritizing discussion topics by inquiring about the patients primary concerns early, keeping any personal
    physician disclosures brief, and using scenarios during
    informed consent.8 Acknowledging a patients emotions
    and values recognizes their individuality.

    Education

    1: Principles of Orthopaedics

    Educational information, when successfully communicated, enhances the patients knowledge and increases
    his or her capacity to deal with treatment options while
    decreasing anxiety. Patients generally prefer detailed
    and extensive disclosure of alternative therapies; however, only 50% of physicians believe that patients want
    information about alternative treatments.25 Patients
    also prefer information regarding risks (even those that
    are rare), whereas physicians often believe that such detailed information regarding drugs will decrease the
    placebo effect, increase adverse effects, and decrease
    compliance. Patients express the opposite view. For example, explaining the potential benefits and adverse effects of a nonsteroidal anti-inflammatory drug will increase rather than decrease adherence to the treatment
    plan.
    Patients often lack the skill to ask appropriate questions during an interview.26 Inquiring about the patients primary concerns at the beginning of the educational phase of a new patient interview will both open a
    focused discussion and save time. Patients should be
    encouraged to ask questions at any time. Physicians
    may mistake a patients respect or reserve as a lack of
    interest. Conversely, assertive patients who push for detailed information may be perceived as litigation
    risks.27
    Physicians should avoid long educational monologues. Stopping to check the patients verbal understanding (not just their nonverbal expressions) is important, but rare. For example, the physician can say,
    I have given you one explanation, so how does this fit
    with what youve been thinking? The physician also
    can inquire about the patients concerns about a
    planned surgery. It should be recognized that every patient presents with a self-diagnosis. The physician
    should be wary of patients who do not engage in open
    discussion; those patients may later complain that important information was not provided.1

    Enlistment
    Enlistment extends an offer to the patient to actively
    participate in decision making. Enlistment acknowledges that patients control much of their treatment
    plan. To achieve successful outcomes, orthopaedic patients must be confident that their treatment will help
    them and must be convinced that they can achieve
    treatment plan goals in the face of competing interests
    for their time and energy.23 A perfect flexor tendon repair or knee replacement will stiffen and fail without
    the cooperation of a well-informed and motivated patient.
    Missed clues by patients regarding possible barriers
    to treatment often lead to misunderstandings and
    112

    Orthopaedic Knowledge Update 10

    wasted time during interviews.24 Older patients, especially African Americans, are quite selective in disclosing important information during interviews with orthopaedic surgeons. A 2008 study reported that
    orthopaedic surgeons responded inadequately to 29%
    of patient concerns (23 of 80)9 (Table 2). A minimal
    acknowledgment was the most common response to
    the concerns of patients about their ability to meet the
    challenges of surgery.
    A 2001 study showed that patients do not adhere to
    treatment plans when they disagree with the physician
    (37%), are concerned about cost (27%), find the instructions too difficult to follow (25%), think the recommendations are in conflict with their personal beliefs
    (20%), or do not understand the plan (7%).28 Patients
    can help to reduce medical errors in the hospital when
    they are fully informed of their treatment plan on a
    daily basis during the physicians morning rounds.29

    Communicating Bad News


    Specific techniques are useful in communicating adverse events.30 A physician may feel defensive when an
    unexpected complication or medical error occurs, resulting in the patient not being fully informed. Discussions between team members will help prepare an appropriate response, thereby reducing the possible
    perception by the patient and family members that the
    event has been handled insensitively. Apologies without
    accepting blame should be offered. The focus should be
    on the disease, not the team members. Adequate time
    should be allowed for difficult and often emotional discussions. The physician should listen carefully, avoid
    interruptions, and frequently check for understanding.
    A proactive, timely plan with clear statements and documentation should be presented. The physician should
    remain hopeful, regroup before moving on to other
    tasks, and follow up on the announced plan in a timely
    manner. Patients who receive full disclosure are reported to have more trust and a more positive emotional response.31 Patients were more likely to litigate
    following errors if there was not full disclosure.32

    Culture

    Definition
    At its most basic, culture is defined as a combination of
    acquired beliefs and behaviors that are shared among a
    particular group or groups. The culture of medicine often clashes with that of patient groups, resulting in disparities of care. The National Center for Cultural Competence defines culture as an integrated pattern of
    human behavior that includes thoughts, communications, languages, practices, beliefs, values, customs,
    courtesies, rituals, manners of interacting, roles, relationships, and expected behaviors of a racial, ethnic, religious, or social group.33 Six realities of cultural programming that should be considered by clinicians in

    2011 American Academy of Orthopaedic Surgeons

    Chapter 9: Patient-Centered Care: Communication Skills and Cultural Competence

    Table 2

    Table 3

    Orthopaedic Surgeon Responses to 80 Concerns


    Expressed by Older Patientsa

    Six Realties of Cultural Programming

    Positive Acknowledgment
    by the Surgeon

    We all think that our own culture is best

    Surgeon Responses to
    Patient Concerns

    Culture is not obvious

    40

    We misinterpret the actions of others if we do not


    understand their interpretations of their own observations

    With explanation

    27

    We may not know when we are offending others

    Without explanation

    13

    Awareness of difference and possible barriers improves our


    chances for successful interactions

    Reassurance

    Supportive/accommodating

    12

    Empathy

    Minimal acknowledgment

    13

    Failure to address concern

    Premature acknowledgment

    The Culture of Medicine

    Negative Response by the Surgeon


    Inappropriate humor

    Denial

    Termination of conversation

    Older patient concerns about surgery (80) were separated from a total of 155
    concerns identified. (Reproduced with permission from Hudak PL, Armstrong K,
    Braddock C III, Frankel RM, Levinson W: Older patients unexpressed concerns
    about orthopaedic surgery. J Bone Joint Surg Am 2008;90(7):1427-1435.)

    managing their patients are summarized in Table 3.


    Culture is very dynamic and includes many characteristics, such as education, socioeconomic class, sexual
    orientation, and sex. These characteristics combine and
    react with the life experiences of an individual to form
    that persons identity and current cultural perspective.34,35 It has been argued that culture must be defined
    and explored in light of these influences to get a true
    picture of the individual and their perceptions, preferences, and needs.36 For example, an African-American
    female cardiac surgeon has life experiences that are
    multifaceted. To classify her within the boundaries of a
    stereotypic definition of African-American women
    would be incomplete. She is African American, female,
    her socioeconomic class is high, she is well educated,
    and nonAfrican-American men dominate her medical
    specialty. Her culture has many influences.
    Culture is not only an integrated pattern of learned
    beliefs and behaviors that can be shared among groups,
    but it is also thought processes, communication styles,
    views on roles and relationships, values, practices, customs, and methods of interacting. Many factors, including ethnicity, race, nationality, language, sex, socioeconomic status, physical and mental ability, sexual
    orientation, and occupation, influence culture. These
    influences work together to shape values, to help form
    belief systems, and to motivate the behavior of an individual.35

    2011 American Academy of Orthopaedic Surgeons

    (Adapted with permission from from Tongue JR, Epps HR, Forese LL:
    Communication skills for patient-centered care: Research-based, easily learned
    techniques for medical interviews that benefit orthopaedic surgeons and their
    patients. J Bone Joint Surg Am 2005;87:652-658.)

    1: Principles of Orthopaedics

    Inadequate Acknowledgment
    by the Surgeon

    Understanding our own software or value system is a


    crucial step in providing culturally competent care

    Using the definition of culture, it can be shown that


    medicine has attributes and characteristics of a unique,
    distinct, fluid group with its own language, thought
    processes, styles of communication, customs, and beliefs; therefore, medicine has its own culture.34
    The language of medicine is characterized by statistical facts, probability, gradations of severity, and the
    use of acronyms and medical terminology, which are
    frequently not understood by people outside the field.
    It is important to use language that is understood by
    patients.34,37
    Medicine has its own way of speaking and its own
    mannerisms of discussion. For example, physicians often discuss a case rather than a person or a patient. Patients are often considered to be separate from the disease process. When a patient describes his or her
    symptoms, physicians describe this information as subjective rather than factual. To the patient, however, the
    information is very factual.37
    The manner in which physicians conceptualize
    health (the explanatory model) is another example of
    the culture of medicine. A physicians explanatory
    model of a disease process is derived from the perception of its etiology, onset, pathophysiology, course, and
    treatmenta biomedical model. This model is derived
    from the medical school curriculum and environment
    along with interactions with peers and mentors. A patients explanatory model of disease is obtained from
    social network experiences and may determine if treatment is sought. A patients explanatory model of a disease process may be very different from that of the physician. It is, therefore, very important for the physician
    to understand these differences when planning a course
    of therapy that is mutually agreeable.37,38
    Medicine also has its own dress and rituals. The
    white coat has been the traditional attire associated
    with medicine. Doctors began wearing white coats in
    the 19th century and it became a symbol of science and
    the art of healing. The white coat has been shown to
    foster confidence and trust in patients. Students enter-

    Orthopaedic Knowledge Update 10

    113

    Section 1: Principles of Orthopaedics

    ing medical school attend the white coat ceremony.


    This ceremony is an example of a cultural ritual of
    medicine.37-40
    The culture of medicine lacks ethnic and sex diversity. For example, 80% of orthopaedic surgeons are
    white males.41

    Culturally Diverse Patient Populations

    1: Principles of Orthopaedics

    Physicians and staff need to be educated regarding certain cultural norms in the diverse populations they
    serve. Educating medical staff regarding cultural diversity increases the health care providers own comfort
    level with diverse populations and increases patient satisfaction and positive outcomes of treatment.42 When
    studying traditional cultural values, ideas, and beliefs
    of the many diverse populations in this nation, it is important to remember that a group of people may share
    traditional values, beliefs, and behaviors, but they are
    also influenced by their current environment, socioeconomic status, age, sex, sexual orientation, and level of
    education. Every man, woman, and child is a unique
    individual and must be approached as such.
    For example, Latinos or Hispanic Americans are a diverse community. Although Spanish is the main language
    spoken, as in any language, there are many dialects.
    Among Latino/Hispanic Americans, the family bond is
    very strong. The decision maker is the male head of the
    family. Many Hispanic/Latino patients have traditional
    beliefs about what makes them sick and what can heal
    them. Negative emotions, natural phenomena, magic,
    and an imbalance between hot and cold are often believed to be causative factors in disease.43 Fatalismo, the
    belief in fate, may also have an important role in attitudes about illness and treatment.44
    The Muslim community is composed of people who
    follow the religion of Islam (the second largest religion
    in the world) and live in at least 184 different countries.
    Doctors should not shake hands or hug unless such an
    action is initiated by the Muslim patient. Some Muslim
    people avoid prolonged eye contact out of respect.45
    Traditionally, the Muslim faith does not allow the ingestion of pork or alcohol, which can be problematic if
    a medication contains alcohol or is derived from pork,
    such as porcine heparin. Exceptions are often made for
    life-saving emergency treatment. It is important for the
    medical provider to be aware of and sensitive to this issue. While fasting during the month of Ramadan, the
    Muslim faith technically does not allow the use of intravenous drugs and pharmaceutical agents. Consultation with an imam, a Muslim religious leader in the
    community, may be needed to allow medications during Ramadan.45
    Asian American is a term that also includes a wide
    variety of cultures, ethnic groups, and countries. According to a 2002 estimate from the Census Bureau,
    more than 13 million Asian people live in the United
    States. Asians make up 4.5% of the population and are
    the fastest-growing racial group in America. Saving
    face is very important in Asian culture. If an Asian patient is asked if he or she understands something, many
    114

    Orthopaedic Knowledge Update 10

    patients will answer in the affirmative out of respect for


    the physician. It is better to ask open-ended questions
    such as, please explain to me your understanding of
    this. Asian patients may also hesitate to make eye contact, out of respect for the physician. Asian families
    may use traditional Asian and herbal remedies before
    using Western medicine. Physicians need to be aware of
    potential interactions of prescribed medications with
    these herbal remedies.46,47
    Each cultural group has its beliefs, traditions, and
    values. The AAOS has published a guidebook that contains tip sheets with information regarding different
    cultures and ethnic groups.44 This book is a good reference tool and can help increase the cultural competency
    of orthopaedic surgeons.

    Language Divides
    How can language be divisive? Studies have shown that
    patients with limited English proficiency feel less satisfied with their health care, often receive insufficient
    health education, and have increased problems with
    medication errors. It has been shown that the children
    of nonEnglish-speaking families do not receive the
    same access to health care nor do they receive equal
    medical and dental care compared to children from
    English-speaking families.48
    When translators are available, words may get translated but often subtle nuances or cultural variables can
    be missed if the translator is not aware of or trained to
    recognize these factors. The literature refers to these subtle nuances and cultural variables as the shared meaning of words. Everyone involved must use words with
    the same meaning when discussing the care of a patient.
    Miscommunication can cause patient dissatisfaction,
    potential errors, and negative outcomes. People of diverse cultural and language backgrounds require not
    only an exchange of words but also an exchange of
    shared meanings, which can be difficult to achieve in a
    clinical encounter. Effective translators and bilingual
    office staff members must have the skill to translate
    words along with the cultural knowledge and the ability to relate subtle cultural nuances in communication.49
    Language barriers are divisive. Language and/or culture can prevent adequate communication among
    health care providers and patients, which has been
    shown to result in patient dissatisfaction and less than
    desirable outcomes. Even with the help of an interpreter, patients with language barriers require more
    time for visits with the physician and may require more
    visits.50,51 In the absence of a professional interpreter or
    bilingual physician, decision making may become more
    cautious, resulting in an increase in diagnostic testing.52

    Health Disparities
    Health disparities are defined as gaps in the quality of
    health and health care in certain racial, ethnic, and
    other minority groups.53 A 1985 study reported that
    people in racial and ethnic minority groups were dying
    at a faster rate than the average for the population as a

    2011 American Academy of Orthopaedic Surgeons

    Chapter 9: Patient-Centered Care: Communication Skills and Cultural Competence

    2011 American Academy of Orthopaedic Surgeons

    Cobb/NMA Health Institute (Cobb Institute) to focus on


    the strategic goal of eliminating health disparities.53

    Cultural Competency
    What does it mean to be culturally competent? Such
    competency starts with an understanding of the communities and cultures of the region served by the physician. It is the knowledge that a persons ethnicity, race,
    or culture forms an important part of who that person
    is and a recognition that current environment, educational level, socioeconomic status, sex, sexual orientation, and age also influence how a person thinks and
    formulates ideas and beliefs.
    To provide culturally competent care, physicians
    must bring to each patient encounter an understanding
    of varied cultural backgrounds and belief systems and
    their effect on the perception of health, illness, treatment, and diagnosis.44 These cultural differences influence a patients understanding and willingness or preparedness to follow a treatment regimen. A clinician
    who lacks awareness and understanding of cultural
    norms can easily evoke mistrust.
    Stereotyping can be avoided by considering the patients cultural background and his or her current social
    situation. A clinician who assumes that a person has
    certain cultural norms based solely on his or her race or
    ethnicity can be stereotyping the patient and thereby
    creating miscommunication and a sense of unease with
    the patient. Current social influences must always be a
    part of the process of understanding the needs of the
    patient. Physicians must also reflect on their own culture, values, and beliefs that influence their interactions
    with patients. Respect for the patients needs, preferences, and sensitivity to nonmedical and spiritual dimensions are also important components of culturally
    competent care.

    1: Principles of Orthopaedics

    whole.54 The fatal diseases were curable and controllable. Subsequently, research requested by Congress resulted in the widely read Unequal Treatment: Confronting Racial and Ethnic Disparities in Health Care
    published by the Institute of Medicine.55 This report
    documented racial, cultural, and language disparities in
    health care. The study recommended including crosscultural education for health care professionals. Health
    disparities currently are well recognized as a reality in
    the United States and the world.56
    Ninety-eight percent of leaders in the health care industry are white. Minorities represent 28% of the US
    population but represent only 3% of medical school
    faculties. Minorities make up 16% of public health officials and 17% of city and county health officers.
    More diversity in health care system leadership would
    make it easier to teach cultural competency. Minorities
    also make up a small number of the health care workforce. Patient satisfaction and the perception of the
    quality of care are greater when patients are treated by
    health care providers of a similar race or ethnicity.54
    In the United States, it is now well documented that
    African Americans, Asian Americans, Latino/Hispanic
    Americans, and Native Americans have a higher incidence of mortality and chronic disease. These groups
    have higher rates of cardiovascular disease, human immunodeficiency virus, acquired immunodeficiency virus, and infant mortality.56 The incidence of cancer
    among African Americans is 10% higher than that for
    whites.57 African Americans and Latino/Hispanic
    Americans have almost twice the incidence of diabetes.58 African American and Hispanic women in the
    United States are underdiagnosed for osteoporosis.59,60
    Surveys have shown that most Americans, including
    physicians, do not believe that there are ethnic and racial disparities in health care despite strong evidence to
    the contrary. A survey published in the 2003 Harvard
    Forum on Health reported that only 22% of white
    Americans believed that minorities received lowerquality health care based on race or ethnicity; however,
    65% of African Americans and 41% of Hispanics believed that there were racial disparities in health
    care.61,62 National studies have consistently found a
    lower rate of hip and knee joint surgeries for arthritis in
    older black adults than white adults. Further investigation of this disparity is necessary, but access to medical
    care may be a factor.63,64
    Many organizations and academic departments are
    now including the study of cross-cultural education and
    health disparities in their mission statements. The Johns
    Hopkins School of Public Health Primary Care Policy
    Center for Underserved Populations mission includes:
    research, analysis, and education concerning the organization, financing, and mode of delivery for primary
    care to underserved and vulnerable populations.65
    The National Medical Association (NMA), which
    was established in 1895, is the oldest and largest organization in the United States representing the interests of
    physicians of African descent and their patients. A strategic goal of the NMA is the elimination of health disparities. In 2004, the NMA launched the W. Montague

    Summary
    Patient-centered care recognizes and enhances the necessary trust between patients and their doctors and depends on quality communications as well as the assumption that physicians will strive to give equal care
    to all patients. Communication skills should be taught
    with the same rigor as other core clinical skills; however, like all skills, communication skills can be retained or lost over time. Current role models in orthopaedic training are not effective in encouraging patientcentered care. Experience alone rarely causes a change
    in behavior.
    Physicians must treat some patients differently to offer them equal treatment. Unconscious stereotypical
    views regarding race, class, or age tear at the fabric of
    the unique patient-physician relationship. Culturally
    competent care requires physicians to be aware, understanding, and inclusive. A physician does not need to
    know or understand every nuance about every culture
    because this is impossible. Physicians must bring four

    Orthopaedic Knowledge Update 10

    115

    Section 1: Principles of Orthopaedics

    things to the physician-patient encounter: a heightened


    awareness, sensitivity, and curiosity; compassion; communication skills; and an open accepting mind. Physicians must recognize and accept the increased time and
    cost required to provide equal care for patients of a different culture, ethnicity, or language.

    These court decisions set a high standard for informed


    consent for all relevant treatment alternatives and risks.
    9.

    Hudak PL, Armstrong K, Braddock C III, Frankel RM,


    Levinson W: Older patients unexpressed concerns
    about orthopaedic surgery. J Bone Joint Surg Am 2008;
    90(7):1427-1435.
    The Levinson group reviewed the patient audiotapes of
    900 Chicago-area orthopaedic surgeons. Patients raised
    only 50% of their concerns and were more likely to
    raise concerns during a discussion rather than in response to an inquiry. A patients limited capacity to
    meet the demands of surgery may impinge on their willingness to agree to treatment.

    10.

    Kramer D, Ber R, Moore M: Impact of workshop on


    students and physicians rejecting behaviors in patient
    interviews. J Med Educ 1987;62(11):904-910.

    11.

    Jimenez RL, Lewis VO, Frick SL: Residency training


    programs, in Jimenez RL, Lewis VO, eds: The AAOS
    Culturally Competent Care Guidebook. Rosemont, IL,
    American Academy of Orthopaedic Surgeons, 2007, pp
    7-8.
    Written by orthopaedic surgeons, this guidebook discusses residency training, ethnic and racial patient
    groups, and issues related to sex and faith.

    12.

    Tongue JR, Jenkins L, Wade A: Low-touch surgeons in a


    high-touch world. American Academy of Orthopaedic
    Surgeons Web site. http://www.aaos.org/news/aaosnow/
    may09/cover1.asp. Accessed February 25, 2010.
    A 10-year tracking study by the AAOS showed the
    changing image of orthopaedic surgeons, who are now
    better known and more highly valued by the public. The
    surgeons self-image is now more modest; however, interpersonal skills are undervalued by orthopaedic surgeons but rate highly with patients.

    13.

    Levinson W, Roter DL, Mullooly JP, Dull VT, Frankel


    RM: Physician-patient communication: The relationship
    with malpractice claims among primary care physicians
    and surgeons. JAMA 1997;277(7):553-559.

    14.

    Fine VK, Therrien ME: Empathy in the doctor-patient


    relationship: Skill training for medical students. J Med
    Educ 1977;52(9):752-757.

    15.

    Leigh JP, Kravitz RL, Schembri M, Samuels SJ, Mobley


    S: Physician career satisfaction across specialties. Arch
    Intern Med 2002;162(14):1577-1584.

    16.

    Quick JC, Saleh KJ, Sime WE, et al: Symposium: Stress


    management skills for strong leadership. Is it worth dying for? J Bone Joint Surg Am 2006;88(1):217-225.

    17.

    Beckman HB, Markakis KM, Suchman AL, Frankel


    RM: The doctor-patient relationship and malpractice:
    Lessons from plaintiff depositions. Arch Intern Med
    1994;154(12):1365-1370.

    18.

    Keller VF, Carroll JG: A new model for physicianpatient communication. Patient Educ Couns 1994;23:
    131-140.

    Annotated References

    1: Principles of Orthopaedics

    1.

    2.

    3.

    Epstein RM, Street RL: Patient-centered communication


    in cancer care. National Cancer Institute. http://
    www.outcomes.cancer.gov/areas/pcc/communication/
    pccm_ch1.pdf. Accessed July 19, 2010.
    The authors present a detailed review of patientcentered care.
    Lundine K, Buckley R, Hutchison C, Lockyer J: Communication skills training in orthopaedics. J Bone Joint
    Surg Am 2008;90(6):1393-1400.
    Communication skills should be taught with the same
    rigor as other core clinical skills and can be taught, retained over time, and lost. Current role models are not
    effective. Experience alone rarely causes a change in behavior.

    4.

    Frymoyer JW, Frymoyer NP: Physician-patient communication: A lost art? J Am Acad Orthop Surg 2002;
    10(2):95-105.

    5.

    Roter DL, Stewart M, Putnam SM, Lipkin M Jr , Stiles


    W, Inui TS: Communication patterns of primary care
    physicians. JAMA 1997;277(4):350-356.

    6.

    7.

    8.

    116

    Tongue JR, Epps HR, Forese LL: Communication skills


    for patient-centered care: Research-based, easily learned
    techniques for medical interviews that benefit orthopaedic surgeons and their patients. J Bone Joint Surg Am
    2005;87:652-658.

    Clark PA: Return on Investment in Satisfaction Measurement and Improvement: Working Paper from Press
    Ganey Associates, vol 1, edition 1, August 31, 2005.
    http://www.pressganey.com/files/roi1.pdf. Accessed February 25, 2010.
    Braddock C III, Hudak PL, Feldman JJ, Bereknyei S,
    Frankel RM, Levinson W: Surgery is certainly one
    good option: Quality and time-efficiency of informed
    decision-making in surgery. J Bone Joint Surg Am 2008;
    90(9):1830-1838.
    Time-efficient strategies for informed surgical decision
    making include using scenarios to illustrate choices, encouraging patient input, and addressing primary patient
    concerns. In more than 140 consent interviews, none received perfect scores. The surgeon should prioritize to
    save time.
    Sorrel AL: Two state courts, same ruling: Informed consent must include all options. Posted August 24, 2009.
    Dylan McQuitty vs. Donald Spangler, MD, Maryland
    Court of Appeals. American Medical News Web site.
    http//:www.ama-assn.org/amednews/2009/08/24/
    prl20824.htm#s1. Accessed February 25, 2010.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 9: Patient-Centered Care: Communication Skills and Cultural Competence

    19.

    Tongue JR. Approaching new orthopaedic patients


    AAOS Bulletin. 2003;51(4):31-32.

    20.

    Tongue JR: Communication skills mentoring program:


    Patient encounter tips. AAOS Web site. http://
    www3.aaos.org/education/csmp/
    InitialMedEncounter.cfm. Accessed February 25, 2010.
    The information is presented as an outline of interview
    tips and pitfalls specific to orthopaedic patient needs.
    Marvel MK, Epstein RM, Flowers K, Beckman HB: Soliciting the patients agenda: Have we improved? JAMA
    1999;281(3):283-287.

    22.

    Wolff JL, Roter DL: Hidden in plain sight: Medical visit


    companions as a resource for vulnerable older adults.
    Arch Intern Med 2008;168(13):1409-1415.
    Sick patients benefit most when accompanied by companions who record instructions, ask questions, provide
    information, and explain physician instructions.

    23.

    Keller V, White M: Choices and changes: A new model


    for influencing patient health behavior. J Clin Outcomes
    Manag 1997;4(6):33-36.

    Mazor KM, Simon SR, Yood RA, et al: Health plan


    members views about disclosure of medical errors. Ann
    Intern Med 2004;140(6):409-418.

    32.

    Wu AW, Cavanaugh TA, McPhee SJ, Lo B, Micco GP:


    To tell the truth: Ethical and practical issues in disclosing medical mistakes to patients. J Gen Intern Med
    1997;12(12):770-775.

    33.

    Georgetown University Center for Child and Human


    Development Web site. National Center for Cultural
    Competence: Curricula Enhancement Module Series.
    http://www.nccccurricula.info/glossary.html. Accessed
    February 25, 2010.
    An online resource for accessing organizations to teach
    interested parties about cultural competence is presented.

    34.

    Boutin-Foster C, Foster JC, Konopasek L: Viewpoint:


    Physician, know thyself. The professional culture of
    medicine as a framework for teaching cultural competence. Acad Med 2008;83(1):106-111.

    35.

    Betancourt JR, Green AR, Carrillo JE: Cultural competence in health care: Emerging frameworks and practical
    approaches. The Commonwealth Fund. October 2002.
    http://www.commonwealthfund.org/usr_doc/
    betancourt_culturalcompetence_576.pdf. Accessed February 25, 2010.

    24.

    Levinson W, Gorawara-Bhat R, Lamb J: A study of patient clues and physician responses in primary care and
    surgical settings. JAMA 2000;284(8):1021-1027.

    25.

    Faden RR, Becker C, Lewis C, Freeman J, Faden AI:


    Disclosure of information to patients in medical care.
    Med Care 1981;19(7):718-733.

    36.

    Green AR, Betancourt JR, Carrillo JE: Integrating social


    factors into cross-cultural medical education. Acad Med
    2002;77(3):193-197.

    26.

    Hughes D: Control in medical consultation: Organizing


    talk in a situation where co-participants have differential competence. Sociology 1982;16(3):359-376.

    37.

    27.

    Studdert DM, Mello MM, Sage WM, et al: Defensive


    medicine among high-risk specialist physicians in a volatile malpractice environment. JAMA 2005;293(21):
    2609-2617.

    The Culture of Medicine. January 5, 2009. Science


    Daily Web site. http://www.sciencedaily.com/releases/
    2008/12/081231182014.htm. Accessed August 2, 2009.
    A brief review of a study dealing with the environment
    of American academic medicine from the perspective of
    faculty is presented.

    38.

    Lerner EB, Jehle DV, Janicke DM, Moscati RM: Medical communication: Do our patients understand? Am J
    Emerg Med 2000;18(7):764-766.

    39.

    Rehman SU, Nietert PJ, Cope DW, Kilpatrick AO:


    What to wear today? Effect of doctors attire on the
    trust and confidence of patients. Am J Med 2005;
    118(11):1279-1286.

    40.

    Van Der Weyden MB: White coats and the medical profession. Med J Aust 2001;174(7):324-325.

    41.

    Jimenez RL: Current activities in orthopaedic culturally


    competent care education. J Am Acad Orthop Surg
    2007;15(suppl 1):S76-S79.
    Legislation for culturally competent care has been
    passed in California and New Jersey, and legislation is
    pending in Arizona, Illinois, New York, and Texas. The
    Diversity Advisory Board of the AAOS has advanced
    the education of diversity for orthopaedic surgeons.

    42.

    National Institute for Childrens Health: Improving

    28.

    29.

    30.

    2001 Commonwealth Fund Health Care Quality Survey.


    The Commonwealth Fund Web site. http://
    www.commonwealthfund.org/Contents/Surveys/2001/
    2001-Health-Care-Quality-Survey.aspx. Accessed February 25, 2010.
    Levin PE, Levin EJ: The experience of an orthopaedic
    traumatologist when the trauma hits home: Observations and suggestions. J Bone Joint Surg Am 2008;
    90(9): 2026-2036.
    This personal essay explores the psychosocial upheaval
    that accompanies major physical trauma. The authors
    report that breakdowns in communication cause misunderstandings and medical errors. The authors also discuss the appropriate role of the orthopaedic trauma surgeon in providing the emotional support and hope
    necessary for healing.
    Epps HR, Tongue JR. Communicating adverse outcomes. AAOS Bulletin. 2003;51(2):29, 33.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    21.

    31.

    117

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    cultural competency in childrens health care. Expanding perspectives. http://www.nichq.org/pdf/NICHQ_


    CulturalCompetencyFINAL.pdf. Accessed February 25,
    2010.
    An extensive reference aimed at reducing disparities in
    health care for children is presented.
    43.

    Weiss B: Caring for Latino patients. Med Econ 2004;


    81(8):34-40.

    44.

    Jimenez RL, Lewis VO, eds: Culturally Competent Care


    Guidebook: Companion to the Cultural Competency
    Challenge CD-ROM. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2007.
    The guidebook was developed by the AAOS to help educate orthopaedic surgeons on culturally competent
    care.

    45.

    Pennachio DL: Caring for your Muslim patients: Stereotypes and misunderstandings affect the care of patients
    from the Middle East and other parts of the Islamic
    world. Med Econ 2005;82(9):46-50.

    46.

    Pennachio DL: Caring for Chinese, Japanese, and Korean patients. Med Econ 2004;81(13):54-59.

    47.

    Pennachio DL: Cultural competence: Caring for your


    Filipino, Southeast Asian and Indian patients. Modern
    Medicine Web site. October 22, 2004. http://
    www.modernmedicine.com/modernmedicine/Medical
    +Practice+Management%3A+Patient+Relations/
    Cultural-Competence-Caring-for-your-Filipino-South/
    ArticleStandard/Article/detail/128909. Accessed February 25, 2010.

    48.

    49.

    118

    Flores G, Tomany-Korman SC: The language spoken at


    home and disparities in medical and dental health, access to care, and use of services in US children. Pediatrics 2008;121(6):e1703-e1714.
    This multivariable analysis of children in non-English
    primary language households reports specific disparities
    in medical health and in access and use of medical services.
    Johnstone MJ, Kanitsaki O: Culture, language, and patient safety: Making the link. Int J Qual Health Care
    2006;18(5):383-388.

    50.

    Kravitz RL, Helms LJ, Azari R, Antonius D, Melnikow


    J: Comparing the use of physician time and health care
    resources among patients speaking English, Spanish,
    and Russian. Med Care 2000;38(7):728-738.

    51.

    Derose KP, Baker DW: Limited English proficiency and


    Latinos use of physician services. Med Care Res Rev
    2000;57(1):76-91.

    52.

    Hampers LC, McNulty JE: Professional interpreters and


    bilingual physicians in a pediatric emergency department: Effect on resource utilization. Arch Pediatr Adolesc Med 2002;156(11):1108-1113.

    Orthopaedic Knowledge Update 10

    53.

    Morgan RC Jr, Davis SJ: Cobb Institute strategies for


    the elimination of health disparities. J Am Acad Orthop
    Surg 2007;15(suppl 1):S59-S63.
    The W. Montague Cobb/NMA Health Institute studies
    and provides solutions to eliminate health disparities in
    African Americans and other underserved populations.
    The Cobb Institute provides information regarding the
    health of African Americans.

    54.

    Secretarys Task Force on Black and Minority Health:


    Report of the Secretarys Task Force on Black and Minority Health. Washington, DC, US Department of
    Health and Human Services, 1985.

    55.

    Smedley BD, Stith AY, Nelson AR: Unequal Treatment:


    Confronting Racial and Ethnic Disparities in Health
    Care. Washington, DC, National Academies Press,
    2002.

    56.

    Centers for Disease Control and Prevention: Disease


    Burden & Risk Factors. Washington, DC, Office of Minority Health, 2007.
    The CDC has published exhaustive data of deaths and
    disease rates by religion and ethinc/racial patient
    groups.

    57.

    National Cancer Institute: Cancer health disparities: A


    fact sheet. Benchmarks 2005;5:2.

    58.

    Centers for Disease Control and Prevention: National


    Diabetes Fact Sheet: United States 2005. Atlanta, GA,
    Centers for Disease Control and Prevention, 2005.

    59.

    Thomas PA: Racial and ethnic differences in osteoporosis. J Am Acad Orthop Surg 2007;15(suppl 1):S26-S30.
    In the United States, osteoporosis is underdiagnosed in
    women in minority racial groups. Disparities exist for
    diagnosing osteoporosis based on racial and ethnic lines.

    60.

    National Osteoporosis Foundation: Fast Facts. Washington, DC, National Osteoporosis Foundation, 2006.

    61.

    Harvard Forums on Health: Americans Speak Out on


    Disparities in Health Care. Boston, MA, Harvard
    School of Public Health, 2003.

    62.

    Nelson CL: Disparities in orthopaedic surgical intervention. J Am Acad Orthop Surg 2007;15(suppl 1):S13S17.
    Research in health care has shown the existence of disparities in orthopaedic care. The disparities in total hip
    and knee replacement have been the most studied.

    63.

    Dunlop DD, Manheim LM, Song J, et al: Age and


    racial/ethnic disparities in arthritis-related hip and knee
    surgeries. Med Care 2008;46(2):200-208.
    Black adults younger than 65 years self-report similar
    rates of hip/knee arthritis surgeries, yet national data
    document lower rates of arthritis-related hip/knee surgeries for older black adults compared with those for
    white adults age 65 years or older.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 9: Patient-Centered Care: Communication Skills and Cultural Competence

    64.

    Manheim LM, Chang RW: Racial disparities in joint replacement use among older adults. Med Care 2003;
    41(2):288-298.

    65.

    The Johns Hopkins School of Public Health Primary


    Care Policy Center for Underserved Populations: Mis-

    sion statement. http://www.jhsph.edu/pcpc/.


    This federally-funded academic program has produced
    evidence of the importance of primary care, including
    musculoskeletal conditions.

    1: Principles of Orthopaedics

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    119

    Chapter 10

    Practice Management
    Craig R. Mahoney, MD

    Stephen P. Makk, MD, MBA

    Introduction

    Dr. Mahoney or an immediate family member serves as a


    paid consultant to or is an employee of Smith & Nephew; and has received research or institutional support
    from Smith & Nephew. Dr. Makk or an immediate family
    member serves as a board member, owner, officer, or
    committee member of AAOS Practice Management
    Committee, Biomedical Engineering Committee, and
    DocsFACTS; is a member of a speakers bureau or has
    made paid presentations on behalf of Baxter; serves as
    an unpaid consultant to Pradama, 3DR, Kentucky Seed
    Fund, Metacyte Business Incubator, and Healthcoast; and
    has stock or stock options held in Schering Plough, Cytori, RTI, Novadaq, and Pradama.

    2011 American Academy of Orthopaedic Surgeons

    Currently there is a move by nonprofit, communitybased hospitals to buy orthopaedic practices and hire
    orthopaedic surgeons as employees. This trend, however, is not unique to orthopaedics. In 2007 and 2008,
    approximately 50 large cardiology practices were purchased by nonprofit hospitals. There have also been
    other large cardiology groups that have entered into
    close relationships with hospitals, avoiding direct employment but integrating management and sharing of
    services and revenue using existing models.1
    Over the past 20 years, hospitals have been active in
    purchasing primary care practices. These purchases
    were thought to aid hospitals in supplying themselves
    with a steady stream of patients through referrals from
    their employed physicians. By controlling referral patterns through employment of the referring physician, it
    was thought that hospitals could more efficiently organize the delivery of care and ancillary services. Utilization of inpatient and outpatient services increases with
    a rise in referrals. Further, it was thought that a larger
    number of patients being integrated into a health sys-

    Figure 1

    1: Principles of Orthopaedics

    The volume of information required to successfully


    practice orthopaedics in America continues to expand.
    Diagnostic and therapeutic breakthroughs are reported
    daily, and those breakthroughs allow orthopaedic surgeons to improve patient care and the quality of life.
    More than 60% of orthopaedic surgeons in the
    United States own their practices. Therefore, they must
    not only be clinically competent, but must also understand the basic principles required to manage the business aspect of their practice. Given the recent political
    landscape, the physician must keep informed of issues
    that will change the economics of health care and affect
    income. In this ever-changing environment, information
    addressing practice management is critical in ensuring
    the success of the physician and the practice itself (Figure 1).
    The number of orthopaedic surgeons working for
    hospitals as employees has steadily risen. It is important to study ownership trends in orthopaedics, specifically comparing physician-owned practices with
    hospital-owned practices and examining the concept of
    concierge medical practice. The management strategy
    used by a medical practice is vital to the success of the
    business, along with practice governance, a topic that is
    often overlooked. The chapter will also address the advantages and disadvantages of using electronic medical
    records (EMRs).

    Ownership Trends of Orthopaedic Practices

    Orthopaedic surgeon practice setting. (Reproduced from the American Academy of Orthopaedic Surgeons Research and Scientific Affairs:
    Orthopaedic Practice in the US 2008. Rosemont,
    IL, 2008. Http://www3.aaos.org/research/opus/
    2008CensusMembers.cfm.)

    Orthopaedic Knowledge Update 10

    121

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    tem would improve negotiating strategies when dealing


    with managed care payers. In many instances, physicians joined hospitals because of incentives offered
    by the hospitals (capital expenditures for physician
    practices, reduced overhead because of economies of
    scale, and enhanced ability to negotiate with insurers
    due to size).2
    Unfortunately, many hospital-owned primary care
    practices were not successful. In 1997, Coopers and Lybrand, Ltd., reported mean losses for acquired practices
    of $97,000 per physician per year. Because of this perceived failure, hospital ownership of physician offices
    has decreased.3
    Changes in how health care is delivered and recognized financially have increased interest in hospital
    practice ownership. However, this is now occurring on
    the subspecialty side. Medicare and private insurance
    companies are now placing more emphasis on bundling
    of payments for related services and payment for disease management rather than reimbursing for individual procedures. The Medicare Payment Advisory Commission (MedPAC) is an independent congressional
    agency established by the Balanced Budget Act of 1997
    (P.L. 105-33) to advise the US Congress on issues affecting the Medicare program.4 MedPAC has proposed
    merging Part A and Part B of Medicare in a bundled
    fashion whereby both the hospital payment and professional component would be grouped together when delivering services. The Centers for Medicare and Medicaid Services has piloted this bundling in 28 inpatient
    cardiac surgery centers.1
    Hospitals continue to perceive the need to be closely
    aligned with medical staff, specifically to ensure loyalty,
    to align incentives when delivering care, and to control
    costs in delivering care. Recognizing physician effort in
    a direct employment environment is easier when trying
    to avoid violation of Stark regulation in a hospital situation. In an effort to enhance employment packages,
    hospitals have divided revenues from professional services with employed physicians. This process is still under some legal scrutiny, and some nonprofit hospitals
    have also been challenged because of potential conflicts.5
    Physicians have been motivated to pursue employment with the hospital for several reasons. Currently,
    there is great economic uncertainty in the practice of
    medicine. Incomes in many surgical subspecialties have
    decreased over the past 5 years. Reimbursement for
    many services provided by physicians offices, such as
    imaging, has decreased.6 There continues to be a large
    number of regulations regarding physician self-referral
    and in-office imaging. Office overhead for many orthopaedic offices has increased steadily, but there has been
    no consistent increase in fees received through delivery
    of services. The threat of further increases in overhead
    exists because of implementation of newer technology,
    such as the EMR, and compliance with governmental
    and private insurance quality initiatives.
    122

    Orthopaedic Knowledge Update 10

    Physician-Owned Medical Practice


    When considering hospital employment, several different issues need to be considered. Maintaining a level of
    autonomy and control of his or her practice is important to many orthopaedic surgeons. Regardless of the
    location or scope of a particular practice, there will
    need to be involvement with a hospital in most instances. When the physician owns his or her practice,
    he or she can determine the level of involvement with
    the hospital and the extent to which patients are committed to using the services provided by the hospital.
    As an employee of a hospital there may be contractual
    obligations that encourage patients to use a particular
    hospital, a practice that can alienate patients from physicians.
    Maintaining financial independence offers huge advantages for most independent orthopaedic groups.
    There have been changes in the tax law recently that
    have motivated practices to reevaluate their ownership
    structure in response to those tax law changes.7 It is
    also easier to maintain a level of transparency in an orthopaedic practice when it is not involved with a hospital. Nonprofit hospitals purchasing orthopaedic practices are large organizations with many layers of
    bureaucracy. Obtaining accurate and up-to-date financial records and benchmarking production levels with
    income is much easier in a physician-owned practice
    than a hospital-owned practice. Maintaining ancillary
    income is also an advantage for the physician-owned
    practice. Because of declining reimbursement for many
    procedures, passive income sources continue to be
    stressed in most practices. Passive income sources and
    ancillary income sources include ownership in ambulatory surgery centers, employing physician extenders
    such as physician assistants and nurse practitioners,
    ownership of imaging modalities, durable medical
    equipment, and ownership of physical therapy and occupational therapy services. Many orthopaedic practices remain profitable because of the existence of these
    passive income sources. Ownership in surgery centers
    has been reported to generate close to $170,000 per
    physician, ownership in MRI up to $66,000 per physician, ownership in physical therapy or occupational
    therapy services up to $67,000, and durable medical
    equipment can generate up to $25,000.8
    There are many inherent risks to private ownership.
    An owner employs many people to assist in the delivery
    of care. Management of those employees is vital to the
    success of the practice. As the size of the group expands, there is increased need to hire managers to appropriately guide employees. These layers of management increase overhead costs for physicians without a
    direct return on investment. Further, the cost of employing managers, nurses, and radiology technicians
    continues to outpace increases in reimbursement seen
    for procedures.
    Although there are many opportunities to earn
    money through ancillary sources, current proposed legislation could place this opportunity at risk. HR 2962

    2011 American Academy of Orthopaedic Surgeons

    Chapter 10: Practice Management

    is the Integrity in Medicare Advanced Diagnostic Imaging Act of 2009. The bill would close the in-office ancillary service exemption for MRI, CT and positronemission tomography currently allowed under the Stark
    self-referral law and end the practice of self-referral for
    those modalities under Medicare.9 If this legislation
    were to pass, then the income provided by those ancillary services would be eliminated.

    Hospital Employment

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    In many instances, medical practices and orthopaedic


    practices consider selling to a hospital because of the
    great economic uncertainty of the current environment.
    Some practices have seen their incomes fall over the
    past 5 to 10 years, in part because of increasing overhead and decreasing fees received for services provided.
    There is a threat that with the implementation of EMRs
    and further compliance issues, practice expenses could
    rapidly increase in the near future, adding to the stress
    of running an orthopaedic office. Orthopaedic surgeons
    also list lifestyle concerns as a primary reason for making a transition to a hospital practice. Most think that a
    hospital-based practice would decrease the administrative duties required by physicians.8
    The relationship that exists between the hospital and
    the physician is critical to successful employment, and
    this includes the ability for both parties to fairly negotiate contracts. The contracts drafted would need to
    clearly outline work expectations and the salary that will
    be paid if those expectations are met. Further, a bonus
    structure will need to be outlined for physicians who are
    motivated to do extra work. On-call requirements and
    pay for call will also need to be outlined in initial contract negotiation. Despite the perception that administrative issues may lessen in a hospital-based practice,
    there will certainly be administrative responsibilities and
    staff support issues that continue to arise regardless of
    practice setting. Clear delineation of these administrative
    responsibilities and financial recognition for fulfilling
    those responsibilities also need to be included in the contract. Benefit packages and support for continuing medical eduction (CME) also need to be clearly delineated in
    any hospital-based practice situation.
    There are many risks associated with being employed by a hospital; the first and most important issue
    is loss of autonomy and control. Any physician who
    moves into a hospital-based situation will be moving
    into an employee/employer relationship. With this relationship comes a decrease in leverage/bargaining power
    for the physician. In a hospital with other subspecialty
    employees, theres a possibility that the orthopaedic
    surgeon could be subsidizing physicians who do not
    produce similar revenue. Currently, orthopaedics is an
    integral part of most hospitals income streams, and yet
    the number of orthopaedic surgeons who are required
    to create this income stream are far outnumbered by
    the rest of the medical staff. There is risk that the orthopaedic surgeons could be marginalized by the medical staff. As an employee, the orthopaedic surgeon

    would need to be comfortable with the hospital form of


    management and with having a limited view of all
    things financial. Most hospitals are large organizations
    that cannot act as quickly as smaller physician organizations.
    The Internal Revenue Service has looked closely at
    nonprofit hospitals and their benefit to the community.
    Specifically, the tax-exempt status and executive compensation practices have been scrutinized. This is an
    important consideration for physicians who are considering hospital employment, as the tax-exempt status of
    the hospital allows greater latitude in subsidizing
    employee-physician salaries. Without this exemption, a
    theoretic reduction in physician salaries in employed
    situations could occur.10

    Other Options
    One possible hybrid employment option available to
    physicians involves contracting with a hospital to provide orthopaedic care while maintaining physician
    ownership of the medical practice. This scenario could
    exist under many forms, with the most common being
    a management services agreement.
    A management services agreement is a business
    agreement that outlines services provided by a physician group, and then that group is paid directly by the
    hospital. This would be similar to using consultants or
    outside managers in private business where those personnel are not employees of a business, but rather work
    for a business for a given amount of time with a welldefined reimbursement schedule. Businesses can experience cost savings when using consultants in a way that
    decreases the number of full-time employees that they
    use. Expenses for recruitment benefits and bonuses can
    be theoretically bypassed in a management services
    agreement.
    Hospitals are also exposed to these expenses and
    would be in a situation where physicians are hired to
    work at the hospital as an employee. By contracting
    with the physician group for specific medical services or
    service lines, there would be a theoretic reduction in
    cost. Other advantages would include defining the
    length of the contract rather than creating an employment agreement between the hospital and the physician.
    This would allow the contract to be reworked on a periodic basis and avoid the process of hiring and firing.
    From a physician standpoint, working under a management services agreement is attractive. Physicians can
    negotiate on the front end with the hospital regarding
    the amount of work they provide and the reimbursement per work unit used (relative value units could be
    used as quantification for work in many instances).
    This process would allow the physician to skip the process of billing and submitting claims and would decrease the physicians overhead by decreasing the need
    for billing and coding staff.
    Another benefit to physicians would be negotiating a
    base salary that would be paid on a monthly or quarterly basis. This guarantee would allow a consistent in-

    Orthopaedic Knowledge Update 10

    123

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    come for the physician and also create an alliance between the hospital and the physician group. Both
    entities would have the same incentive to recruit patients to be served by the physicians under the management services agreement. The hospital could use this as
    leverage for the physician group when discussing referrals with other employed or engaged physician groups,
    such as a primary care. As a part of a management services agreement, clinical comanagement agreements
    could be drafted. Physicians and hospitals have been
    asked by the Centers for Medicare and Medicaid Services to launch focused quality initiatives. A clinical comanagement agreement could be a model used for integration of hospital services. In the arrangement,
    physicians will provide management of medical services
    with the hospital at a level that would exceed conventional medical director agreements. These arrangements
    typically occur between an organized group of physicians and a health care system. The physicians are then
    empowered to improve care, making a specific service
    line competitive in a targeted market but are also recognized financially for their efforts. The physicians
    would be charged with day-to-day management of hospital processes. It can benefit the hospital by engaging
    physicians in direct participation in design and oversight of a specific service line but also in capital and operating budgets. Physicians can also be engaged in assisting quality initiatives by setting up audit programs
    monitoring outcomes.
    A clinical comanagement arrangement can compensate physicians either on an hourly or annual basis with
    bonuses based on performance, clinical outcomes, patient satisfaction, or improved operating efficiencies.
    Compensation can also be awarded based on a predetermined, negotiated sum regardless of method of payment. Both parties are well served under the clinical comanagement model.
    Finally, physician groups can also pursue affiliations
    with hospitals through outpatient joint ventures. This
    involves capital investment on behalf of both the hospital and the physician group. This again aligns the hospital and the physician group in increasing the likelihood of success of the specific venture.
    Regardless of who owns a practice, physicians need
    to maintain a very active role in the management and
    direction of whatever practice situation they choose.
    Physicians who do not stay involved risk losing autonomy and the ability to direct the group in ways they
    deem appropriate.

    Concierge Medicine
    Concierge medicine is a term used to describe a personal relationship that a physician has with a patient,
    whereby the patient pays a retainer or an annual fee to
    maintain the relationship with the physician. Most concierge medicine relationships involve an enhanced form
    of care for the patient.
    Because of the personal attention provided by the
    physician and the extra time physicians take in admin124

    Orthopaedic Knowledge Update 10

    istering care, concierge medical practices often maintain a smaller number of patients in comparison with a
    conventional physician practice. The annual fees required vary widely based on the type of medicine practiced, the geographic region, and the exclusivity of the
    services being provided to the individual. More exclusive relationships have required up to $25,000 per year
    from a family to a specific physician.11
    The fee does not substitute for insurance and does
    not cover patients for consultations that would fall
    outside of the typical scope of the practice engaged.
    This means that outside of the care provided by the
    concierge medical specialists, and the access provided
    by the relationship, insurance typically is still purchased by the involved patients to cover medical costs
    that fall outside of the concierges relationship. This includes further laboratory procedures, medications,
    hospitalizations, and emergency care from other providers.
    Dr. Howard Maron is thought to be the first physician to offer concierge medicine as formal practice. He
    initially founded a company called MD2 International
    in 1996. His company currently charges patients up to
    $20,000 per year for exclusive primary care services.
    He reports that he has fewer than 100 patients in his
    practice and in an average day may be required to see
    only one or two patients. Prior to moving to a concierge situation, his patient roster numbered greater
    than 4,000. Many physicians employed in concierge situations are able to increase their yearly salary and also
    spend more time on their patients. One physician practicing in Boca Raton, FL, stated, Its allowed me to focus on being a doctor again.12
    Reported advantages include spending more time
    with each patient and having the time to research each
    individual complaint that a patient brings to the physician. Physicians also report less stress regarding financial concerns due to declining reimbursements. Many
    physicians report increased patient compliance and better outcomes when their concierge patients are compared with those in a more conventional practice.
    Orthopaedic applications in a concierge medicine
    situation could include a conventional model, which
    would provide exclusive orthopaedic care for an individual or an individuals family. This is not attractive to
    most patients, though, because of the limited frequency
    with which most visit the orthopaedic surgeon.
    Another possibility would include increased patient
    access and timeliness of that access with a physician or
    group in return for an upfront annual retainer fee. This
    retainer would ensure that the patients would receive
    timely consultations with physicians of their choice.
    Other services that could be provided would include orthopaedic screening, house calls, or even emergency department visits in some situations. The concept of access is important to consider. The average age of the
    United States population is rising, and that population
    will require more orthopaedic care. There is a relatively
    static number of US orthopaedic surgeons, so providing
    care when the patient requests it may hold real value.13
    Assuring access in an environment of scarcity may ulti-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 10: Practice Management

    mately be the key when the concept of concierge medicine is considered.


    Concerns with concierge medicine include abandonment of existing patients, care for indigent or uninsured
    patients, and the perception that only the rich could afford this type of care. The current economic and political climate also does not easily lend itself to a concierge situation.
    A more likely scenario in the field of orthopaedics
    would be up-front guarantees for patients to ensure access to their orthopaedic surgeon of choice. Current
    legislation regarding health care reform will in all likelihood determine future directions for concierge medicine.

    One of the most critical aspects of running a successful


    medical practice or business involves setting up a successful management structure. Many practices do not
    have a formal outline of their management practices
    but rather settle into a method of governance based on
    past history or ease of administration.
    Successful forms of management in a medical practice have key characteristics in common.14 First, forms
    of governance within a practice need to allow the practice principals or shareholders to make decisions on
    major issues impacting the business. There has to be
    shared acceptance of responsibility by the principals in
    a group for the decisions they make. If no one in the
    group is ultimately held accountable for the decisions,
    then key decision makers would never be rewarded for
    good decisions and bad decision makers would never
    be educated. Shareholders need adequate clerical and
    administrative support provided by their staff to run
    day-to-day activities so the shareholders can focus on
    the major issues impacting the business. If the shareholders are required to address day-to-day activities
    that would otherwise keep them from efficiently and effectively seeing patients, then the income stream of the
    medical practice may suffer. Efficient and cost-effective
    support provided by clerical and administrative staff is
    key in the overall management of a medical practice.
    A commonly overlooked characteristic of a successful practice is having a well-thought-out mission statement.14 A mission statement should define the services
    that are provided by the group and the geographic region where those services are provided. It should also
    address why those services are being provided in a specific geographic region and when the services are available. If the mission statement is not given the attention
    that it deserves, it will be poorly done and not beneficial to the practice.
    Medical practices need legal agreements that document practice structure. Articles of Incorporation or
    Ownership, such as exist with S Corps, C Corps, partnerships, and LLCs, need to be documented and easily
    accessible for the group. Along with those documents,
    bylaws of the group are also critical to maintain. This
    would include documents outlining buying into a prac-

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    Governance

    tice and exiting a practice, employment contracts, and


    standards of care and professionalism. Effective forms
    of governance provide a framework for good professional relations between practice principals and support
    staff. Behavior of the principals needs to be assessed
    and monitored, and standards need to be placed on this
    behavior. Well-outlined standards allow the principals
    themselves to assess their own behavior and set or
    modify standards as appropriate. A standard for work
    quality also needs to be outlined, specifically regarding
    patient care. From a quality standpoint, the group is
    benefitted not only by the improved outcomes but also
    by having a quality assurance program in place. When
    obtaining professional liability insurance, a quality assurance process often is necessary and in some instances can lower rates.
    Work expectations such as time off, on-call responsibilities, and day-to-day responsibilities need to be
    documented and well outlined, especially within a
    larger group. Including the shareholders in the formulation of these work expectations engenders a sense of
    ownership from the members of the group, and also decreases the risk of having a disgruntled member failing
    to uphold his or her end of the bargain when it comes
    to work effort. Organizational structure needs to be
    formally defined, providing all the employees with a
    role and a template defining who they report to and
    who they are responsible for.
    Finally, the way that the group financially rewards
    work needs to be well defined and easy to follow for
    the owners and employees of the group. Compensation
    formulas need to recognize not only work effort but
    also the ability to gather revenue. Compensation formulas may need to be modified on a periodic basis;
    however, it is imperative that all the partners are included in the process of computing the compensation
    formula.
    Work plans outline pathways to achieve short- and
    long-term goals, and should be updated on at least an
    annual basis to reflect the mission of the group but also
    reflect the individual needs of group members. A lack
    of planning can contribute to financial instability, high
    turnover, and high levels of dissatisfaction. The plan
    should address the description and intensity of the services that will be provided by the group, the supporting
    activities involved in maintaining those services, any
    marketing initiatives that will be instituted to support
    the group, the anticipated staffing requirements to support the group, planning in terms of physical facility,
    and investments in practice infrastructure.
    A good governance strategy is important to medical
    groups in several different ways. Consistent management strategies will improve efficiency, allowing workers to maximize their potential. This improved efficiency will often translate into increased revenues
    and/or decreased expenses. In the event of an audit, a
    consistent, well-documented governance system will allow information to be easily obtained by an outside auditing firm. More favorable audits typically will result
    in lower penalties in the event of a problem being discovered.
    125

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    Consistent, well-planned governance can also lower


    the groups risk of litigation. Intraoffice relationships
    between personnel and physicians are always well defined within a well-run group. People who understand
    and accept their roles are happier in their jobs, and
    happy employees and partners would be less apt to sue
    based on personnel decisions. A satisfied workforce
    also relates better to customers. Patients and payers
    who sense a satisfied workforce will likely have a better
    interaction during their exposure to the group and are
    less likely to sue.
    When examining the organizational structure of a
    group, there are signs of organizational dysfunction to
    look for. Inability to obtain or out-of-date corporate
    documents often signal a lack of organizational control
    within a group. Physician contract disputes may indicate a dysfunctional organizational structure. Employees in a dysfunctional organization can exhibit a disdain for authority. Principals of the group may exhibit
    inappropriate, selfish behavior or act in a unilateral
    fashion while not risking their personal position within
    the group. Many times, selfish or inappropriate behavior may involve the management of money. Many times
    the shareholders themselves will exhibit selfish behavior, specifically as it relates to money. In addition, principals of the group may commonly exhibit inappropriate behavior, and are sometimes disrespectful toward
    staff. They may actively act in a unilateral fashion and
    will not risk their personal position in the group to stop
    illegal or immoral behavior.
    Strategies to improve governance within a group include engaging the support of the practice administrator. Many of the issues determining successful governance need the full support of the administrator. The
    administrator has a very large stake in this and is critical to the development and success of a governance
    strategy.
    Principals within the group need to be educated regarding the importance of governance. Unless there is
    buy-in to a governance strategy, it is doomed to fail.
    One way to educate partners is to discuss governancerelated issues at business meetings and continue to update members when changes occur in governance strategies. Meetings need to be held at least on an annual
    basis and effectively run. Protocols should be established to manage disagreements that may arise and
    should be followed when other techniques of conflict
    resolution fail.
    Corporate documents should be reviewed annually
    to make sure they remain relevant. Changes to these
    documents need to be recommended after their review.
    If specific documents that have been mentioned above
    do not exist, then they need to be created, and the principals of the group should be engaged in this process.
    It is important to remember that governance does
    not happen on its own. It is a learned behavior that will
    not improve overnight. When good governance is absent, there will be resistance to change, but over time,
    most principals will realize the benefits of having a stable governance strategy in place.
    126

    Orthopaedic Knowledge Update 10

    Electronic Medical Records


    As of 2009, EMRs are at the forefront of medicine.
    Currently less than 10% of orthopaedic practices use a
    full EMR technology or technologies; however, the current US governments proposed stimulus package offers
    up to $44,000 per physician (up to $65,000 in some
    underserved areas) to be used to adopt EMRs with a
    national standard. Costs for EMR adoption have been
    estimated to be $44,000 per physician, with $8,500 for
    annual maintenance. There are annual hardware costs
    and also interest costs to consider if these systems are
    financed.15 The thought is that EMRs can create efficiencies and savings in medicine as well as high-quality
    recordkeeping and the avoidance of errors.8 It is difficult to measure the return on investment in smaller to
    medium-sized practices, especially when considering
    the cost of these systems and the verification of real or
    perceived quality improvement. Nonetheless, most
    agree that using EMRs will change future practice patterns. It should be noted that there are challenges in
    adopting EMRs and that failure rates exist.
    A full EMR helps document pertinent patient demographic data, the patient encounter, and the physicians
    actions so that he or she gets paid. Advantages of a full
    EMR include the establishment of a database that uses
    medical terms for storing medical records, laboratory
    and imaging results, findings, and treatment actions.
    Additionally, a properly implemented EMR can facilitate patient interaction and speed office work flow in
    comparison with traditional paper charts. Ultimately, it
    is hoped that the EMR will decrease practice operating
    costs (overhead), including those associated with paper
    charts, issues with evaluation and management coding
    compliance, real-time notes, and transcription. Disadvantages include implementation and a learning curve,
    procedural changes that affect office work flow, and
    high start-up costs.
    EMR implementation challenges involve creating
    templates, installing and maintaining workstations, and
    changing physician behavior pertaining to the entry of
    clinical information. Clinical information can be input
    by point and click, which is the preferred route by
    surgeons; voice recognition; keyboarding; and scanning.
    Work flow requires new processes and physician and
    staff training, and the dynamic of the physician/patient
    encounter is changed. It is important to have physician
    leaders in this regard in order to obtain successful results. EMRs interface with other technologies, including billing systems and picture archiving and communication systems.
    The US government currently is developing the
    Health Information Technology for Economic and
    Clinical Health (HITECH) Act, better known as part of
    the stimulus package of President Obamas administration. Final regulations are forthcoming. Terms that
    need to be defined in this Act include meaningful use
    and reporting requirements. Implementation of the
    EMR mandate will begin in 2011, with $18 billion ear-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 10: Practice Management

    management of the successful practice. Having a successful business is difficult, and organized, welldocumented governance will put orthopaedic surgeons
    in the best position to succeed.

    Annotated References
    1.

    Wann S: Nonprofit hospitals buying up cardiology practices. Cardiology Today. http://www.cardiologytoday.


    com/view.aspx?rid=33243. Published December 1,
    2008. Accessed August, 29 2009.
    The author discusses the relationship between cardiology groups and nonprofit hospitals. Specifically, the
    risks and benefits of hospital ownership are outlined.

    2.

    Boblitz MC, Thompson JM: 7 steps for evaluating primary care practice ownership: Burned by physician
    practice ownership in the past? Chances are your strategy was ill-fated from the start. BNET. http://
    findarticles.com/p/articles/mi_m3257/is_11_58/
    ai_n7069413/. Published November 2004. Accessed
    August 29, 2009.
    The authors examine practice ownership from the hospital perspective. A seven-step approach is offered to analyze primary practice ownership.

    3.

    Bakhtiari E: Facilities learn from physician management


    and compensation mistakes. HealthLeaders Media.
    http://www.healthleadersmedia.com/content/92849/
    topic/WS_HLM2_HOM/Facilities-learn-fromphysician-management-and-compensationmistakes.html. Published October 4, 2007. Accessed
    August 29, 2009.
    The author outlines the risks and benefits of physician
    hospital employment.

    4.

    About MedPAC. MedPAC. http://www.medpac.gov/


    about.cfm. Accessed August 29, 2009.
    The Medicare Payment Advisory Commission (MedPAC) is a congressional agency established by the Balanced Budget Act of 1997 (P.L. 105-33) that advises
    Congress on issues affecting Medicare.

    5.

    Leys T: Waterloo hospital pays feds $4.5 million. Des


    Moines Register. http://www.desmoinesregister.com/
    apps/pbcs.dll/article?AID=2009908260358. Published
    August 26, 2009. Accessed August 30, 2009.
    The author reports on a hospital being fined by the US
    attorneys office for reportedly overpaying physicians in
    an alleged scheme to boost its business.

    6.

    Ross JR: Radiology practices fight declining technical revenues. http://www.imagingbiz.com/articles/view/


    radiology-practices-fight-declining-technical-revenues/.
    Published February 15, 2010. Accessed August 19,
    2010.
    This article outlines declining technical revenues for radiology procedures.

    Summary
    The technical aspects of running an orthopaedic practice continue to become increasingly more complex.
    Remaining informed and engaged is key to making decisions that benefit the individual and the practice.
    Questions regarding practice ownership will continue
    to be discussed in the foreseeable future. Although
    there may be some short-term benefits related to hospital ownership, surgeons need to be cognizant of the loss
    of autonomy this situation brings. As health care reform evolves, new business relationships between doctors and hospitals will also develop. The successful
    business will be one that can maintain income streams
    while limiting overhead growth.
    Concierge medicine allows the orthopaedic practice
    an opportunity to continue to provide care to everyone
    in addition to a level of care that is perceived as enhanced by some. A guarantee of prompt, efficient, and
    patient-centered service may allow surgeons to market
    themselves to patients outside of the current practice
    model. Governance will continue to be important in the

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    marked for funding. Funds are to be paid over 5 years.


    The take-home message is that the physician has time
    to do his or her homework and evaluate how to best
    implement these developments in his or her practice.
    Other considerations would be whether or not the physician has a current EMR. If so, it may not meet the
    certification requirements, which are yet to be defined.
    As for EMR standards, few systems have
    orthopaedic-specific modules or templates, although
    some exist. There is also no defined set of requirements
    for an orthopaedic practice or for EMR system service.
    Defined training programs are lacking, although these
    are likely to arise in the next several years. Current concerns and also part of the HITECH Act are that there is
    interoperability between EMR systems. The current
    Health Level-7 standards are generally met by most
    EMRs; however, there is little or no interoperability between systems. Stimulus legislation required for formal
    certification, currently a certifying body, the Certification Commission for Healthcare Information Technology, deals with interoperability, date of security, privacy, and compliance in prescribing health information
    networks and ambulatory and hospital EMRs.
    Failure rates are a concern; learning and adoption
    curves are not underestimated. Challenges include the
    integrity of the clinical information, usability, quality of
    care, and work flow guided by the record and malpractice protection, sometimes with a lack of complete documentation. All information needs to be checked for
    evaluation management compliance.
    The Practice Management Committee created in
    February 2007 The Electronic Medical Record: A
    Primer for Orthopaedic Surgeons. This document is
    free to members and can be accessed at www.aaos.org.
    The document explains the economics of EMRs, lessons learned, standards, data file security, and the political landscape.

    127

    Section 1: Principles of Orthopaedics

    7.

    5-Year Carryback of 2008 and 2009 Net Operating


    Losses (NOLs) for Eligible Small Businesses. http://
    www.irs.gov/formspubs/article/0,,id=207330,00.html.
    Accessed August 19, 2010.
    This Web site describes two laws that can affect businesses with net operating losses.

    8.

    American Association of Orthopaedic Executives


    (AAOE): 2008 Orthopaedic Benchmark Survey, 2009.

    11.

    Sack K: Despite Recession, Personalized Health Care


    Remains in Demand. New York Times. http://
    www.nytimes.com/2009/05/11/health/policy/
    11concierge.html. Published May 10, 2009. Accessed
    August 30, 2009.
    The author describes concierge medicine and its appeal
    despite the recent downturn in the economy.

    12.

    OShaughnessy P: Michael Jacksons death puts concierge doctors in the spotlight. NY Daily News. http://
    www.nydailynews.com/entertainment/michael_jackson/
    2009/07/05/2009-07-05_concierge_doctors_
    for_the_rich__famous.html#ixzz0Le1XQWMl).
    Published July 5, 2009. Accessed August 30, 2009.
    The author outlines the risks associated with the practice of concierge medicine.

    13.

    Medscape. http://www.medscape.com/viewarticle/588854.
    Accessed August 30, 2010.
    This article outlines anticipated shortages in the orthopaedic workforce.

    14.

    Fisher SE: Six steps to effective group practice governance. http://www2.aaos.org/aaos/archives/bulletin/aug05/


    fline9.asp. Accessed August 19, 2010.
    The development of effective governance is discussed.

    15.

    Miller RH, West C, Brown TM, Sim I, Ganchoff C: The


    value of electronic health records in solo or small group
    practices. Health Aff (Millwood) 2005;24(5):11271137.

    A survey comparing financial information from multiple


    orthopaedic practices is presented.

    1: Principles of Orthopaedics

    9.

    10.

    128

    ACR Action Alert: Congressmen Anthony Weiner (DNY) and Bruce Braley (D-IA) to Offer Self-Referral
    Amendment to House Health Care Reform Package.
    RadRounds http://www.radrounds.com/profiles/blogs/
    acr-action-alert-congressmen. Published July 20, 2009.
    Accessed August 29, 2009.
    This radiology Web site encourages congressional support of HR 2962, a bill designed to close in-office ancillary service exemptions for MRI, CT and positron emission tomography.
    Internal Revenue Service. http://www.irs.gov/pub/irstege/execsum_hospprojrept.pdf.
    An IRS study of nonprofit hospitals was conducted for
    the IRS and other stakeholders to better understand
    nonprofit hospitals and their community benefit and executive compensation practices.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 11

    Polytrauma Care
    Hans-Christoph Pape, MD, FACS

    Philipp Lichte, MD

    Initial Assessment

    Hemorrhagic Shock, Volume


    Treatment, and Fracture Care
    From the orthopaedic point of view it is understood
    that early fracture stabilization is a major goal. Prior to
    clearing a patient for an orthopaedic procedure, severe

    Neither Dr. Pape nor Dr. Lichte nor any immediate family member has received anything of value from or owns
    stock in a commercial company or institution related directly or indirectly to the subject of this chapter.

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    In patients with severe injuries, fatal outcome continues


    to be a major concern.1 The trimodal pattern of death
    described by Trunkey is a valuable tool to assess the
    treatable conditions. Death occurring within the first
    hours after trauma is usually due to severe hemorrhage
    or head trauma. In patients who succumb within several hours, death is usually a result of airway, breathing, or cardiovascular issues and has been identified to
    be potentially preventable. The third mortality peak is
    caused by sepsis and multisystem organ failure and appears more than 1 week after trauma.
    Polytrauma may be defined as injuries to at least two
    organ systems associated with a potentially lifethreatening condition. To quantify the severity of multiple injuries, several trauma scores have been described. The most common ones are the Injury Severity
    Score (ISS) and the New Injury Severity score, both of
    which are based on the Abbreviated Injury Scale (AIS).
    Injuries of six body regions (head, face, chest, abdomen, extremities [including pelvis], and external structures) are classified from 1 (mild) to 6 (usually fatal).2
    Based on the ISS, a polytrauma is considered if the ISS
    exceeds 16 points. To achieve reliable data, clinical and
    radiologic assessment should be completed. During the
    ongoing process of achieving reliable patient information, the clinical scenario can change. Hemorrhage can
    become more severe, or improvement can be achieved
    by volume therapy. In addition to the extent of the anatomic injuries, assessment of the pulmonary and hemodynamic status is required as described in the Advanced Trauma Life Support (ATLS) algorithm. ATLS
    requires ruling out other causes of acute decompensation such as tension pneumothorax, cardiac tamponade, and herniation.

    hemorrhage should be identified and controlled. Ongoing hemorrhagic shock has to be ruled out, and it is important to recognize that alterations in pulse and blood
    pressure are late signs, especially among patients
    younger than 40 years. Due to the cardiovascular reserve of younger patients, the extent of hypovolemia
    can be underestimated in adolescents and young adults.
    In these patients, capillary refill is a valid clinical parameter. Another secondary parameter is urine output,
    along with arterial pH, base excess, and plasma lactate
    levels. The plasma lactate levels may serve for assessment of the end points of volume therapy. The four major sources of bleeding are usually external, thoracic,
    abdominal, and pelvic.
    External blood loss is usually apparent. The exact
    quantity of blood loss may be difficult to assess, especially in cases of prolonged extrication. Initial treatment before rushing the patient to the operating room
    may be the use of a compressing towel or a tourniquet.
    Internal sources of hemorrhage can be identified by
    clinical examination, abdominal ultrasound, or CT
    scan. Unstable pelvic fractures can also be a source of
    massive hemorrhage, requiring acute external tamponade by pelvic sheets or binders, or internal tamponade
    during surgery. Some centers apply an external fixator
    or a pelvic clamp. Selective angiography and embolization of the source of bleeding is becoming more common.

    Principles of Stabilizing the Cardiovascular


    Status of a Multiply Injured Patient
    Volume therapy should be administered using several
    large-bore intravenous lines. Although some controversy remains, crystalloid fluids are widely used. The
    use of hypertonic saline for small-bolus infusions seems
    to be beneficial for those with intracranial injuries but
    not for polytraumatized patients without brain injury.
    In severe hemorrhage, replacement of red blood cells is
    necessary to improve oxygen-carrying capacity. If there
    is no improvement with volume treatment, other causes
    such as pneumothorax should be considered and the indications for chest drains should be evaluated.
    Recent data confirm that concentrated amounts of
    hemoglobin, 5 g/L, may be acceptable for normovolemic volunteers. In trauma patients, concentrations
    between 7 and 9 g/L appear to be sufficient. Dilution
    effects and depletion of components of the coagulation
    cascades represent one aspect of posttraumatic coagulopathy. Hypothermia and acidosis can cause further

    Orthopaedic Knowledge Update 10

    129

    Section 1: Principles of Orthopaedics

    Table 1

    Criteria to Diagnose a Borderline Condition


    ISS > 40
    Body temperature below 95F
    Multiple injuries (ISS > 20) in combination with thorax
    trauma
    Multiple injuries in combination with severe abdominal or
    pelvic injury and hemorrhagic shock on admission
    Radiographic evidence of pulmonary contusion
    Bilateral femur fractures

    1: Principles of Orthopaedics

    Moderate or severe head trauma in addition to other major


    fractures
    (Adapted with permission from Pape HC, Giannoudis P, Krettek C. The timing of
    fracture treatment in polytrauma patients: Relevance of damage control
    orthopaedic surgery. Am J Surg 2002;183:622-629.)

    Figure 1

    Approach for ipsilateral femur and tibia fractures, treated by initial retrograde femoral and
    antegrade tibial nailing in a stable patient.

    deterioration and should be avoided or corrected in a


    timely fashion. Replacement of blood products and alternate strategies such as recombinant factor VII in selected cases may be of value.

    Grading of the Patient Condition


    Completion of the initial assessment implies the diagnosis of major fractures and the cardiovascular, pulmonary, and inflammatory status as a decision guide for
    surgical therapy. Four categories have been identified:
    stable, borderline, unstable, and in extremis.3
    Figure 2

    Stable Condition
    Stable patients have no immediate life-threatening injuries, respond to initial interventions, and are hemodynamically stable. They are normothermic and show no
    physiologic abnormalities. These patients should undergo initial surgical fixation of their major fractures4
    (Figure 1).
    Borderline Condition
    Patients in this category respond to resuscitation but
    may have a delayed response to resuscitation and can
    have other sources of occult bleeding.5 The criteria
    listed in Table 1 have proved useful to classify a patient
    as borderline. In these patients, a higher possibility of
    deterioration of the patients condition has to be considered. If these patients are stabilized appropriately,
    early definitive care can be used safely in the treatment
    of their major fractures.6 In case of deterioration, conversion to damage control techniques should be considered. Some authors consider damage control nailing to
    130

    Orthopaedic Knowledge Update 10

    Extremity of an unstable patient with bilateral


    open femur fractures, liver laceration, and lung
    contusions. The external fixator is placed anteriorly to allow treatment in the rotatory bed
    (RotoRest, Kinetic Concepts, San Antonio, TX).

    minimize the duration of initial surgery. In these cases,


    an unreamed, unlocked nail is used initially and locking
    and/or further reduction is performed secondarily.
    Unstable Condition
    If patients do not respond to initial resuscitation and
    remain hemodynamically unstable, a rapid deterioration in the patients condition can occur. Surgical treatment consists of lifesaving surgery followed by temporary stabilization of major fractures7 (Figure 2). The
    patient should then be monitored in the intensive care
    unit. Complex reconstruction procedures should be
    postponed several days until the patient is stable and
    the acute immunoinflammatory response has subsided.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 11: Polytrauma Care

    In Extremis Condition
    In these patients, uncontrolled bleeding occurs and the
    response to resuscitation is inadequate. Hypothermia,
    acidosis, and coagulopathy are present, thus allowing
    lifesaving procedures only. Reconstructive surgical procedures can be done in course, if the patient survives.8

    Interactions Between Hemorrhage,


    Coagulation, Hypothermia, and Inflammation

    Management of Extremity Injuries


    Fracture stabilization is important to reduce pain, minimize fat embolization, and allow for early patient mobilization. Primary definitive osteosynthesis is the best
    way to achieve this goal. Usually, temporary external
    fixation, splints, or casts should be avoided. Exceptions
    may apply according to the status of the patient (Tables
    2 and 3).

    Grading of Local Injury


    Severity in Closed Fractures
    The assessment of true soft-tissue damage in closed
    fractures may be difficult immediately after injury. Both
    a puncture wound in an open fracture and a skin contusion can represent similar damage to the skin barrier.
    The result can be skin necrosis, resulting in increased
    risk of infection. Early quantification of the soft-tissue
    injury should be attempted by using scoring systems, as
    shown in Table 4.
    Special Situations: Crush Injury
    In the presence of severe soft-tissue injuries, complete
    dbridement of necrotic tissue is crucial. In a polytrauma situation, amputation is the treatment of choice
    more frequently than in isolated fracture management.
    Antibiotic coverage should be instituted, and some centers advocate the use of hyperbaric oxygen therapy. The
    most important focus of therapy should be to minimize
    tissue necrosis and the risk of secondary infection. Repeated revisions and staged surgical dbridements are
    required to achieve this goal.

    Management of Open Fractures


    Primary surgical therapy in open fractures implies dbridement, extensive irrigation, assessment of the dam-

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    Various interactions induced by hemorrhage occur that


    affect the cascade systems of coagulation, hypothermia,
    and inflammation. Ongoing hemorrhage can cause sustained coagulopathy and disseminated intravascular coagulation. Also, hypothermia can induce a coagulopathic state. Both systems also interfere with
    inflammation. Thus, all four systems can interfere with
    each other and cause another system to deteriorate.
    The assessment of just a single parameter or end point
    of resuscitation is not sufficient. Table 2 summarizes
    various staging systems of patients with multiple injuries and reflects the four different systems and patient
    status.

    age, and fixation of the fracture. The first careful assessment is an important step for planning the
    therapeutic strategy. Knowledge of the extent of the
    vascular and nerve damage is essential in order to decide whether to reconstruct or amputate a severely injured limb. Other important factors include the time
    and mechanism of injury, energy of causative force, and
    severity of the fracture. Open fractures following lowenergy trauma produce soft-tissue damage that often is
    minor. These fractures usually can be treated in a manner similar to that of closed fractures after the initial
    dbridement.
    Many fracture types in polytraumatized patients can
    be handled in a manner similar to that of isolated injuries. Intra-articular open fractures require special treatment strategies. Usually, a two-step strategy consisting
    of initial dbridement followed by reconstruction of the
    joint surface is advised. Often, the joint surface is reduced by temporary fixation with Kirschner wires followed by fixation with lag screws and adjusting screws.
    After consolidation of the soft tissue, definitive osteosynthesis is achieved. Some authors favor the use of a
    hybrid fixator system.

    Management of Bilateral
    Fractures and Fracture Combinations
    Simultaneous treatment can be a useful concept for the
    treatment of bilateral fractures. In bilateral tibia factures, both legs can be prepped and draped simultaneously. Because of the handling of the fluoroscope, fixation should be performed sequentially. The same
    process applies for bilateral femur fractures. In these injuries, a higher kinetic energy has occurred and additional injuries imply a higher risk of acute respiratory
    distress syndrome (ARDS) and multiple organ dysfunction syndrome (MODS).9,10 If the condition of the patient deteriorates, external fixation should be considered. For the management of ipsilateral femoral and
    tibia fractures, a staged management is advised, as
    shown in Table 3.

    Unstable Pelvic Injuries


    Clinical and radiologic examination of the pelvis are
    part of the initial assessment. Pelvic injuries can be classified on the basis of the examination results considering the history of the trauma.11 Type A fractures include stable fractures of the anterior pelvic ring that do
    not require surgical treatment. Type B injuries are characterized by partially intact posterior structures. Rotational instability may be possible. Open-book fractures
    with externally rotated alae have an increased risk of
    hemorrhage complications and urogenital lesions.
    However, type B injuries may initially be in internal rotation, which results in bony compression and selfstabilization of the pelvis. Type B injuries require osteosynthesis of the anterior pelvic ring only.12
    The differentiation of type B and C fractures may be
    difficult.11 A CT scan can give important additional information on stable patients. If a CT scan is not available, inlet and outlet radiographic views should be ob-

    Orthopaedic Knowledge Update 10

    131

    Section 1: Principles of Orthopaedics

    Table 2

    Criteria Used to Facilitate Determination of the Clinical Condition of Multiple-Trauma Patientsa

    1: Principles of Orthopaedics

    Patient Status
    Factor

    Parameter

    Stable

    Borderline

    Unstable

    In extremis

    Shock

    Blood pressure
    (mm Hg)

    100

    80-100

    <80

    70

    Blood units given in a


    2-h period

    0-2

    2-8

    5-15

    >15

    Lactate levels (mg/dL)

    Normal range
    according to local
    laboratory

    2.5

    >2.5

    Severe acidosis

    Base deficit level


    (mmol/L)

    Normal range
    according to local
    laboratory

    No data

    No data

    >6-8

    ATLS classification

    I
    (normovolemia)

    II-III
    (slight shock)

    III-IV
    (severe shock)

    IV
    (life-threatening
    shock)

    Platelet count (/mm3)

    >110,000

    90,000- 110,000

    <70,000- 90,000

    <70,000

    Factor II and V (%)

    90-100

    71-89

    50-70

    <50

    Fibrinogen (g/dL)

    >1

    <1

    Disseminated
    intravascular
    coagulation

    D-dimer (g/mL)

    Normal range
    according to local
    laboratory

    Abnormal

    Abnormal

    Disseminated
    intravascular
    coagulation

    Coagulation

    Temperature

    C (F)

    <33

    33-35

    30-32

    30

    Soft-tissue
    injuries

    Lung function;
    Pao2/Fio2 (mm Hg)

    350-400

    300-350

    200-300

    <200

    Chest trauma scores;


    AIS

    AIS I or II
    (eg, abrasion)

    AIS 2
    (eg, 2-3 rib
    fractures)

    AIS 3
    (eg, serial rib
    fixation >3)

    AIS 3
    (eg, unstable chest)

    Chest trauma score;


    TTS

    0 concussion

    I-II slight thoracic


    trauma

    II-III moderate

    IV severe

    No, slight,
    moderate,
    severe

    Abdominal trauma
    (Moore)

    grade II

    grade III

    Grade III

    Grade III

    No, slight,
    moderate,
    severe

    Pelvic trauma (AO


    classification)

    A type

    B or C type

    C type

    C type
    (crush, rollover abd.

    No, slight,
    moderate,
    severe

    External

    AIS I-II
    (eg, abrasion)

    AIS II-III
    (eg, multiple tears
    >20 cm)

    AIS III-IV
    (eg, <30% burn)

    Crush injury (>30%


    burn)

    Three of the four criteria should be met to classify for a certain grade. Patients who respond to resuscitation qualify for early definitive fracture care provided that
    prolonged surgeries are avoided. ATLS = Advanced Trauma Life Support; AIS = Abbreviated Injury Scale; PaO2 = partial pressure of oxygen in arterial blood; FiO2 = Fraction
    of inspired oxygen; TTS = thoracic trauma score.
    It is of note that the clinical status can change rapidly. The initial assessment therefore can change during the first hours. Also, the existing scores have not necessarily been
    designed to differentiate between borderline, stable, and unstable patients nor has this table been validated prospectively. Nevertheless, it may be helpful to facilitate an
    overview of several clinical conditions and may be a guide to treatment.
    (Adapted with permission from Pape HC, Giannoudis P, Krettek C, Trentz O: Timing of fixation of major fractures in blunt polytrauma: Role of conventional indicators in
    clinical decision making. J Orthop Trauma 2005;19:551-562.)

    tained. Type C fractures are characterized by


    translational instability of the dorsal pelvis, which results in separation of one or both pelvic halves from the
    trunk. These injuries are associated with a high risk of
    hemorrhagic complications and concomitant injuries of
    132

    Orthopaedic Knowledge Update 10

    intrapelvic organs. Type C injuries require stabilization


    of the anterior and posterior pelvic ring.
    More than 80% of all unstable pelvic injuries are associated with multiple injuries. The goal of initial treatment of unstable pelvic injuries in multiply injured pa-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 11: Polytrauma Care

    Table 3

    Management of Ipsilateral Femur and Tibial Shaft Fractures


    Stable

    Borderline

    Unstable

    In extremis

    Femur: nail

    Femur:
    Femur:
    resuscitation successful; nail
    external fixation/traction
    resuscitation difficult: traction
    consider damage control
    nailing

    Femur: traction

    Tibia: nail

    Tibia: nail

    Tibia:
    external fixation/traction

    Tibia: traction

    N/A

    Femur: nail

    Femur: nail

    Femur: nail

    Tibia: nail

    Tibia: nail

    Initial treatment

    Staged treatment
    1: Principles of Orthopaedics

    N/A

    Table 4

    Soft-Tissue Injury Classification


    Soft-tissue injury

    Type of fracture

    Closed fracture G0

    No or very minor

    Simple fractures, ie, caused by indirect


    trauma

    Closed fracture G1

    Superficial abrasions or contusions from internal


    fragment pressure

    Simple to moderate

    Closed fracture G2

    Deep, contaminated abrasions or local dermal and


    muscular contusions due to tangential forces
    Compartment syndrome

    Moderate to severe, usually caused by direct


    forces

    Closed fracture G3

    Extensive skin contusion or muscular destruction,


    subcutaneous decollement
    Obvious compartment syndrome

    Severe and comminuted

    Closed fracture G4

    Same injury as G3 with significant vascular damage

    Severe and comminuted

    tients is adequate stabilization and bony compression


    of the pelvis to avoid massive bleeding. Therefore, stabilization techniques with the patient supine are preferred during this primary period.

    Unstable Injuries of the Spine


    In all cases, the spine should be assessed with radiographs or CT scans. To rule out the presence of fragments in the spinal canal, further diagnostic procedures
    (MRI) are required.
    Surgical treatment of unstable spine injuries is mandatory. The length of immobilization and intensive care
    unit stay are significantly reduced due to internal fixation of the spine. Internal stabilization of spinal fractures (even without neurologic symptoms) has been advocated more commonly in the last few years.
    Closed reduction of unstable spine injuries without
    neurologic symptoms is performed in fractures of the
    cervical spine and rotational injuries of the lower thoracic or lumbar spine. In multiply injured patients,
    closed reduction may be difficult because of injuries of

    2011 American Academy of Orthopaedic Surgeons

    the extremities. In these cases, surgery is required for


    proper correction of rotation and axis.
    If bony fragments or an intervertebral disk are interposed or displaced into the spinal canal, open reduction
    and extraction of the fragment should be performed to
    avoid spinal cord injury.
    The standard approach to surgical management of
    the cervical spine is the ventral approach. Injuries of
    the thoracic or lumbar spine requiring dorsal and ventral stabilization should be treated in a two-stage fashion. Despite the presence of thoracic or intraabdominal injuries, prone positioning can be done if
    performed carefully.

    Intensive Care Unit Aspects


    One of the challenges in intensive care therapy is the
    management of ARDS and multiple organ failure. In
    polytraumatized patients a pulmonary parenchymal lesion (lung contusion) can alter pulmonary function di-

    Orthopaedic Knowledge Update 10

    133

    Section 1: Principles of Orthopaedics

    Table 5

    1: Principles of Orthopaedics

    Criteria for Patient Assessment on the Intensive


    Care Unit
    Input/output ratio

    Negative (> 500 mL) for 2 consecutive


    days

    Lung function

    PaO2 / FiO2 > 250


    No chest radiograph infiltrates

    Coagulation

    Platelet count 90,000/mm3 and rising,


    or no requirement for replacement
    of blood products

    Acid / base status


    Hepatic function

    Normal values for pH and base excess


    Hepatic malperfusion should be ruled
    out

    Cardiac function

    Vasopressors: none or minimal

    Inflammation

    Decreasing interleukin values


    (IL-6 < 500 and dropping)
    Figure 3

    rectly. In addition, vascular and endothelial permeability is increased in the entire body secondary to
    hemorrhagic shock. Increased water content in all organs occurs and in the lung it increases the risk of
    ARDS.
    Pulmonary failure usually develops first in MODS,
    the most severe complication after severe trauma. Onephase MODS is characterized by rapid failure of all organs, whereas in two-phase MOF, lung dysfunction is
    followed by cardiovascular and renal failure. To avoid
    two-phase MODS, ventilation strategies help decrease
    mortality. Once the full-blown syndrome of MODS has
    developed, treatment is based on the patients symptoms.
    Distinct criteria are known to be important when assessing a patient during the course of intensive care.
    First, hypothermia has to be normalized because it is
    known to interfere with coagulopathy induced by
    platelet loss and loss of coagulatory factors due to the
    initial hemorrhage. Second, the capillary leak caused by
    ischemia and blood loss is known to last for several
    days and usually peaks around day 3 or 4 after the initial injury. A positive input/output ratio usually is indicative of an ongoing capillary leak. A negative fluid balance of 500 mL or more should be present for a day or
    two before taking a patient to the operating room for a
    prolonged procedure. Third, coagulation factors should
    be normalized and platelet count exceeding 90,000/
    mm3 or rising for 2 consecutive days is a good parameter. Fourth, the chest radiograph should not show
    signs of edema or infiltration. Fifth, inflammatory parameters, such as proinflammatory cytokines (IL-6,
    IL-8) may be helpful, if available. Likewise, the systemic inflammatory response syndrome score can be
    counted to assess the inflammatory status as it has been
    shown to correlate with IL-6 levels. An overview of the
    intensive care unit assessment criteria is presented in
    Table 5. Usually, days 2 through 4 are difficult in terms
    of ongoing edema, coagulopathy, and inflammation,
    134

    Orthopaedic Knowledge Update 10

    Transverse wound with little contamination.


    Initial closure can be performed.

    whereas after day 6 the inflammatory status usually has


    normalized.

    Soft-Tissue Reconstruction
    Wound healing of multiply injured patients is complicated by the relative hypoxia of the tissues, which
    raises the risk of delayed wound healing and wound infections. Therefore, forced primary wound closure
    should not be performed.
    Small wounds can be closed (Figure 3) or covered
    with artificial skin replacements, or negative pressure
    used until the swelling decreases. Definitive closure of
    the wound or mesh graft transplantation is an option.
    For the past decade, the vacuum-assisted closure has
    been increasingly used for temporary closure of softtissue injuries and to prepare the wound for definitive
    closure. Advantages include low infection rates and
    proper granulation of the wound.
    If implants, bones, joints, or tendons are visible on
    the ground of the wound, every attempt should be undertaken to cover them rapidly with vital and wellperfused soft tissue (Figure 4). If wound coverage is not
    achieved within a few days, there is a sustained risk of
    infection and nonunions. Close cooperation between
    the orthopaedic surgeon and plastic surgery services is
    recommended for an optimal overall result.
    Medium-sized wounds can often be closed by local
    transposition of the surrounding tissue after mobilization. This secondary covering procedure should be performed in the period of 72 hours after trauma. Rotational flaps consist of different combinations of muscle,
    fascia, and skin and should be fit in the defect without
    tension. Among multiply injured patients it can be difficult to find enough healthy tissue to perform a local

    2011 American Academy of Orthopaedic Surgeons

    Chapter 11: Polytrauma Care

    Figure 4

    flap due to serial injuries. Distant flaps are often required in the treatment of these patients. Distant flaps
    are also indicated if the defect zone is too large to be
    covered with a rotational flap. Free microvascular flaps
    are usually preferred by plastic surgeons. However, it
    has to be kept in mind that prolonged surgical procedures stress the general condition of the patient. If a
    distant flap is required, the general condition should be
    kept in mind for this prolonged operation. Yet, coverage of the defect continues to be an urgent issue.

    Rehabilitation
    Mobilization of all major joints should be initiated during the course of the intensive care treatment. This may
    imply continuous passive motion therapy. Delayed and
    aggressive mobilization has been shown to increase the
    risk of heterotopic ossifications and should be avoided.
    On the ward these measures usually are accompanied
    by active exercises performed under supervision of a
    physical therapist. Mobilization should occur several
    times a day. Weight bearing is determined according to
    the combination of fractures and the fracture type.

    Annotated References
    1.

    Rotondo MF, Esposito TJ, Reilly PM, et al: The position


    of the Eastern Association for the Surgery of Trauma on
    the future of trauma surgery. J Trauma 2005;59(1):
    77-79.

    2.

    Baker SP, ONeill B, Haddon W Jr, Long WB: The injury severity score: a method for describing patients
    with multiple injuries and evaluating emergency care.
    J Trauma 1974;14(3):187-196.

    3.

    Pape HC, Giannoudis PV, Krettek C, Trentz O: Timing


    of fixation of major fractures in blunt polytrauma: Role
    of conventional indicators in clinical decision making.
    J Orthop Trauma 2005;19(8):551-562.

    4.

    Canadian Orthopaedic Trauma Society: Reamed versus


    unreamed intramedullary nailing of the femur: Comparison of the rate of ARDS in multiple injured patients.
    J Orthop Trauma 2006;20(6):384-387.

    5.

    Pape HC, Rixen D, Morley J, et al: Impact of the


    method of initial stabilization for femoral fractures in
    patients with multiple injuries at risk for complications
    (borderline patients). Ann Surg 2007;246(3):491-499.
    This was a prospective randomized study that eliminated patients at high risk for ARDS and multiple organ
    failure. Patients were randomized to acute intramedullary nailing of the femur versus external fixation. The
    authors separated stable from borderline multiple
    trauma patients and looked at the incidence of acute
    lung injuries that developed postoperatively. In stable
    patients, early definitive fixation of the femur was associated with a shorter ventilation time. In borderline patients, early definitive fixation was associated with a
    higher incidence of acute lung injury. The authors conclude that the indication for initial definitive fixation
    should be selected according to the condition of the patient.

    6.

    Pape HC, Giannoudis P, Krettek C: The timing of fracture treatment in polytrauma patients: Relevance of
    damage control orthopedic surgery. Am J Surg 2002;
    183(6):622-629.

    Summary
    Polytrauma may be defined as injuries to at least two
    organ systems associated with a potentially lifethreatening condition or an ISS higher than 16 points.
    The initial assessment should detect at first acute lifethreatening injuries. In patients with multiple injuries
    the clinical condition can change rapidly within the
    first hours after trauma. Next to severe head trauma,
    ongoing or uncontrolled hemorrhage is the major reason for the development of a life-threatening condition.
    The four sources of major bleeding usually derive from
    an extremity (vascular tear), thoracic, abdominal, and
    pelvic trauma. Four categories have been identified: stable, borderline, unstable, and in extremis. These four
    categories can help the surgeon decide whether the patients condition allows early definitive care of major

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    Tendons are visible. Coverage should be achieved


    as soon as possible.

    fractures or if temporary stabilization by external fixation is advised. The assessment to categorize these patients includes the volume status, pulmonary and renal
    function, body temperature, coagulation and acid-base
    status. The decision whether the patient is cleared for
    definitive surgery can be made on the basis of these parameters.
    From the orthopaedic point of view, stabilization of
    major extremity fractures is an important goal. The
    time points of stabilization are control of major, lifethreatening bleeding (minutes to hours); stabilization of
    major fractures (first day of surgery); planned revisions
    and complex fixations (fourth day after surgery and afterward); and late reconstruction (after the second
    week for example, maxillofacial).

    Orthopaedic Knowledge Update 10

    135

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    136

    7.

    Scalea TM, Boswell SA, Scott JD, Mitchell KA, Kramer


    ME, Pollak AN: External fixation as a bridge to intramedullary nailing for patients with multiple injuries
    and with femur fractures: damage control orthopedics.
    J Trauma 2000;48(4):613-621, discussion 621-623.

    8.

    Morshed S, Miclau T III, Bembom O, Cohen M, Knudson MM, Colford JM Jr: Delayed internal fixation of
    femoral shaft fracture reduces mortality among patients
    with multisystem trauma. J Bone Joint Surg Am 2009;
    91(1):3-13.
    The study used the US National Trauma Databank and
    included fractures of the femoral shaft; an ISS of greater
    than or equal to 15; and internal fixation of the femur.
    Five time periods were selected a priori. The authors
    used an inverse-probability-of-treatment-weighted analysis to estimate the risk of mortality for a defined treatment time. Their results document that definitive fixation in all but one (24 48 hours) of the four delayed
    treatment categories was associated with a significantly
    lower risk of mortality to about 50% of that expected
    with early treatment (< 12 hours). Also, patients with
    serious associated injuries demonstrated greater risk reductions from delayed fixation when compared with
    those with less serious or no abdominal injury. The authors conclude from this study that a cautious approach
    to early definitive femoral shaft fracture fixation among
    multisystem trauma patients should be performed, and
    reinforce this for patients who present with serious associated abdominal injuries.

    Orthopaedic Knowledge Update 10

    9.

    Nork SE, Agel J, Russell GV, Mills WJ, Holt S, Routt


    ML Jr: Mortality after reamed intramedullary nailing of
    bilateral femur fractures. Clin Orthop Relat Res 2003;
    415(415):272-278.

    10.

    Copeland CE, Mitchell KA, Brumback RJ, Gens DR,


    Burgess AR: Mortality in patients with bilateral femoral
    fractures. J Orthop Trauma 1998;12(5):315-319.

    11.

    Olson SA, Burgess A: Classification and initial management of patients with unstable pelvic ring injuries. Instr
    Course Lect 2005;54:383-393.

    12.

    Cothren CC, Osborn PM, Moore EE, Morgan SJ,


    Johnson JL, Smith WR: Preperitonal pelvic packing
    for hemodynamically unstable pelvic fractures: A paradigm shift. J Trauma 2007;62(4):834-839, discussion
    839-842.
    The authors describe a close cooperative effort between
    orthopaedic surgeons and general surgeons to perform
    initial surgical fixation of patients with unstable pelvic
    ring fractures. They brought them to the operating
    room and performed external or internal fixation and
    initial packing of major intrapelvic bleedings. Their results are in favor of this management plan. It is understood that the usage of pelvic binders also provides
    hemorrhage control temporarily, although it does not
    reduce the pelvic fracture anatomically.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 12

    Coagulation, Thromboembolism,
    and Blood Management in
    Orthopaedic Surgery
    Charles R. Clark, MD

    Venous thromboembolic disease and prophylaxis are


    subjects of controversy in orthopaedic surgery. Venous
    thromboembolism is a major risk in patients undergoing total hip and knee arthroplasty as well as repair of
    a hip fracture. In addition, patients sustaining major orthopaedic trauma including spinal cord injury as well
    as patients undergoing treatment of various other musculoskeletal conditions are at potential risk for thromboembolism. Morbidity and mortality are associated
    with both thromboembolic disease and prophylaxis.
    Various forms of pharmacologic and mechanical
    prophylaxis are available and are presented in the
    American Academy of Orthopaedic Surgeons guideline
    on prevention of pulmonary embolism.1 This clinical
    practice guideline was based on a systematic review of
    published studies of patients undergoing total hip and
    total knee arthroplasty to prevent pulmonary embolism.2 The guideline found no difference in the pulmonary embolism rate, death rate, or death related to
    bleeding from prophylaxis among different thromboembolic prophylactic measures1 (Table 1).
    The Surgical Care Improvement Program (SCIP) of
    the Centers for Medicare and Medicaid Services (CMS)
    was initiated in an attempt to minimize venous thromboembolic disease and includes pay-for performance
    programs. This program has focused additional attention on thromboembolic disease. Specifics of the basic
    guidelines will be presented later in this chapter. A
    2008 study determined the incidence, risk factors, and
    long-term sequelae of postoperative hematomas requiring surgical evacuation after primary total knee arthro-

    Dr. Clark or an immediate family member serves as a


    board member, owner, officer, or committee member of
    University of Iowa Hospitals and Clinics; has received
    royalties from DePuy; serves as a paid consultant to or is
    an employee of DePuy and Smith & Nephew; and has received research or institutional support from DePuy and
    Smith & Nephew.

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    Coagulation and Thromboembolism

    plasty and pointed out the potential for adverse sequela


    of anticoagulation.3 The authors found a significantly
    increased risk of the development of deep infection
    and/or subsequent major surgery in patients who returned to the operating room within 30 days after the
    index total knee arthroplasty for evacuation of a postoperative hematoma. The authors concluded that these
    results support all efforts to minimize the risk of postoperative hematoma formation. Consequently, when
    patients are managed with pharmacologic prophylaxis
    it is important to prevent the development of a postoperative hematoma, to monitor for the development of a
    hematoma, and to practice techniques that will minimize its occurrence.
    One study found that patients treated with aspirin or
    warfarin were somewhat less likely to have associated
    bleeding complications than were patients treated with
    low-molecular-weight heparin (LMWH) or subcutaneous heparin.4

    Pharmacologic Prophylaxis
    The ideal prophylactic agent should be effective, have
    minimal adverse effects, not require monitoring, be administered orally, and be cost-effective.5 Of all of the
    interventions (reviewed by the Agency for Healthcare
    Research and Quality [AHRQ]) in terms of the ability
    to reduce adverse events while decreasing overall costs,
    prophylaxis for deep venous thrombosis has received
    the highest safety rating.5
    The four most common pharmacologic prophylaxis
    agents used in the United States are warfarin, LMWH,
    pentasaccharide, and aspirin (acetylsalicylic acid). It is
    important to appreciate the evidence supporting the use
    of the various pharmacologic prophylactic agents.
    Evidence-based medicine typically includes a level of
    evidence as well as an indication of the strength of a
    recommendation. Table 2 describes the levels of evidence commonly cited in the medical literature, including The Journal of Bone and Joint Surgery. The levels
    range from level I, which includes a high-quality randomized trial, to level V, expert opinion. Strengths of
    recommendation (Table 3) range from grade A, which

    Orthopaedic Knowledge Update 10

    137

    Section 1: Principles of Orthopaedics

    Table 1

    American Academy of Orthopaedic Surgeons Clinical Practice Guideline on the Prevention of


    Symptomatic Pulmonary Embolism in Patients Undergoing Total Hip or Knee Arthroplasty:
    Summary of Recommendations
    Recommendation 3.3
    Chemoprophylaxis of patients undergoing hip or knee replacement
    Recommendation 3.3.1
    Patients at standard risk for both PE and major bleeding should be considered for one of the chemoprophylactic agents
    evaluated in this guideline, including, in alphabetical order: aspirin, LMWH, synthetic pentasaccharides, and warfarin. (Level
    III, Grade B [choice of prophylactic agent], Grade C [dosage and timing])
    Note: The grade of recommendation was reduced from B to C for dosage and timing because of the lack of consistent evidence in the literature
    defining a clearly superior regimen.

    1: Principles of Orthopaedics

    Recommendation 3.3.2
    Patients at elevated (above standard) risk for PE and at standard risk for major bleeding should be considered for one of the
    chemoprophylactic agents evaluated in this guideline, including, in alphabetical order: LMWH, synthetic pentasaccharides,
    and warfarin. (Level III, Grade B [choice of prophylactic agent], Grade C [dosage and timing])
    Note: The grade of recommendation was reduced from B to C for dosage and timing because of the lack of consistent evidence in the literature
    on risk stratification of patient populations.

    Recommendation 3.3.3
    Patients at standard risk for PE and at elevated (above standard) risk for major bleeding should be considered for one of the
    chemoprophylactic agents evaluated in this guideline, including, in alphabetical order: aspirin, warfarin, or none. (Level III,
    Grade C)
    Note: The grade of recommendation was reduced from B to C for dosage and timing because of the lack of consistent evidence in the literature
    on risk stratification of patient populations.

    Recommendation 3.3.4
    Patients at elevated (above standard) risk for both PE and major bleeding should be considered for one of the
    chemoprophylactic agents evaluated in this guideline, including, in alphabetical order: aspirin, warfarin, or none. (Level III,
    Grade C)
    Note: The grade of recommendation was reduced from B to C for dosage and timing because of the lack of consistent evidence in the literature
    on risk stratification of patient populations. No studies currently include patients at elevated risk for major bleeding and/or pulmonary
    embolism (PE) in study groups.
    (Reproduced from the American Academy of Orthopaedic Surgeons: Clinical Practice Guideline on the Prevention of Pulmonary Embolism. Rosemont, IL, American Academy
    of Orthopaedic Surgeons, May 2007. Http://www.aaos.org/Research/guidelines/PEguide.asp.)

    Table 2

    Table 3

    Levels of Evidence

    Strengths of Recommendation
    A

    Good evidence: level I studies with consistent


    findings (adequate quality and applicability)

    Fair evidence: level II or III studies with consistent


    findings (adequate quality and applicability)

    Poor evidence: level IV or V studies with consistent


    findings

    Insufficient or conflicting evidence not allowing a


    recommendation

    High-quality randomized trial

    II

    Cohort study (good control)

    III

    Case-control study

    IV

    Uncontrolled case series

    Expert opinion

    (Reproduced with permission from Haas SB, Barrack RL, Westrich G, Lachiewicz PF:
    Venous thromboembolic disease after total hip and total knee arthroplasty:
    An instructional course lecture, American Academy of Orthopaedic Surgeons.
    J Bone Joint Surg Am 2008;90:2764-2780.)

    consists of good evidence based on level I studies with


    consistent findings that have adequate quality, to grade
    D, in which there is insufficient or conflicting evidence
    that precludes a recommendation.
    Warfarin
    Warfarin is a vitamin K antagonist that is attractive because it is an oral agent. Based on the American College
    of Chest Physicians (ACCP) Guidelines6 there is grade
    IA data supporting its use in prophylaxis in patients
    undergoing elective hip replacement and elective knee

    138

    Orthopaedic Knowledge Update 10

    (Reproduced with permission from Haas SB, Barrack RL, Westrich G, Lachiewicz PF:
    Venous thromboembolic disease after total hip and total knee arthroplasty:
    An instructional course lecture, American Academy of Orthopaedic Surgeons.
    J Bone Joint Surg Am 2008;90:2764-2780.)

    replacement, with an international normalized ratio


    (INR) target of 2.5 and a range from 2.0 to 3.0. It is
    also effective in the prophylaxis of patients undergoing
    hip fracture surgery with a grade of IB when the INR
    range is 2.0 to 3.0 with a target of 2.5. Limitations of
    warfarin include the need for monitoring, interaction
    with other drugs, and variable metabolism based on a
    genetic basis; it has a long half-life and its effects are
    difficult to reverse.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 12: Coagulation, Thromboembolism, and Blood Management in Orthopaedic Surgery

    Pentasaccharide
    Fondaparinux is a synthetic pentasaccharide and an inhibitor of factor Xa. In a study of patients undergoing
    elective major knee surgery, a significantly decreased
    rate of thromboembolic complications (P < 0.001) was
    reported, but the rate of bleeding was significantly increased (P < 0.006) when compared with that of patients treated with enoxaparin.9
    Aspirin
    Aspirin is a safe, inexpensive oral agent that does not
    require monitoring. However, it is less effective in terms
    of prophylaxis when used alone. A prospective randomized study was conducted comparing treatment
    with LMWH and a calf mechanical compression device
    along with aspirin.10 The rates of deep venous thrombosis were assessed with ultrasonography and there
    were no significant differences between the two groups,
    showing that aspirin in combination with mechanical
    compression may be as effective as and safer than more
    aggressive anticoagulant therapy.

    Mechanical Prophylaxis
    Mechanical prophylaxis primarily consists of compressive devices that provide prophylaxis by decreasing venous stasis and increasing fibrinolysis. One of the major drawbacks of compression devices is compliance,
    not only in terms of the amount of time in which the
    patient is in the device, but also how effectively the device is applied to the extremity. A 2006 study of 275
    patients undergoing unilateral total knee replacement
    evaluated the use of a mechanical compression device
    and aspirin compared with enoxaparin for prophylaxis
    following total knee replacement and found that when
    used in combination with pneumatic compression,
    enoxaparin was not superior to aspirin in preventing
    deep venous thrombosis.10
    Inferior Vena Cava Filter
    An inferior vena cava (IVC) filter functions by preventing a pulmonary embolus as opposed to preventing a
    deep venous thrombosis. Typically, this device is indi-

    2011 American Academy of Orthopaedic Surgeons

    cated for patients with a previous history of deep venous thrombosis and/or pulmonary embolism as well
    as those who sustain major trauma and in whom pharmacologic prophylaxis is contraindicated. IVC devices
    are expensive. Retrievable devices are now available.

    Thromboembolic Disease After


    Total Hip and Knee Arthroplasty
    Many orthopaedic surgeons have taken issue with
    whether deep venous thrombosis should be the surrogate marker for pulmonary embolism or death in
    thromboembolic disease.5,11 Based on an AAOS systematic review, the rate of deep venous thrombosis does
    not correlate with pulmonary embolism or death following total hip and total knee arthroplasty. This view
    is not shared by the ACCP. The rate of deep venous
    thrombosis is two to three times greater in patients undergoing total knee arthroplasty compared with patients undergoing total hip arthroplasty; however, the
    pulmonary embolism rate is equivalent.11 As previously
    noted, a 2007 study reported poor results with the
    ACCP 1A protocol using enoxaparin.8 These authors
    found that patients were returned to the operating
    room for wound care three times more frequently when
    the ACCP protocol was followed compared to a previous group of patients in whom the authors used a nonACCP protocol with warfarin.

    1: Principles of Orthopaedics

    Low-Molecular-Weight Heparin
    LMWH is attractive because it has rapid antithrombotic activity5 and a half-life of approximately 4.5
    hours. LMWH does not require regular monitoring;
    however, it is associated with increased cost and a risk
    of bleeding. All heparin agents have some risk of
    heparin-induced thrombocytopenia as well as a higher
    risk of postoperative drainage. According to one study,
    there was a significantly increased risk of minor
    bleeding events in patients undergoing total hip replacement in comparison with patients who received
    warfarin prophylaxis.7 According to the ACCP guidelines6 there is grade IA data for prophylaxis with
    LMWH for patients undergoing elective hip replacement, elective knee replacement, and hip fracture surgery. However, one study showed both low efficacy and
    a high complication rate with the enoxaparin protocol.8

    Thromboembolic Disease After Spine Surgery


    An evidence-based analysis of thromboprophylaxis in
    patients with acute spinal injuries was performed.12 The
    authors studied patients who underwent surgery following spinal injury and compared the groups with and
    without spinal cord injury. The authors found an increased incidence of deep venous thrombosis in patients
    with spinal cord injury compared to those without.
    They recommended that prophylaxis begin as soon as
    possible once it is deemed safe in terms of bleeding potential. Further, the authors found that the use of
    LMWH was more effective with respect to deep venous
    thrombosis prophylaxis than unfractionated heparin
    with less bleeding. In addition, it was concluded that
    prevention of pulmonary embolism appeared successful
    with the use of vitamin K antagonists.
    The American Academy of Orthopaedic Surgeons
    Clinical Guideline on Prevention of Symptomatic Pulmonary Embolism in Patients Undergoing Total Hip or
    Knee Arthroplasty1 recommendations are based on an
    assessment of the patient risk for pulmonary embolism
    and the risk for major bleeding. The guideline stratified
    patients into one of four categories based on whether
    the patient has a standard or elevated risk of pulmonary embolism and a standard or elevated risk of major
    bleeding, hence the recommendations are patient specific (Table 4). Patients at standard risk for both pulmonary embolism and major bleeding should be considered for treatment with one of the following
    chemoprophylactic agents, listed in alphabetical order:
    aspirin, LMWH, synthetic pentasaccharide, and warfarin. Patients at an elevated risk for pulmonary embo-

    Orthopaedic Knowledge Update 10

    139

    Section 1: Principles of Orthopaedics

    Table 4

    General Recommendations Derived With the


    Consensus Process

    1: Principles of Orthopaedics

    Recommendation

    Level of Evidence/
    Strength of
    Recommendationa

    Assess all patients preoperatively


    to determine whether risk of
    pulmonary embolism is
    standard or high

    III/B

    Assess all patients preoperatively


    to determine whether risk of
    bleeding complications is
    standard or high

    III/C

    Consider use of vena cava filter


    in patients who have
    contraindications to
    anticoagulation

    V/C

    Consider intraoperative and/or


    immediate postoperative
    mechanical compression

    III/B

    Consider regional anesthesia for


    the procedure (in consultation
    with anesthesiologist)

    IV/C

    Consider continued use of


    mechanical prophylaxis
    postoperatively

    IV/C

    Rapid patient mobilization

    V/C

    Routine screening for


    thromboembolism is not
    recommended

    III/B

    Educate patient about symptoms


    of thromboembolism after
    discharge

    V/B

    See Tables 2 and 3


    (Reproduced with permission from Haas SB, Barrack RL, Westrich G, Lachiewicz PF:
    Venous thromboembolic disease after total hip and total knee arthroplasty: An
    instructional course lecture, American Academy of Orthopaedic Surgeons. J Bone
    Joint Surg Am 2008;90:2764-2780.)

    lism and at standard risk for major bleeding should be


    considered for treatment with LMWH, a synthetic pentasaccharide, and warfarin. Patients at standard risk
    pulmonary embolism and at an elevated risk for major
    bleeding should be considered for treatment with aspirin, warfarin, or neither agent. Patients at an elevated
    140

    Orthopaedic Knowledge Update 10

    risk for both pulmonary embolism and major bleeding


    should be considered for prophylaxis with aspirin, warfarin, or neither agent. In addition, patients should be
    considered for intraoperative and postoperative mechanical compression. Patients with known contraindications to anticoagulation should be considered for
    vena cava filter placement.
    The AAOS clinical guideline provides additional recommendations based on the results of the objective
    AAOS Consensus Process in which the work group
    members participated, and these recommendations are
    provided in Table 5. General recommendations include
    use of an IVC filter in patients who have contraindications for anticoagulation, rapid patient mobilization,
    and educating patients about symptoms of thromboembolism after discharge.
    A risk assessment was performed for patients undergoing total hip and knee arthroplasties, and a multimodal protocol for thromboprophylaxis was developed.13 Patients were divided into two groups based on
    low or high risk. Low risk factors are cardiac disease
    (congestive heart failure) classified as class I (according
    to the system of the New York Heart Association),14
    prior deep venous thrombosis that occurred more than
    5 years previously, inactive malignant disease, current
    use of hormone replacement therapy (HRT), chronic
    tobacco use, and blood disorders consisting of sickle
    cell trait, polycythemia vera, or thrombocytopenia.
    Some patients had a combination of these risk factors.
    High risk factors are a history of a venous thromboembolic event that occurred within the previous 5 years,
    congestive heart failure classified as class II or III according to the system of the New York Heart Association, atrial fibrillation with cardiac disease and the use
    of warfarin, recent surgery for the treatment of malignant disease, or current adjuvant drug therapy and
    thrombophilia, including factor V Leiden, prothrombin
    disorders, protein-S deficiency, antithrombin disorders,
    or hypercoagulability states. In addition, some patients
    had a combination of these factors. Low-risk patients
    were managed with aspirin, dipyridamole, or clopidogrel bisulfate as well as intermittent pneumatic calf
    compression devices. High-risk patients were managed
    with LMWH or warfarin and intermittent calf compression. The authors concluded that a multimodal
    thromboembolic prophylactic regimen is consistent
    with protecting patients while limiting adverse clinical
    outcomes secondary to thromboembolic, vascular, and
    bleeding complications. The level of evidence was therapeutic level III.

    Blood Management in Orthopaedic Surgery


    Rather than relying on an automatic transfusion trigger, the surgeon should identify patient-specific risk factors such as the anticipated difficulty of the proposed
    surgical procedure, the preoperative hemoglobin level,
    and comorbidities and develop a plan for blood management.15 Medical errors in orthopaedic surgery were
    examined in a recent study, and 5.5% of errors were re-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 12: Coagulation, Thromboembolism, and Blood Management in Orthopaedic Surgery

    Table 5

    Recommendations for Medication Derived From Literature Review and Analysis Process
    Level of Evidence/Strength
    of Recommendationb

    Agentsa

    Standard risk of pulmonary embolism and


    major bleeding

    Aspirin, LMWH, pentasaccharide,


    warfarin (INR 2)

    III/B (C for dosing and timing)

    Elevated risk of pulmonary embolism;


    standard risk of bleeding

    LMWH, pentasaccharide, warfarin (INR <2)

    III/B (C for dosing and timing)

    Standard risk of pulmonary embolism;


    elevated risk of bleeding

    Aspirin, warfarin, (INR <2), no prophylaxis

    III/C

    Elevated risk of pulmonary embolism and


    bleeding

    Aspirin, warfarin (INR 2), no prophylaxis

    III/C

    1: Principles of Orthopaedics

    Risk

    The agents in each row are given in alphabetical order.


    See Tables 2 and 3
    (Reproduced with permission from Haas SB, Barrack RL, Westrich G, Lachiewicz PF: Venous thromboembolic disease after total hip and total knee arthroplasty:
    An instructional course lecture, American Academy of Orthopaedic Surgeons. J Bone Joint Surg Am 2008;90:2764-2780.)
    b

    lated to a blood or tissue event.16 An algorithm of


    blood management was developed based on anticipated
    blood loss in patients undergoing total hip and total
    knee arthroplasty.17 When the algorithm was followed
    the transfusion rate with allogeneic blood was 2.1%,
    which was significantly lower (P < 0.001) than a transfusion rate of 16.4% when the algorithm was not followed (Figure 1).

    Preoperative Blood Management


    It has been reported in patients undergoing lower extremity total joint arthroplasty that if the preoperative
    hemoglobin level was less than 13 g/dL, the risk of requiring an allogeneic blood transfusion was four times
    greater compared with a hemoglobin level of 13 to 15
    g/dL and was 15.3 times greater compared to patients
    with a preoperative hemoglobin level of greater than 15
    g/dL.18 These data indicate that preoperative hemoglobin levels can be used to dictate the need for different
    blood management strategies. It has been recommended that preoperative anemia be corrected with
    oral iron supplementation.19 Preoperative medical conditions can influence risks, including the need for transfusions. A 2009 study found that uncontrolled diabetes
    mellitus, whether type I or type II, was significantly associated with additional surgical and systemic complications including postoperative hematoma, transfusion
    risk, and infections following lower extremity total
    joint arthroplasty.20 Patient-specific factors such as age,
    sex, whether or not the patient was hypertensive, and
    body mass index were evaluated.21 The authors found
    that when a patient had two or more of these factors,
    there was a significantly increased risk of allogeneic
    blood transfusion (P < 0.02).

    2011 American Academy of Orthopaedic Surgeons

    Autologous Donation
    A snapshot assessment of 9,482 patients undergoing
    lower extremity total joint arthroplasties was performed and the then-current blood usage was described.22 Sixty-one percent of patients predonated autologous blood. However, 45% of the predonated
    autologous blood was not used. Nine percent of patients required allogeneic blood despite predonated autologous blood. For each unit of donated blood, the hemoglobin level is decreased approximately 1.2 to 1.5
    g/dL. Autologous donation is an option that the surgeon should consider for the patient, bearing in mind
    concerns regarding wasted donated units and the resultant associated preoperative decrease in hemoglobin.
    Donor-Directed Donation
    The risk of hepatitis B and C transmission as well as
    the risk of human immunodeficiency virus (HIV) transmission is increased in patients who received donordirected donations as opposed to autologous blood.15
    This increased risk is possibly because directed donations are from family members or friends who often
    may be reluctant to disclose risk factors for viruses
    such as hepatitis and/or HIV. Donor-directed donation
    is rarely used because of these concerns.
    Erythropoietin is effective for rapidly increasing the
    hemoglobin level and is indicated for patients with a
    hemoglobin level of 10 to 13 g/dL. Further, erythropoietin is an important component of the blood conservation algorithm shown in Figure 1; in that study, patients who followed the algorithm and were given
    erythropoietin if the anticipated hemoglobin was below
    a certain level had a reduced need for blood transfusion
    following total hip and total knee arthroplasty.17

    Orthopaedic Knowledge Update 10

    141

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 1

    Flow chart illustrating patient-specific recommendations. The preoperative hemoglobin is the hemoglobin level before the patient enters the algorithm. The baseline hemoglobin is the hemoglobin level at the time of surgery.

    Intraoperative Blood Management


    Methods for intraoperative blood management include
    effective anesthetic techniques, intraoperative blood
    salvage, acute normovolemic hemodilution, the use of
    antifibrinolytic agents, the use of a bipolar ceiling device, perioperative injections, and topical agents. Patients undergoing total knee arthroplasty were compared using a computer-assisted minimally invasive
    technique with a standard technique in a prospective
    randomized study.23 The authors found that despite increased duration of surgery, patients treated with the
    computer-assisted minimally invasive technique had a
    decreased length of hospital stay and decreased blood
    loss.
    A meta-analysis of the use of antifibrinolytic agents
    in spine surgery found that aprotinin, tranexamic acid,
    and epsilon-aminocaproic acid were effective in reducing blood loss and transfusions.24 These agents were
    particularly effective in patients undergoing correction
    of spinal deformities and in patients with long arthrodesis constructs. However, at the present time, these
    agents are not approved by the United States Food and
    Drug Administration for these indications. The use of
    tranexamic acid in patients undergoing total hip replacement was evaluated in a 2009 study. Intravenous
    administration of 1 g of tranexamic acid during induction resulted in decreased early postoperative blood
    142

    Orthopaedic Knowledge Update 10

    loss and total blood loss, but intraoperative blood loss


    was not affected.25 Tranexamic acid acts during the
    early phase of the fibrinolytic cascade. Concerns about
    the use of antifibrinolytic agents include an increased
    risk of thrombosis; however, an increased incidence of
    deep venous thrombosis was not found. Concern has
    also been expressed about the cost of these agents;
    however, tranexamic acid was cost-effective in reducing
    blood loss and transfusion requirements after total hip
    replacement, especially in women, in the 2009 study.
    Topical agents such as a fibrin sealant have been
    studied in patients undergoing total knee arthroplasty.
    According to results from a prospective randomized
    trial, the use of the fibrin sealant safely decreased blood
    drainage while maintaining higher hemoglobin levels.26
    Fibrin sealant should be considered as part of a blood
    management strategy, particularly in patients undergoing total knee arthroplasty and especially in those who
    have an inflamed synovium.

    Postoperative Blood Management


    Patients undergoing total hip and total knee replacement who preoperatively had mild anemia and hemoglobin levels ranging from 10 to 13 g/dL were studied.27 Treatment of patients with preoperative
    erythropoietin injections was found to be more effective but more costly in reducing the need for allogeneic

    2011 American Academy of Orthopaedic Surgeons

    Chapter 12: Coagulation, Thromboembolism, and Blood Management in Orthopaedic Surgery

    Summary
    Coagulation, thromboembolism, and blood management are important topics related to patient management, particularly for those patients undergoing total
    hip or total knee arthroplasty. The AAOS clinical
    guideline on the prevention of symptomatic pulmonary
    embolism in these patients is based on a systematic review of the literature and is evidence based. This guideline provides useful information related to patient management regarding pulmonary embolism prophylaxis.
    In addition, ACCP provides evidence-based guidelines,
    which include deep venous thrombosis and pulmonary
    embolism. Prevention of deep venous thrombosis is important; however, orthopaedic surgeons are most concerned with prevention of pulmonary embolism, which
    can be fatal. A patient-specific plan for blood management should be developed based on factors including
    preoperative hemoglobin level and anticipated blood
    loss of the proposed surgical intervention. Patients undergoing a particularly difficult revision will more urgently need multiple blood management strategies than
    the patient undergoing an anticipated straightforward
    unilateral primary joint arthroplasty.

    2.

    Johanson NA, Lachiewicz PF, Lieberman JR, et al: Prevention of symptomatic pulmonary embolism in patients undergoing total hip or knee arthroplasty. J Am
    Acad Orthop Surg 2009;17(3):183-196.
    This is a summary of the AAOS clinical practice guideline on the prevention of symptomatic pulmonary embolism in patients undergoing total hip or knee arthroplasty.

    3.

    Galat DD, McGovern SC, Hanssen AD, Larson DR,


    Harrington JR, Clarke HD: Early return to surgery for
    evacuation of a postoperative hematoma after primary
    total knee arthroplasty. J Bone Joint Surg Am 2008;
    90(11):2331-2336.
    The authors found that patients who returned to the operating room within 30 days following a primary total
    knee arthroplasty for evacuation of a hematoma were at
    significantly increased risk for the development of deep
    infection and are undergoing subsequent major surgery.

    4.

    Brookenthal KR, Freedman KB, Lotke PA, Fitzgerald


    RH, Lonner JH: A meta-analysis of thromboembolic
    prophylaxis in total knee arthroplasty. J Arthroplasty
    2001;16(3):293-300.

    5.

    Haas SB, Barrack RL, Westrich G, Lachiewicz PF:


    Venous thromboembolic disease after total hip and knee
    arthroplasty. J Bone Joint Surg Am 2008;90(12):27642780.
    A summary of venous thromboembolic disease after total hip and knee arthroplasty is presented.

    6.

    Hirsh J, Guyatt G, Albers GW, Harrington R, Schnemann HJ; American College of Chest Physicians: Executive summary: American College of Chest Physicians
    Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 2008;133(6, Suppl):71S-109S.
    This is an executive summary of the 2008 ACCP
    evidence-based clinical guidelines.

    7.

    Colwell CW Jr, Collis DK, Paulson R, et al: Comparison


    of enoxaparin and warfarin for the prevention of venous thromboembolic disease after total hip arthroplasty. Evaluation during hospitalization and three
    months after discharge. J Bone Joint Surg Am 1999;
    81(7):932-940.

    8.

    Burnett RS, Clohisy JC, Wright RW, et al: Failure of the


    American College of Chest Physicians-1A protocol for
    lovenox in clinical outcomes for thromboembolic prophylaxis. J Arthroplasty 2007;22(3):317-324.
    The authors compared their results of prophylaxis following an ACCP 1A protocol using Lovenox and found
    that returning to the operating room for wound complications occurred three times more frequently with the
    use of Lovenox than a previous study using warfarin.

    9.

    Bauer KA, Eriksson BI, Lassen MR, Turpie AG; Steering


    Committee of the Pentasaccharide in Major Knee Surgery Study: Fondaparinux compared with enoxaparin
    for the prevention of venous thromboembolism after
    elective major knee surgery. N Engl J Med 2001;
    345(18):1305-1310.

    Annotated References
    1.

    American Academy of Orthopaedic Surgeons: American


    Academy of Orthopaedic Surgeons Clinical Guideline
    on Prevention of Symptomatic Pulmonary Embolism in
    Patients Undergoing Total Hip or Knee Arthroplasty:
    Summary of Recommendations. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2007, pp 1-63.
    This is an executive summary of the recommendations
    of the AAOS clinical guideline on prevention of pulmonary embolism in patients undergoing total hip or knee
    arthroplasty.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    blood transfusion in mildly anemic patients than the


    use of postoperative reinfusion of autologous shed
    blood. In a randomized controlled trial of patients undergoing total knee replacement, the use of autologous
    retransfusion was evaluated.28 No adverse reactions associated with retransfusion of autologous blood were
    found. This study confirmed the safety of reinfusion
    drains in total knee arthroplasty but casts doubt regarding their efficacy in reducing the need for allogeneic transfusion compared with standard suction drainage after total knee arthroplasty.
    The use of allogeneic blood transfusion is part of the
    strategy for blood management and is an option that
    should be considered. Allogeneic blood is currently
    safer than ever before because blood can be screened
    for various viruses. However, a risk of viral transmission as well as bacterial contamination of the blood exists but has greatly decreased. In 1984 the risk of HIV
    transmission was greater than 1 per 1,000, and in 2001
    it was less than 1 per 1 million.29 Further, administrative errors persist.19

    143

    Section 1: Principles of Orthopaedics

    Westrich GH, Bottner F, Windsor RE, Laskin RS,


    Haas SB, Sculco TP: VenaFlow plus Lovenox vs VenaFlow plus aspirin for thromboembolic disease prophylaxis in total knee arthroplasty. J Arthroplasty 2006;
    21(6, Suppl 2):139-143.

    18.

    Salido JA, Marin LA, Gmez LA, Zorrilla P, Martnez


    C: Preoperative hemoglobin levels and the need for
    transfusion after prosthetic hip and knee surgery: Analysis of predictive factors. J Bone Joint Surg Am 2002;
    84(2):216-220.

    11.

    Callaghan JJ, Dorr LD, Engh GA, et al; American College of Chest Physicians: Prophylaxis for thromboembolic disease: Recommendations from the American
    College of Chest Physiciansare they appropriate
    for orthopaedic surgery? J Arthroplasty 2005;20(3):
    273-274.

    19.

    Lemaire R: Strategies for blood management in orthopaedic and trauma surgery. J Bone Joint Surg Br 2008;
    90(9):1128-1136.
    This paper considers the various strategies available for
    the management of blood loss in patients undergoing orthopaedic and trauma surgery.

    12.

    Ploumis A, Ponnappan RK, Maltenfort MG, et al:


    Thromboprophylaxis in patients with acute spinal injuries: An evidence-based analysis. J Bone Joint Surg Am
    2009;91(11):2568-2576.
    The incidence of deep venous thrombosis is higher in
    spinal cord injury patients undergoing spine surgery
    than in patients without spinal cord injury. LMWH was
    more effective for the prevention of deep venous thrombosis with less bleeding complications than on fractionated heparin. Prevention of pulmonary embolism appeared to be successful with the use of vitamin K
    antagonists.

    20.

    Marchant MH Jr, Viens NA, Cook C, Vail TP, Bolognesi MP: The impact of glycemic control and diabetes
    mellitus on perioperative outcomes after total joint arthroplasty. J Bone Joint Surg Am 2009;91(7):16211629.
    Regardless of diabetes type, patients with uncontrolled
    diabetes mellitus exhibited significantly increased odds
    of surgical and systemic complications including postoperative hemorrhage during their index hospitalization
    following lower extremity total joint arthroplasty.

    21.

    Pola E, Papaleo P, Santoliquido A, Gasparini G, Aulisa


    L, De Santis E: Clinical factors associated with an increased risk of perioperative blood transfusion in
    nonanemic patients undergoing total hip arthroplasty.
    J Bone Joint Surg Am 2004;86(1):57-61.

    22.

    Bierbaum BE, Callaghan JJ, Galante JO, Rubash HE,


    Tooms RE, Welch RB: An analysis of blood management in patients having a total hip or knee arthroplasty.
    J Bone Joint Surg Am 1999;81(1):2-10.

    23.

    Dutton A, Yeo SJ, Yang KY, Lo NN, Chia KU, Chong


    HC: Computer-assisted minimally invasive total knee
    arthroplasty compared with standard total knee arthroplasty: A prospective, randomized study. J Bone Joint
    Surg Am 2008;90(1):2-9.
    The authors found there was less blood loss and no increase in the rate of short-term complications in the
    group undergoing computer-assisted, minimally invasive
    total knee arthroplasty compared with standard total
    knee arthroplasty.

    24.

    Gill JB, Chin Y, Levin A, Feng D: The use of antifibrinolytic agents in spine surgery: A meta-analysis. J Bone
    Joint Surg Am 2008;90(11):2399-2407.
    The authors performed a meta-analysis of antifibrinolytic agents in spine surgery and found that they were effective for reducing blood loss in transfusions. The use
    of these agents, which include aprotinin, tranexamic
    acid, and epsilon-aminocaproic acid, is not an FDA approved indication for these agents.

    25.

    Rajesparan K, Biant LC, Ahmad M, Field RE: The effect of an intravenous bolus of tranexamic acid on
    blood loss in total hip replacement. J Bone Joint Surg Br
    2009;91(6):776-783.
    The authors found that a preoperative bolus of 1 g of
    tranexamic acid was cost-effective in reducing blood
    loss in transfusion requirements after total hip replace-

    1: Principles of Orthopaedics

    10.

    13.

    14.

    Hunt SA, Baker DW, Chin MH, et al; American College


    of Cardiology/American Heart Association: ACC/AHA
    guidelines for the evaluation and management of
    chronic heart failure in the adult: Executive summary. A
    report of the American College of Cardiology/American
    Heart Association Task Force on Practice Guidelines
    (committee to revise the 1995 guidelines for the evaluation and management of heart failure). J Am Coll Cardiol 2001;38(7):2101-2113.

    15.

    Clark CR: Perioperative blood management in total hip


    arthroplasty. Instr Course Lect 2009;58:167-172.
    Patient-specific risk factors such as the anticipated difficulty of the procedure, preoperative hemoglobin level,
    and comorbidities should be identified and the surgeon
    should develop a plan for blood management.

    16.

    17.

    144

    Dorr LD, Gendelman V, Maheshwari AV, Boutary M,


    Wan Z, Long WT: Multimodal thromboprophylaxis for
    total hip and knee arthroplasty based on risk assessment. J Bone Joint Surg Am 2007;89(12):2648-2657.
    A multimodal thromboembolic prophylactic regimen
    was consistent with protecting patients while limiting
    adverse clinical outcome secondary to thromboembolic,
    vascular, and bleeding complications.

    Wong DA, Herndon JH, Canale ST, et al: Medical errors in orthopaedics: Results of an AAOS member survey. J Bone Joint Surg Am 2009;91(3):547-557.
    This review of medical errors in orthopaedics based on
    an AAOS survey revealed that 5.5% of the events were
    a blood or tissue event.
    Pierson JL, Hannon TJ, Earles DR: A bloodconservation algorithm to reduce blood transfusions after total hip and knee arthroplasty. J Bone Joint Surg
    Am 2004;86(7):1512-1518.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 12: Coagulation, Thromboembolism, and Blood Management in Orthopaedic Surgery

    ment especially in women. The results suggest that fibrin sealant can safely reduce blood drainage following
    total knee arthroplasty while maintaining higher hemoglobin levels.
    Wang GJ, Hungerford DS, Savory CG, et al: Use of fibrin sealant to reduce bloody drainage and hemoglobin
    loss after total knee arthroplasty: A brief note on a randomized prospective trial. J Bone Joint Surg Am 2001;
    83(10):1503-1505.

    27.

    Moonen AF, Thomassen BJ, Knoors NT, van Os JJ, Verburg AD, Pilot P: Pre-operative injections of epoetinalpha versus post-operative retransfusion of autologous
    shed blood in total hip and knee replacement: A prospective randomised clinical trial. J Bone Joint Surg Br
    2008;90(8):1079-1083.
    Preoperative epoetin injections were more effective but
    more costly in reducing the need for allogeneic blood

    2011 American Academy of Orthopaedic Surgeons

    28.

    Amin A, Watson A, Mangwani J, Nawabi D, Ahluwalia


    R, Loeffler M: A prospective randomised controlled
    trial of autologous retransfusion in total knee replacement. J Bone Joint Surg Br 2008;90(4):451-454.
    The authors concluded the cost-effectiveness and continued use of autologous drains in total knee replacement
    should be questioned.

    29.

    Vamvakas EC, Blajchman MA: Transfusion-related


    mortality: The ongoing risks of allogenic blood transfusion and the available strategies for their prevention.
    Blood 2009;113(15):3406-3417.
    This article reports that levels of allogenic blood
    transfusion-transmitted virus in the United States are exceedingly low.

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    26.

    transfusions in mildly anemic patients who had postoperative retransfusion of autologous blood.

    145

    Chapter 13

    Work-Related Illness, Cumulative


    Trauma, and Compensation
    J. Mark Melhorn, MD, FAAOS, FAADEP, FACOEM, FACS

    All states in the United States have a workers compensation system. Each states system is unique, but they all
    have some common features. Workers compensation
    injuries or illnesses represent a significant percentage of
    case volume in some orthopaedic practices. Physicians
    should learn the states rules that are applicable to a
    given case. At times, such as in cases in which an employee lives in one state, works for a company located
    in a different state, and is injured in a third state, it can
    be challenging to determine which rules apply.

    History
    Workers compensation pays for medical care for workrelated injuries or illnesses beginning immediately after
    the injury occurs, pays temporary disability benefits
    (partial wage replacement) after a waiting period of 3
    to 7 days, pays permanent partial and permanent total
    disability benefits to workers who have lasting consequences from injuries caused on the job, pays rehabilitation and training benefits for those unable to return
    to preinjury careers (in some states); and pays benefits
    to the survivors of workers who die of work-related
    causes. One program under the Social Security Admin-

    Dr. Melhorn or an immediate family member serves as a


    board member, owner, officer, or committee member of
    the American Academy of Orthopaedic Surgeons, American Society for Surgery of the Hand, American Association for Surgery of the Hand, American Academy of Disability Evaluating Physicians, and American College of
    Occupational and Environmental Medicine; serves as a
    paid consultant to or is an employee of Auxilium; and
    has stock or stock options held in Abbott, Eli Lilly, GlaxoSmithKline, Johnson & Johnson, Merck, Pfizer, Procter &
    Gamble, and Bristol-Myers Squibb. Dr. Talmage or an immediate family member serves as a board member,
    owner, officer, or committee member of the American
    Academy of Disability Evaluating Physicians and the
    American College of Occupational and Environmental
    Medicine.

    2011 American Academy of Orthopaedic Surgeons

    istration, in contrast, pays benefits to workers with


    long-term disabilities resulting from any cause, but only
    when the disabilities preclude any type of work and
    usually only after the individual is off work for more
    than 1 year.
    Although there is considerable variation in rules
    from state to state, workers compensation is designed
    to function as a no-fault system involving numerous
    parties, including the worker, the physician, the employer, the employers insurance carrier, case managers,
    and others. Even though workers compensation systems are designed to be no fault, many injured workers hire legal counsel. Although the goal should be to
    return the injured worker to maximal function in the
    shortest period of time with the least residual disability
    and the shortest absence from work, there are often
    conflicting goals among the involved parties. Most patients want to receive care and get better; however,
    some noninjury-related issues or barriers are often involved. On occasion, patients may not want to return
    to work because of issues as far ranging as a hostile
    work environment to possible secondary monetary
    gain. In some systems, injured workers who do not return to work receive greater financial compensation. In
    all systems it is probable that the injured workers lawyer will receive more income if the worker cannot return to work. Attorney involvement typically delays
    claim closure and increases costs.1 Most treating physicians prefer to administer care as expeditiously as possible. Employers generally want employees to receive as
    little sick or compensable time away from work as possible, and insurance carriers want to resolve cases with
    as little expense as possible.

    1: Principles of Orthopaedics

    Introduction

    James B. Talmage, MD, FAADEP, FACOEM

    Costs
    The medical cost of treating workers injuries and illnesses can be considered from the standpoint of the total medical cost for these patients or from the standpoint of the practice overhead experienced by the
    physician who treats these patients. The most recent review from the National Council on Compensation Insurance2 determined a number of relevant findings.
    Workers compensation pays more than group health
    insurance to treat comparable injuries. The differences

    Orthopaedic Knowledge Update 10

    147

    Section 1: Principles of Orthopaedics

    Table 1

    Odds of Worse Results in Workers Compensation Patients for Conditions Commonly Treated by
    Orthopaedic Surgeons
    Procedure

    Number of Studies

    Odds Ratio

    95% Confidence Interval

    Shoulder acromioplasty

    13

    4.48

    2.71 7.40

    Lumbar fusion

    19

    4.33

    2.81 6.62

    Lumbar diskectomy

    24

    4.77

    3.51 6.50

    3.67

    2.45 5.51

    10

    4.24

    2.43 7.40

    Lumbar intradiskal chymopapain

    1: Principles of Orthopaedics

    Carpal tunnel release

    in the utilization of medical services dominate price differences and explain 80% of the difference in overall
    treatment costs. Utilization of services varies principally
    based on the type of injury, with all the injuries considered showing higher medical service utilization for
    workers compensation patients than for group health
    insurance patients. Traumatic injuries to arms or legs
    consistently have smaller cost and utilization differences, whereas chronic pain-related injuries such as
    bursitis, back pain, and carpal tunnel syndrome have
    larger differences. Differences in payment between
    workers compensation and group health insurance depend on the type of service provided. Evaluation, management, and physical therapy costs are higher in
    workers compensation cases because of greater use of
    those medical services. Radiology costs are higher in
    workers compensation cases than in group health insurance cases because of higher prices and greater utilization. Greater use of physical therapy services is more
    prominent for workers compensation patients with
    acute traumas than for those with other injuries.
    Greater use of office visits and radiology services is
    more prominent for workers compensation patients
    with chronic pain-related injuries than for patients with
    other injuries.
    The overhead expenses of the physicians practice
    are substantially higher for treating workers compensation patients than for treating patients with other
    forms of payment or insurance.3 For example, in one
    practice the total orthopaedic expense per episode of
    care in 2000 for patients was $123 for self-payers,
    $195 for those with an indemnity plan, $148 for Medicare patients, $178 for those with preferred provider
    organizations, $208 for patients with health maintenance organizations/point-of-service plans, and $299
    for workers compensation patients. These differences
    among payer types persisted even after accounting for
    patient age, sex, treatment type (nonsurgical versus surgical), and the number of office visits.
    According to 2007 data published by the Bureau of
    Labor Statistics, the employers costs of workers compensation vary among industries and occupations, depending on the number of workers employed. Costs
    also vary if an employer is union or nonunion and by
    geographic location within the United States.4 Statistics
    148

    Orthopaedic Knowledge Update 10

    also showed that litigation results in an increased number of subjective patient complaints, poorer medical
    outcomes, increased patient use of health care, and increased physician workloads.5
    Many states have workers compensation fee schedules and most pay physicians somewhat more than the
    rate paid by Medicare for the same current procedural
    terminology (CPT) code, which is reasonable because
    these cases generate increased practice overhead. Despite slightly higher rates of pay for office visits, procedures, and other medical care, the main reason for the
    increased cost in workers compensation cases is overutilization of medical services.
    Documented overutilization of services and societal
    concern for controlling costs in the workers compensation system to promote US competitiveness in the
    global marketplace have led an increasing number of
    states to impose utilization review requirements that
    approve or deny requested care using evidence-based
    treatment guidelines. The trend of using evidence-based
    treatment guidelines to determine authorized care is expected to increase over the next decade for both workers compensation and health insurance patients, regardless of the outcome of government health care
    reform.
    The human cost of workers compensation injuries is related to medical outcomes and residual impairment and/or disability. Results of a meta-analysis of
    211 studies found that the same injury or condition
    treated in a compensation setting (usually workers
    compensation) was much more likely to have a poorer
    outcome than if the injury or illness had been treated
    under personal health insurance.6 In the 211 reviewed
    studies, 175 showed worse outcomes with workers
    compensation when compared with noncompensation
    patients, 35 found no difference, and 1 study found improved outcomes in workers compensation patients.
    Table 1 summarizes the odds of worse results in workers compensation patients for conditions commonly
    treated by orthopaedic surgeons.
    The poorer outcomes were not determined by objectively measurable outcomes such as range of motion or
    neurologic deficit but were based on outcome assessments by validated questionnaires that recorded selfreported symptoms and descriptions of functional abil-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 13: Work-Related Illness, Cumulative Trauma, and Compensation

    ity. If two seemingly identical injuries are treated in a


    workers compensation patient and a patient with a
    health insurance payer, the patient treated under the
    workers compensation system would be expected to
    receive more medical treatments, have higher medical
    costs, and have a much poorer outcome than the patient with the health insurance payer. Therefore, the
    treating physicians initial decision on causation (determining if a given injury or illness is related to work) is
    not only a matter of cost allocation and ethical fairness
    but a potential determinant of the patients outcome. A
    similar relationship between compensation status and
    increasing disability has been reported.7

    Many physicians make causation determinations based


    on their understanding of tradition (for example, prior
    training, prior experience, or consensus among other
    doctors in the community) rather than based on science. This reasoning leads to anecdotal determinations,
    such as attributing nonspecific back pain with the
    teaching occupation because the teacher either sits or
    stands all day, or attributing limping from a meniscal
    tear in one knee as the causative factor in a meniscal
    tear in the contralateral knee and nonspecific back
    pain.
    Causation determinations are complicated because
    legal causation is not medical causation. States differ in
    the percentage of the cause that must be attributed to a
    work-related injury or exposure for the patient to qualify for coverage in the workers compensation system
    under the legal theory of aggravation of a preexisting
    condition. This area of understanding is critical. The
    concept that causation does not equal compensability is
    poorly understood by both physicians and patients.
    Physicians need to understand the rules of the system
    when asked to provide an opinion about causation because many believe that when asked about medical causation that this will automatically be applied to the legal issue of compensability, and this is not necessarily
    the case. Several states, such as Kansas and Tennessee,
    have very liberal rules allowing almost any change in a
    condition imagined by a physician to qualify a worker
    for treatment in the workers compensation system.
    California has a 1% rule (1% or more of the causation
    must be from the industrial injury or exposure). Texas
    has a 3% threshold, whereas states such as Arkansas,
    Florida, and Missouri require more than a 50% threshold. Consequently, the statutory or case-law basis that
    defines aggravation of the patients condition for each
    state will tremendously impact the number of cases
    treated in the workers compensation system and the
    costs to industry and society. These rules make the physicians causation decisions problematic because there is
    no scientific literature to determine, for example, if
    walking at work may play a less than 1% role or a
    more than 3% role in knee osteoarthritis. For many of
    the causation questions that arise in cases with potential compensation for injury or illness, the only science

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    Causation

    available is case-control studies, which can provide hypotheses for testing, but which cannot establish causation.8,9 Physicians are forced to use their own understanding of the legal standard of causation in a state,
    even if there is no scientific support for the interpretation. This factor explains why two apparently equally
    well-trained, competent physicians can testify in a case,
    agreeing completely on the diagnosis and treatment,
    and yet have opposite opinions on causation and
    whether the case should be treated in the workers
    compensation system.
    The literature on the epidemiology of occupational
    musculoskeletal disorders is often confusing because of
    conflicting evidence on the importance of various potential risks or causal factors. Occupational exposures
    and their association with, or causation of, injuries and
    illnesses are often debated. Because a determination for
    association or causation is required to establish eligibility for compensation and financial responsibility for
    workers compensation or tort cases, debates and disputed legal cases often ensue.10 The significance of such
    disputes is underscored by the reported direct health
    care costs for the nations workforce of more than $418
    billion and indirect costs of more than $837 billion.11
    It is important that common perceptions or popular
    opinions of causation be based on the best available
    scientific evidence. For example, the speculation that
    carpal tunnel syndrome is related to arm use is widely
    accepted, but is unproven.9 Because this proposed linkage is appealing and pervasive and seems to make
    sense, the lay press has advanced this association despite quality scientific investigations that have found
    little or no relationship between carpal tunnel syndrome and occupation or hand use.12,13
    Recent studies on causation indicate that many conditions that have been routinely accepted as workrelated by workers compensation systems are actually
    not scientifically caused by work. For example, a 2006
    study reported that most of the minor common injuries
    of life do not cause episodes of chronic significant back
    pain, unless those episodes of pain occur in a compensation setting, in which case they are often erroneously
    attributed to minor trauma.14 In a different study, the
    authors obtained preinjury (baseline) lumbar MRIs,
    in an attempt to document which MRI finding commonly seen in asymptomatic individuals is the weak
    link in the chain that breaks when chronic back
    pain subsequently develops.15 The authors reported
    that none of the preexisting changes on MRI correlated
    with the subsequent development of adult chronic back
    pain; follow-up MRIs after the onset of low back pain
    were typically unchanged from the baseline MRIs. It
    was concluded that in the cohort study, minor trauma
    did not appear to increase the risk of serious low back
    pain episodes or disability and that most incidentadverse low back pain events can be predicted by a
    small set of demographic and behavioral variables
    rather than by structural findings or minor trauma.
    A 2009 systematic review of methodologically sound
    studies on spinal mechanical loading as a risk factor for
    low back pain reported conflicting evidence that leisure
    149

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 1

    Identical twins study using MRI to establish


    determinants of disk degeneration. (Adapted
    with permission from Batti MC, Videman T,
    Gibbons LE, Fisher LD, Manninen H, Gill K:
    Determinants of lumbar disc degeneration: A
    study relating lifetime exposures and magnetic
    resonance imaging findings in identical twins.
    Spine 1995;20:2601-2612.)

    activities, whole-body vibration, and the performance


    of nursing tasks, heavy physical work, and working
    with the trunk in a bent or twisted position were associated with adult low back pain, whereas sitting, prolonged standing and/or walking, and participation in
    leisure sports activities were not associated with low
    back pain.16
    In a study of pairs of identical twins from the Finnish Twin Registry, the authors found a substantial genetic influence in degenerative back disorders and provided a list of the genes associated with the disorders.17
    Despite an extraordinary discordance between twin siblings in occupational and leisure time physical loading
    conditions on the spine throughout adulthood, surprisingly little effect on disk degeneration was observed.
    No evidence was found to suggest that exposure to
    whole-body vibration in motor vehicles leads to accelerated degenerative changes. Some evidence was found
    that routine spinal loading was actually beneficial to
    lumbar disks. The effects of personal physical factors
    such as body weight and muscle strength on disk degeneration were modest, and much greater than the
    minimal effect of occupational physical demands. The
    most striking visual evidence in this article, and in prior
    publications from the same study group, is the series of
    MRIs that show identical lumbar MRIs in identical
    twins regardless of the physical loading. The authors
    found that familial aggregation (heredity) was the best
    predictor of lumbar disk degeneration as seen in
    Figure 1.
    Thus, the idea that repetitive activity, minor trauma,
    or lifting is actually the cause of low back disorders in
    adults of working age is being seriously questioned in
    150

    Orthopaedic Knowledge Update 10

    scientific studies, despite compensation systems accepting these long-held beliefs.


    The decision on causation in cases of potentially
    compensable injuries is further confounded by the patient history. In many instances, the key piece of evidence alleging that a spinal disorder should be considered work-related or compensable is the patients own
    reported history of no prior spinal pain or problems before the onset of pain at work, and of no potential confounders such as substance abuse or psychiatric disorders. In a 2009 study, 335 adults who reported back
    pain after a motor vehicle crash were randomly selected
    from the outpatient clinics of five spine specialists.18
    The authors correlated information retrieved from a
    search of prior medical records with the patients selfreported history. They found that approximately 50%
    of the patients had previously reported axial pain based
    on the medical record audit; however, none had reported the prior pain to the spine specialist after their
    motor vehicle crash. The medical record audit also
    showed that approximately 75% of the patients had
    one or more preexisting comorbid conditions (alcohol
    abuse, illicit drug use, and psychological diagnosis) that
    were not reported to the spine specialist. In the patients
    who perceived that the crash was the fault of another
    person, the rate of documented previous back and neck
    pain based on the past medical records was more than
    twice the self-reported rate (P < 0.01). The rate of documented preexisting psychological disorders in the past
    medical records was more than seven times the rate of
    self-reported psychological problems (P < 0.001). In
    patients who perceived that the crash was their own
    fault or no ones fault, a decreased rate of underreporting of axial pain and comorbid conditions was found.
    Therefore, if a physician bases causation decisions
    solely on the alleged temporality of a condition without
    a review of prior medical records, causation conclusions may be flawed.
    The physician must understand that occupational
    causation involves medical and legal requirements.19
    Medical causation deals with scientific cause and effect.
    Legal causation arises from a desire for social justice,
    not science, and requires two separate and distinct
    components: cause in fact and proximate (or legal)
    cause.9 Proximate cause is the defendants (employers)
    alleged action that started the chain of events that led
    to the injury, whereas cause in fact is typically the actual traumatic event (for example, the proximate cause
    could be a defective warning signal at a railroad crossing, and the cause in fact could be the train striking the
    car crossing the railroad tracks).
    A systematic approach for assessing epidemiologic
    studies and their application for determining workrelatedness (occupational causation) is in the public domain and is available on the Internet20 and in the published literature.21 This approach is consistent with the
    principles of using evidence-based medicine for establishing clinical treatment guidelines.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 13: Work-Related Illness, Cumulative Trauma, and Compensation

    Return to Work

    Assessing the Patients Risk, Capacity, and Tolerance for Work


    Physicians are often asked for medical information and
    work status certification. In other words, How do I
    fill out the return-to-work forms indicating what a patient should be safely able to do at work? The key
    concepts for the physician to understand are risk, capacity, and tolerance.28
    Risk refers to the chance of harm to the patient or to
    the general public if the patient engages in specific
    work activities. Risk is the basis for physician-imposed
    work restrictions, which are requested on many returnto-work forms. The physician should consider risk as
    two parts. First is the concept of risk reduction, which
    involves preventing a patient from doing something
    that the patient may be able to do but might cause
    harm. The second concept involves having the physician avoid preventing a patient from doing something
    that they are otherwise capable of doing (avoiding iatrogenic disability behavior). Unfortunately, there is little scientific literature on the entailed risks of working
    for employees with known medical conditions. For example, patients with osteonecrosis of the femoral head
    may be restricted from medium, heavy, or very heavy
    labor to minimize the progressive collapse of the femoral head. Although such a restriction would appear to
    be based on common sense, there are no published
    studies to indicate exactly how much weight an employee with femoral head osteonecrosis can safely handle.
    Capacity refers to the ability to perform a task and is
    usually measured by strength, flexibility, and endurance. Capacity implies that the individual is already
    maximally trained and fully acclimated to the job or
    activity in question. Current ability can often be increased toward achieving maximum capacity by conditioning, which can either be accomplished with formal

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    Why is staying at work or returning to work in the patients best interest? For most people, work plays an important role in giving meaning and purpose to life as
    well as providing income for lifes necessities.22 Being
    unemployed when young or old enough to be working
    actually causes physical disease, premature mortality,
    and emotional problems.22 Consensus statements by the
    Canadian Medical Association,23 the American College
    of Occupational and Environmental Medicine,24 the
    American Academy of Orthopaedic Surgeons,25 and the
    American Medical Association (AMA)26 all support
    and strongly recommend that physicians return patients
    to their usual work roles as soon as possible. Another
    view of the importance of staying at work or returning
    to work is a 2008 study that showed that inactivity was
    the only modifiable factor found to be predictive of total health care costs; this factor also appears to have an
    increasing effect with advancing age.27

    physical therapy or by work restrictions that progressively decrease over time. Capacity is the basis for
    physician-described work limitations. Many return-towork forms ask the physician to provide work limitations for the patient based on the concept of capacity or
    ability. For example, if after a rotator cuff repair, a patient lacks the shoulder motion to reach an overhead
    control of a factory punch press, the patient lacks the
    capacity (has a work limitation) to do this task. The
    physicians work guideline describes what the patient is
    not physically able to do.
    Tolerance refers to the biopsychosocial aspect of the
    patient. Tolerance is the basis for a patients decision if
    the rewards of work (such as money and self-esteem)
    exceed the cost of work (such as pain and fatigue). The
    tolerance level is one of the factors that makes a person
    unique and involves how each person deals with other
    people, stress, pain, and impairment. Tolerance is often
    affected by motivation and rewards and is not scientifically measurable or verifiable. Tolerance is frequently
    less than either capacity or current ability in a compensated population, although tolerance may be higher
    than capacity if there is high incentive or personal motivation. Shortly after a significant injury or surgery,
    tolerance for pain may be a basis for a physician to certify that a patient should not work; however, many
    return-to-work forms do not ask that a physician list
    tolerance issues. Thus, after a rotator cuff repair, a physician may certify a work absence of a few days for a
    patient who performs sedentary desk work that can be
    done with one hand. For chronic conditions, tolerance
    is the basis by which the patient (not the physician) decides if the rewards of the job exceed the costs (symptoms). If there is no significant risk, and the patient can
    do the task despite symptoms, the decision to work, to
    change careers, or to apply for disability should be the
    patients decision. In these cases, the physician should
    not impose restrictions or claim limitations but should
    indicate on evaluation forms that the patient may
    choose to work.
    Studies have been conducted with physicians in
    many specialties using return-to-work vignettes to elicit
    ideal responses. Results show a striking lack of consistency among different physicians in determining work
    guidelines and restrictions; however, there is less variability in the decisions of an individual physician in implementing similar guidelines on different occasions for
    patients with similar cases.29

    Point of View
    The biologic model of disease used by Western culture
    has typically focused on the physical aspects of illness;
    the nonphysical suffering associated with disease and
    injury are often ignored. With this disease model, a
    physician may be inclined to misinterpret a patients
    distress or anxiety about a medical condition as indicative of a more serious physical condition, requiring
    more elaborate treatment or diagnostic testing, rather
    than understanding the distress as an indication that

    Orthopaedic Knowledge Update 10

    151

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    the patient is having difficulty coping because of psychosocial or other extraneous stressors. It is precisely
    this inability to differentiate, by some clinicians, between a patients pain and/or distress and the underlying pathology that becomes an obstacle to improving
    management of many disorders, especially in workers
    compensation cases.
    Perhaps in part because of personal experience or
    medical school training, physicians have a bias against
    the importance of initially approaching the injury care
    of a patient using a biopsychosocial model of disease
    rather than the purely biologic approach. The initial
    treating physician can and should address the psychosocial issues that play such a large role in cases in
    which the injured worker is not recovering as expected.
    When injured, the patient does not necessarily deal
    with the injury in an appropriate or inappropriate (dysfunctional) manner. Most patients deal with injury in
    stages. Understanding these stages allows for better
    treatment and appropriate intervention. In the acute injury stage, the degree of physical impairment usually
    correlates with identifiable physical and pathologic impairments that are expected with a given type of injury.
    The transition stage is the critical stage at which a physician should identify the patient in whom a chronic
    pain state or a dysfunctional attitude may develop. Often, such a patient will not be recovering as expected.
    The patients subjective complaints exceed objective
    findings. The longer dysfunctional behaviors continue,
    the more entrenched the behaviors become. It is important for the physician to change management strategies
    to reduce the dysfunctional behavior. Physicians may
    administer a questionnaire such as the Fear Avoidance
    Belief Questionnaire and/or the Distress and Risk Assessment Method, which is a simple patient classification to identify distress and evaluate the risk of a poor
    outcome.30,31 More complete guidance in using the biopsychosocial model is available in the literature.32
    The learned stage of injury occurs when additional
    impairments and disabilities result from drug misuse,
    inactivity, and deconditioning. The patient becomes a
    professional patient and incorporates the sick patient
    role into all activities. Avoiding this stage is the key to
    good outcomes. The Ds is a memory device for physicians to aid awareness of the observable factors that
    may result in chronic preventable disability.33,34 These
    factors include: (1) Dramatizationthe patients report
    of vague, diffuse, nonanatomic pain and the use of
    emotionally charged words to describe pain and suffering. Patients exhibit exaggerated histrionic behavior
    and a theatrical display of pain. (2) Drugsthe misuse
    of habit-forming pain medications or alcohol. (3) Dysfunctionstated bodily impairments related to various
    physical and emotional factors and a withdrawal from
    the fabric of life. Patients disengage from work and recreation and alienate friends, family, employers, and
    health care providers. (4) Dependencythe patient exhibits passivity, depression, and helplessness. (5) Disabilitythe patients pain is contingent on financial
    compensation and pending litigation claims. (6) Durationthe pain persists long after tissue damage should
    152

    Orthopaedic Knowledge Update 10

    have healed and the disability persists long after impairments should have resolved. (7) Despairpatients become embittered, defensive, and rigid. The four manifestations of despair are depression, apprehension,
    irritability, and hostility. (8) Disuseprolonged immobilization occurs. Pain is aggravated with attempts to
    resume normal activities.
    To deal effectively with patients who are at risk for
    chronic preventable disability, the physician and employer must be actively involved in the patients care.
    The physician must listen attentively to the patient and
    have a desire for the patient to get better. The physician
    must attempt to understand the patients method of
    dealing with injury and pain, and should help the patient to become a more active and useful participant in
    life activities, including work. The physician needs to
    become a facilitator or rehabilitator by focusing on the
    patients ability to function rather than on his or her
    pain. These patients are stuck, and the physicians challenge is to get them moving again. This concept has
    been paraphrased in Martins Law of Return to Work
    Decision Making Entrophy: A Corollary to the Laws of
    Motion and Dynamics. Things at rest stay at rest,
    things in motion stay in motion unless acted upon by
    an outside force. Workers compensation patients who
    are actively managed and allowed to return to normal
    continue to improve whereas patients left alone without proactive management tend to assume a disorganized state.

    Impairment
    Accurate and consistent impairment ratings continue to
    be a concern for the employee, employer, and rating
    physician. In an attempt to standardize and classify impairments, the AMA publishes the Guides to the Evaluation of Permanent Impairment (Guides). The workers compensation systems of many states mandate the
    use of a specific edition of the Guides to determine an
    impairment percentage, or a number that attempts to
    quantify how serious the residual problems are after a
    compensable injury or illness. This often results in attempts to convert impairment (defined in the Guides as
    a significant deviation, loss, or loss of use of any body
    structure or function in an individual with a health
    condition, disorder or disease) to disability (an umbrella term for activity limitations and/or participation
    restrictions in an individual with a health condition,
    disorder, or disease). The number (impairment percentage) is used in various ways by various jurisdictions to
    determine a financial award for the workers injuries.
    Traditionally, physicians rate impairment (medical disorders) and the judicial system determines disability
    (how the impairment translates into an employment
    handicap). Understanding the differences between impairment and disability is crucial. There is no correlation between impairment and disability except in cases
    with extreme injury. Some physicians develop a reputation as being friendly to injured workers in rating
    impairments, whereas others develop a reputation as

    2011 American Academy of Orthopaedic Surgeons

    Chapter 13: Work-Related Illness, Cumulative Trauma, and Compensation

    Clinical Treatment Guidelines


    The trend in workers compensation is toward legislated clinical guidelines, which have the presumption of
    being correct for determining authorization for treatment. Some clinical guidelines are well developed using
    strict criteria and established levels of evidence. Such
    guidelines result in summarized consensus statements
    that often include discussions of prevention; diagnosis;
    prognosis; therapy, including dosage of medications; indications for tests and invasive treatment; risks and
    benefits; and cost-effectiveness. Additional objectives of
    clinical guidelines are to standardize medical care, to
    raise the quality of care, to reduce risks, and to achieve
    the best balance between cost and medical treatment.

    Independent Medical Evaluations


    An independent medical evaluation (IME) is a medical
    evaluation conducted by a physician who is not involved in the treatment of the individual being examined. Within the context of workers compensation, an
    IME typically documents the workers condition by addressing diagnosis, causation, functional status, treatment needs, maximum medical improvement determination, and impairment.35 This information helps to
    determine appropriate assistance for the individual and
    aids in making a fair decision on the claim. A 2009
    search of independent medical examinations using
    an Internet search engine returned 2,850,000 sites.
    Most of the sites were associated with personal injury
    attorneys with specific instructions (coaching) as to
    what IME examiners are expected to ask and with information on responding to their questions. Unfortunately, such coaching may inject disinformation into
    the evaluation.36,37

    2011 American Academy of Orthopaedic Surgeons

    Ergonomics
    Ergonomics is the science of fitting the job to the
    worker. Ergonomics is designed to consider the workers physical capability, anatomy, and physiology (risk,
    capacity, and tolerance) and match these factors to the
    job requirements. Strategies for preventing workplace
    injuries can begin with epidemiologically-based recommendations regarding relative risks.38,39 Reducing
    workplace risks should logically be balanced with reducing individual risks, such as reducing obesity and
    smoking.40

    Summary

    1: Principles of Orthopaedics

    being friendly to employers. All physicians should be


    neutral and apply the Guides impartially. Differences in
    opinion about impairment ratings may result in extended litigation, which usually impacts treatment outcomes.
    The first five editions of the Guides, published by
    the AMA from 1972 to 2000, used the same concept of
    medical impairment and basically the same methodology. In the sixth edition of the Guides, published in late
    2007, the AMA used an entirely new conceptual model
    of impairment and disability created by the World
    Health Organization and adopted by 192 countries, including the United States. The new methodology is
    used to determine impairment. Physicians who provide
    patient ratings based on the Guides new model of impairment and disability will find it a more diagnosisbased model; however, it is less intuitive to use. Future
    refinement of the Guides should include reduced complexity, improved intrarater and interrater reliability, an
    evidence-based approach when available, and a rating
    more reflective of the loss of function.

    The treatment of workers compensation injury patients is a significant part of many orthopaedic practices. Most orthopaedic residencies prepare their graduates to provide excellent biomedical care but may not
    provide training in the biopsychosocial and legal issues
    that orthopaedic surgeons confront daily when caring
    for workers compensation patients. Recently, important research has been published to help orthopaedic
    surgeons understand the complex issues of medicallegal causation and the biopsychosocial treatment of
    work-related injuries and illnesses.

    Annotated References
    1.

    Bernacki EJ, Tao XG: The relationship between attorney involvement, claim duration, and workers compensation costs. J Occup Environ Med 2008;50(9):10131018.
    A review of 738 claims with attorney involvement and
    6,191 claims without attorney involvement paid by the
    Louisiana Workers Compensation Corporation showed
    that attorney involvement resulted in increased claim
    duration and workers compensation costs.

    2.

    Robertson J, Corro D: Workers Compensation vs.


    Group Health: A Comparison of Utilization. NCCI Research Brief, November, 2006. http://www.ncci.com/
    documents/research-wc-vs-group-health.pdf. Accessed
    March 31, 2010.

    3.

    Brinker MR, OConnor DP, Woods GW, Pierce P, Peck


    B: The effect of payer type on orthopaedic practice expenses. J Bone Joint Surg Am 2002;84A(10):18161822.

    4.

    Blum F, Burton JF Jr: Workers compensation costs in


    2007: Regional, industrial, and other variations. Workers Compensation Policy Review, 2008. John Burtons
    Workers Compensation Resources Web site. http://
    www.workerscompresources.com/WCPR_Public/
    WCPR%20PDFs/MA08.pdf. Accessed March 31, 2010.
    The four types of workers compensation cash benefits
    are examined. The concept of operational versus purpose of benefits is discussed.

    Orthopaedic Knowledge Update 10

    153

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    5.

    Kasdan ML, Vender MI, Lewis K, Stallings SP, Melhorn


    JM: Carpal tunnel syndrome: Effects of litigation on utilization of health care and physician workload. J Ky
    Med Assoc 1996;94(7):287-290.

    6.

    Harris I, Mulford J, Solomon M, van Gelder JM, Young


    J: Association between compensation status and outcome after surgery: A meta-analysis. JAMA 2005;
    293(13):1644-1652.

    7.

    Sander RA, Meyers JE: The relationship of disability to


    compensation status in railroad workers. Spine (Phila
    Pa 1976) 1986;11(2):141-143.

    8.

    Genovese E: Causality, in Demeter SL, Andersson GBJ,


    eds: Disability Evaluations. Chicago, IL, American
    Medical Association, 2003, pp 95-100.

    9.

    Melhorn JM, Ackerman WE, Glass LS, Deitz DC: Understanding work-relatedness, in Melhorn JM, Ackerman WE, eds: Guides to the Evaluation of Disease and
    Injury Causation. Chicago, IL, American Medical Association Press, 2008, pp 13-32.
    The authors discuss work-related issues with regard to
    causation of diseases and injuries using an evidencebased medicine approach.

    10.

    11.

    12.

    Melhorn JM, Ackerman WE: Introduction, in Melhorn


    JM, Ackerman WE, eds: Guides to the Evaluation of
    Disease and Injury Causation. Chicago, IL, American
    Medical Association Press, 2008, pp 1-12.
    The authors discuss the methodology for determining
    causation of diseases and injuries using an evidencebased medicine approach.
    Brady W, Bass J, Moser R Jr , Anstadt GW, Loeppke
    RR, Leopold R: Defining total corporate health and
    safety costs: Significance and impact. Review and recommendations. J Occup Environ Med 1997;39(3):224231.
    Lozano-Caldern S, Anthony S, Ring D: The quality
    and strength of evidence for etiology: Example of carpal
    tunnel syndrome. J Hand Surg Am 2008;33(4):525-538.
    A quantitative scoring system was developed to review
    the literature for quality and strength based on Bradford
    Hill criteria for causal association between carpal tunnel
    syndrome and physical activities. The etiology of carpal
    tunnel syndrome is largely structural, genetic, and biologic, with environmental and occupational factors such
    as repetitive hand use playing a minor and more debatable role.

    13.

    Fisher B, Gorsche R: Diagnosis, Causation and Treatment of Carpal Tunnel Syndrome: An Evidence-Based
    Assessment. Alberta, CA, Workers Compensation
    Board, 2006, pp 1-153.

    14.

    Carragee E, Alamin T, Cheng I, Franklin T, Hurwitz E:


    Does minor trauma cause serious low back illness?
    Spine (Phila Pa 1976) 2006;31(25):2942-2949.

    15.

    Carragee E, Alamin T, Cheng I, Franklin T, van den


    Haak E, Hurwitz E: Are first-time episodes of serious

    LBP associated with new MRI findings? Spine J 2006;


    6(6):624-635.
    16.

    Bakker EW, Verhagen AP, van Trijffel E, Lucas C, Koes


    BW: Spinal mechanical load as a risk factor for low
    back pain: A systematic review of prospective cohort
    studies. Spine (Phila Pa 1976) 2009;34(8):E281-E293.
    A meta-analysis was performed to review the past literature for spinal mechanical loading as a risk factor for
    low back pain. The authors found 18 high-quality methodological articles, which allowed the review of 24,315
    subjects. The authors reported that the evidence for associations was conflicting.

    17.

    Batti MC, Videman T, Kaprio J, et al: The Twin Spine


    Study: Contributions to a changing view of disc degeneration. Spine J 2009;9(1):47-59.
    A multicenter study of twins reported that the once
    commonly held view that disk degeneration is primarily
    a result of aging and mechanical insults and injuries is
    not supported by evidence from this study.

    18.

    Don AS, Carragee EJ: Is the self-reported history accurate in patients with persistent axial pain after a motor
    vehicle accident? Spine J 2009;9(1):4-12.
    A multicenter validation study of 702 patients found
    that the accuracy of a self-reported history for persistent
    axial back pain after a motor vehicle crash was poor; results were worse in patients who perceived that another
    person was at fault for the crash.

    19.

    Hegmann KT, Oostema SJ: Causal associations and determination of work-relatedness, in Melhorn JM, Ackerman WE, eds: Guides to the Evaluation of Disease and
    Injury Causation. Chicago, IL, American Medical Association Press, 2006, pp 33-46.

    20.

    Causation methodology procedure: The approach on


    how to determine causation. Download 8504. CtdMAP
    Web site. http://www.ctdmap.com/DownLoadsInfo/
    default.aspx. Accessed April 2, 2010.
    A method for determining work-relatedness was created
    for evaluating the scientific evidence using standardized
    quality scoring processes. The framework for how to
    determine causation for specific activities, conditions, or
    events is presented. This methodology was placed into
    the public domain and may be freely copied or reprinted
    if the reference source is appropriately acknowledged.

    21.

    Melhorn JM, Ackerman WE, eds: Guides to the Evaluation of Disease and Injury Causation. Chicago, IL,
    American Medical Association Press, 2008.
    This textbook presents a review and detailed discussion
    of the medical literature regarding causation of diseases
    and injuries.

    22. Waddell G, Burton AK: Is Work Good for Your Health


    and Well-Being? Norwich, England, Stationery Office,
    2006.
    23.

    154

    Orthopaedic Knowledge Update 10

    Canadian Medical Association: The physicians role in


    helping patients return to work after an illness or injury.
    CMAJ 1997;156(5):680A-680F.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 13: Work-Related Illness, Cumulative Trauma, and Compensation

    The Personal Physicians Role in Helping Patients with


    Medical Conditions Stay at Work or Return to Work,
    2008. American College of Occupational and Environmental Medicine Web site. http://www.acoem.org/
    guidelines.aspx?id=5460. Accessed March 31, 2010.
    The American College of Occupational and Environmental Medicine provides their position statement on
    the benefits of returning to work after illness or injury.

    25.

    Position statement: Early return to work programs.


    American Academy of Orthopaedic Surgeons Web site.
    http://www.aaos.org/about/papers/position/1150.asp.
    Accessed March 31, 2010.
    AAOS supports safe and early return-to-work programs
    and believes that these programs are in the best interest
    of patients in an effort to help the injured workers improve performance, regain functionality, and enhance
    quality of life. The success of an early return-to-work
    program is dependent on appropriate planning as well
    as attention to a host of physical, psychological, and environmental factors.

    26.

    Report 12 of the Council on Scientific Affairs: Physician


    Guidelines for Return to Work After Injury or Illness.
    2004. American Medical Association Web site. http://
    www.ama-assn.org/ama/no-index/about-ama/
    13609.shtml. Accessed March 31, 2010.

    27.

    Wilkerson GB, Boer NF, Smith CB, Heath GW: Healthrelated factors associated with the healthcare costs of
    office workers. J Occup Environ Med 2008;50(5):593601.
    A study of 214 employees found that inactivity was the
    only modifiable factor predictive of total health care
    costs among officer workers.

    28.

    Talmage JB, Melhorn JM: How to think about work


    ability and work restrictions: Capacity, tolerance, and
    risk, in Talmage JB, Melhorn JM, eds: A Physicians
    Guide to Return to Work. Chicago, IL, American Medical Association, 2005, pp 7-18.

    29.

    30.

    31.

    Rainville J, Pransky GS, Indahl A, Mayer EK: The physician as disability advisor for patients with musculoskeletal complaints. Spine (Phila Pa 1976) 2005;30(22):
    2579-2584.
    Waddell G, Newton M, Henderson I, Somerville D,
    Main CJ: A Fear-Avoidance Beliefs Questionnaire
    (FABQ) and the role of fear-avoidance beliefs in chronic
    low back pain and disability. Pain 1993;52(2):157-168.
    Main CJ, Wood PL, Hollis S, Spanswick CC, Waddell
    G: The distress and risk assessment method: A simple
    patient classification to identify distress and evaluate the
    risk of poor outcome. Spine (Phila Pa 1976) 1992;
    17(1):42-52.

    2011 American Academy of Orthopaedic Surgeons

    32.

    Kendall NA, Burton AK: Tracking Musculoskeletal


    Problems: The Psychosocial Flags Framework: A Guide
    for Clinic and Workplace. London, England, The Stationery Office, 2009.
    This textbook helps treating physicians to better understand the psychosocial impact of musculoskeletal pain
    and the patients ability to perform work tasks.

    33.

    Brena SF, Champman SL: Pain and litigation, in Wall


    PD, Melzack R, eds: Textbook of Pain. New York, NY,
    Churchill Livingstone, 1984, pp 832-839.

    34.

    Melhorn JM: Stay at work and return to work for upper


    limb conditions, in Melhorn JM, Yodlowski ML, eds:
    10th Annual AAOS Occupational Orthopaedics and
    Workers Compensation: A Multidisciplinary Perspective. Rosemont, IL, American Academy of Orthopaedic
    Surgeons, 2008, pp 103-120.
    The author presents a review of factors that predict disability and details information on returning the patient
    to work.

    35.

    Melhorn JM: Forward, in Grace TG, ed: Independent


    Medical Evaluations. Rosemont, IL, American Academy
    of Orthopaedic Surgeons, 2001, pp vii-viii.

    36.

    Barth RJ: Observation compromises the credibility of an


    evaluation. American Medical Association Guides
    Newsletter, July-August 2007, pp 1-5.
    A review of the impact of having an observer present
    during the completion of an independent medical evaluation is presented.

    37.

    Cain DM, Detsky AS: Everyones a little bit biased (even


    physicians). JAMA 2008;299(24):2893-2895.

    1: Principles of Orthopaedics

    24.

    This commentary reviews biases in the developed policies and guidelines in response to increasing concerns
    over potential conflicts of interest.
    38.

    Melhorn JM, Wilkinson LK, OMalley MD: Successful


    management of musculoskeletal disorders. J Hum
    Ecolog Risk Assessment 2001;7:1801-1810.

    39.

    Kasdan ML: Upper-extremity cumulative trauma disorders of workers in aircraft manufacturing. J Occup Environ Med 1998;40(1):12-15.

    40.

    Amadio PC: Work-related illness, cumulative trauma,


    and compensation, in Koval KJ, ed: Orthopaedic
    Knowledge Update 7. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2002, pp 121-125.

    Orthopaedic Knowledge Update 10

    155

    Chapter 14

    Evidence-Based Orthopaedics:
    Levels of Evidence and Guidelines
    in Orthopaedic Surgery
    Kanu Okike, MD, MPH

    Mininder S. Kocher, MD, MPH

    Evidence-based medicine is the conscientious, explicit,


    and judicious use of current best evidence in making
    decisions about the care of individual patients.1 Although this form of medical practice is often contrasted
    with decision making on the basis of opinion and experience (a phenomenon sometimes termed eminencebased medicine2), it is important to note that the ideal
    practice of evidence-based medicine involves integrating individual clinical expertise with the best available
    external clinical evidence from systematic research.1
    Although the term evidence-based medicine did
    not appear in the medical literature until 1992,3 it has
    since become the dominant paradigm in the practice of
    clinical medicine. Orthopaedic surgery has been no
    exception,4-6 as evidence-based medicine has generally
    been welcomed by practicing orthopaedists.7
    Along with this increased emphasis on evidence in
    clinical decision making, there has developed a need for
    the critical analysis of scientific research. Studies may
    be subject to bias, confounding, and other shortcomings, which may limit the extent to which the data may
    be used to guide the clinical care of patients. Therefore,
    hierarchical level of evidence classification systems have
    been developed to aid in the assessment of research
    quality.
    The movement toward evidence-based medicine has
    also created a need for mechanisms to synthesize the

    Dr. Kocher or an immediate family member serves as a


    board member, owner, officer, or committee member of
    The American Orthopaedic Society for Sports Medicine,
    The Arthritis Foundation, and The Pediatric Orthopaedic
    Society of North America; serves as a paid consultant to
    or is an employee of Biomet, CONMED Linvatec, Smith &
    Nephew, Covidien, OrthoPediatrics, and Gerson Lehrman
    Group; and has received research or institutional support from CONMED Linvatec. Dr Okike has received research or institutional support from Depuy Orthopaedics.

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    Introduction

    available evidence and distill it into a form that can be


    used effectively by practicing physicians. The sheer volume of the scientific literature, coupled with everpresent time constraints, means that it is no longer feasible for physicians to critically review all studies
    published in ones field.8 Clinical practice guidelines,
    which provide recommendations for the management
    of specific conditions based on a systematic review of
    the best available evidence, are well placed to satisfy
    this growing need.

    Levels of Evidence

    History and Purpose


    The concept of grading studies on the basis of their
    methodology was first proposed in a 1986 article on
    the use of antithrombotic agents.9 The Journal of Bone
    and Joint Surgery: American volume was the first orthopaedic publication to adopt the classification system, as it began assigning levels of evidence to all clinical studies published in the Journal in 2003.10 In the
    adoption of this classification system, the Journals
    goals were threefold: to familiarize authors, reviewers,
    and readers with the concept of levels of evidence; to
    improve orthopaedic studies via the explicit articulation of a primary research question; and to place clinical research studies into context for the reader.10
    Over the past few years, several other orthopaedic
    journals have adopted similar level of evidence classification systems, including Clinical Orthopaedics and Related Research, Arthroscopy, The American Journal of
    Sports Medicine, and The Journal of Hand Surgery.11-13
    The American Academy of Orthopaedic Surgeons
    (AAOS) followed suit by adopting its own level of evidence classification system in 200514 (Table 1).

    Assigning Levels of Evidence


    There are three basic steps in the assignment of a level
    of evidence to a particular clinical study: determine the
    primary research question, establish the study type, and
    assign a level of evidence.15

    Orthopaedic Knowledge Update 10

    157

    Section 1: Principles of Orthopaedics

    Table 1

    Levels of Evidence for Primary Research Question


    Types of Studiesa
    Therapeutic Studies

    1: Principles of Orthopaedics

    Investigating the results


    of treatment

    Prognostic Studies
    Investigating the effect
    of a patient
    characteristic on the
    outcome of disease

    Diagnostic Studies

    Economic and Decision


    Analyses

    Developing an
    Investigating a diagnostic economic model or
    test
    decision model

    High-quality prospective
    Testing of previously
    Sensible costs and
    studyd (all patients were
    developed diagnostic
    alternatives; values
    criteria on consecutive
    obtained from many
    enrolled at the same
    patients (with universally
    studies; with multiway
    point in their disease
    applied reference gold
    sensitivity analyses
    with 80% follow-up of
    standard)
    Systematic reviewb of
    enrolled patients)
    Systematic reviewb of level Systematic reviewb of level II
    level I studies
    I studies
    studies

    Level I

    High-quality randomized
    trial with statistically
    significant difference but
    narrow CIs
    Systematic reviewb of level I
    RCTs (and study results
    were homogeneousc)

    Level II

    Development of diagnostic Sensible costs and


    Retrospectivef study
    Lesser-quality RCT (eg,
    criteria on consecutive
    alternatives; values
    Untreated controls from
    < 80% follow-up, no
    patients (with universally
    obtained from limited
    an RCT
    blinding, or improper
    applied reference gold
    studies; with multiway
    Lesser-quality prospective
    randomization)
    standard)
    sensitivity review
    study (eg, patients
    Prospectived comparative
    Systematic reviewb of level II Systematic reviewb of
    enrolled at different
    studye
    points in their disease or
    studies
    level II studies
    Systematic reviewb of level II
    < 80% follow-up)
    studies or level I studies
    with inconsistent results

    Level III

    Case-control studyg
    Retrospectivef comparative
    studye
    Systematic reviewb of level
    III studies

    Case-control studyg

    Analyses based on limited


    Study of nonconsecutive
    alternatives and costs;
    patients; without
    poor estimates
    consistently applied
    reference gold standard Systematic reviewb of
    Systematic reviewb of level
    level II studies
    III studies

    Level IV

    Case seriesh

    Case series

    Case-control study
    Poor reference standard

    Analyses with no
    sensitivity analyses

    Level V

    Expert opinion

    Expert opinion

    Expert opinion

    Expert opinion

    RCT = randomized controlled trial; CI = confidence interval


    a
    A complete assessment of quality of individual studies requires critical appraisal of all aspects of the study design.
    b
    A combination of results from two or more prior studies.
    c
    Studies provided consistent results.
    d
    Study was started before the first patient enrolled.
    e
    Patients treated one way (eg, cemented hip arthroplasty) compared with a group of patients treated another way (eg, uncemented hip arthroplasty) at the same
    institution.
    f
    The study was started after the first patient enrolled.
    g
    Patients identified for the study based on their outcome, called cases (eg, failed total arthroplasty), are compared with those patients who did not have outcome, called
    controls (eg, successful total hip arthroplasty).
    h
    Patients treated one way with no comparison group of patients treated another way.
    Reproduced from American Academy of Orthopaedic Surgeons: Levels of evidence for primary research question. Available at:
    http://www.aaos.org/Research/Committee/Evidence/loetable1.pdf. Accessed July 23, 2010.

    It is important to note that levels of evidence are applied to the primary research question of a given study
    only. Although a study may have multiple research
    questions, only one should be designated as primary.
    The primary research question of a given study should
    be specified by the authors, preferably at the time of
    study inception.
    Once the primary research question has been determined, the study type must be established. In the clas-

    158

    Orthopaedic Knowledge Update 10

    sification scheme used by the AAOS as well as several


    orthopaedic journals, including The Journal of Bone
    and Joint Surgery, studies are categorized as therapeutic, prognostic, diagnostic, or economic/decision analysis (discussed in detail in the next sections). Although
    nearly all clinical studies can be placed into one of these
    categories, the categorization scheme is not exhaustive
    and it is possible for a particular study to not fit neatly
    into any one of the above categories. Only after the pri-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 14: Evidence-Based Orthopaedics: Levels of Evidence and Guidelines in Orthopaedic Surgery

    mary research question has been determined and the


    study type has been established can a specific level of
    evidence be assigned (Table 1).

    Therapeutic Studies

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    Therapeutic studies investigate the effect of treatment


    on the outcome of disease and represent the most common type of study in the orthopaedic literature.16-18
    Level I therapeutic studies are high-quality randomized controlled trials (RCTs), which are generally considered to represent the best possible evidence available.
    To be considered a high-quality study, an RCT must satisfy several criteria. It must be appropriately powered,
    either by detecting a significant difference (in the case of
    a positive trial) or documenting sufficient power (in
    the case of a negative trial). High-quality RCTs must
    use an appropriate randomization technique, in which
    allocation of the next study participant cannot be determined by members of the research team before the patient receives his or her treatment allocation. Rates of
    follow-up must be high generally above 80%. Whenever possible, patients, caregivers, and researchers
    should be blinded to the treatment assignment. This is
    by no means an exhaustive list, and there are several
    other characteristics that must be fulfilled for a trial to
    be considered of high quality. However, one can reliably
    assume that studies not fulfilling the above criteria will
    generally not be considered level I evidence.
    Level II therapeutic studies include lesser-quality
    RCTs (as previously discussed), as well as prospective
    comparative studies. Comparative studies (also known
    as cohort studies) involve the comparison of one group
    of patients treated in a particular way with another
    group of patients treated in another way. For example,
    a study comparing the outcomes of patients with intertrochanteric hip fractures treated with a sliding hip
    screw or a cephalomedullary device would be considered a comparative (or cohort) study. Although the distinction between prospective and retrospective can
    sometimes be confusing,15 AAOS considers prospective
    investigations to be those in which the study was initiated (the research question was posed) before the first
    patient was enrolled or treated.
    Level III therapeutic studies include retrospective
    comparative studies (as previously discussed), as well as
    case-control studies. Case-control studies, which are
    retrospective, involve the comparison of one group of
    patients who have a particular outcome with another
    group of patients who do not have the outcome of interest. These case and control groups are compared to each other on the basis of characteristics plausibly associated with the outcome of interest. For
    example, a comparison of children who developed
    slipped capital femoral epiphysis to a similar group of
    children who did not develop this condition would be
    considered to be a case-control study. Such a comparison could be made on the basis of risk factors, such as
    obesity or sex.
    Level IV therapeutic studies, which represent the
    most common type of study in the orthopaedic

    literature,16-19 are case series of patients treated in one


    way without any comparison group of patients treated
    in another way. Although the evidence provided by this
    type of study is relatively low in the level of evidence
    hierarchy, it is important to emphasize that these studies do have their place in the orthopaedic literature. If a
    level IV case series is well executed, it can provide important information to guide patient care. A welldesigned case series is one that has 100% of patients
    with the same diagnosis, strict inclusion and exclusion
    criteria, a standard treatment protocol, patient
    follow-up at specified time intervals, well-defined outcome measures that include clinical parameters, and
    validated patient-derived instruments for functional assessment.17
    Expert opinion, without the support of clinical data,
    is considered to be level V evidence. This is true for all
    study types, including therapeutic studies.
    The terms systematic review and meta-analysis
    are often assumed to be interchangeable, but their definitions do differ slightly. Whereas a systematic review
    is a comprehensive literature search to identify studies
    appropriate for answering a particular clinical question, a meta-analysis is a statistical method of combining the data provided by these studies. Combining multiple studies into a single meta-analysis may address
    problems of small sample size and insufficient power,
    but it will not alter the level of evidence because metaanalyses are assigned levels of evidence based on the
    quality of the studies used in the meta-analysis.

    Nontherapeutic Studies
    Prognostic studies, which represent the second most
    common type of study in the orthopaedic literature,16-18
    investigate the effect of a patient characteristic on the
    outcome of disease. Differentiating between therapeutic
    and prognostic studies can be difficult because both examine the effects of factors with the potential to influence the outcome of disease. James Wright, MD, MPH,
    Associate Editor for Evidence-Based Orthopaedics at
    The Journal of Bone and Joint Surgery: American volume, suggests considering whether the factor of interest
    can be randomized or not: If [a factor] can be randomly allocated, one is dealing with a therapeutic
    study.15 For example, an investigation of physical therapy on outcome after proximal humerus fracture
    would be considered a therapeutic study, whereas an
    investigation of the effect of age following this same injury would be considered to be a prognostic study. The
    criteria for assigning levels of evidence to prognostic
    studies are detailed in Table 1.
    Diagnostic studies are the third most common type
    of study in the orthopaedic literature16-18 and evaluate
    the performance of tests designed to detect the presence
    or absence of a particular condition. Of central importance in the evaluation of a diagnostic test is the gold
    standard, a second diagnostic test generally regarded
    to provide the most definitive evidence for or against
    the presence of a particular condition. For example, a
    study evaluating the ability of physical examination to

    Orthopaedic Knowledge Update 10

    159

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    Figure 1

    Number of RCTs in orthopaedic journals, 19681999. (Data from Gnal I: Do orthopaedic journals provide high-quality evidence for clinical
    practice? Arch Orthop Trauma Surg 2003;123:
    82-85.)

    detect a meniscal tear could use arthroscopy as the gold


    standard. For a diagnostic study to be considered of
    high quality, there must be a gold standard that is universally applied to all cases. (In the previous example,
    all study participants would have to undergo arthroscopy for it to be considered a high-quality diagnostic
    study.) Another feature of high-quality diagnostic studies is the inclusion of consecutive patients, as detailed
    in Table 1.
    The final study type included in the AAOS level of
    evidence classification system is economic and decision
    analyses. This study type is relatively uncommon in the
    orthopaedic literature, as it has been found to represent
    less than 1% of clinical studies published in orthopaedic journals.16-18 Details on the criteria used to assign
    levels of evidence to these types of studies are described
    in Table 1.

    Interrater Reliability in the


    Assignment of Levels of Evidence
    For the level of evidence classification system to be
    most useful, there must be consistency of grade assignment between different raters. Recently, there have
    been several studies assessing interrater agreement in
    the assignment of levels of evidence to orthopaedic research, and interrater reliability has been found to
    range widely.16-18,20,21
    One of the factors that appears to influence interrater
    reliability is the training and experience of the raters who
    are submitting level of evidence grades. For example, in
    a study of individuals reviewing manuscripts for The
    Journal of Bone and Joint Surgery: American volume, the
    authors found that reviewers with training in epidemiology demonstrated near-perfect agreement (intraclass
    correlation coefficient [ICC] of 0.99 to 1.00, versus 0.61
    160

    Orthopaedic Knowledge Update 10

    to 0.75 for reviewers not trained in epidemiology).16 Similarly, the authors of another study found that agreement
    in the assignment of level of evidence was higher among
    experienced reviewers (practicing orthopaedic surgeons)
    than between experienced and inexperienced reviewers
    (orthopaedic residents and medical students) (kappa
    0.75 versus 0.62).17 In addition, the ability of orthopaedic residents to identify the level of evidence of 10
    blinded articles from The Journal of Bone and Joint Surgery: American volume, was assessed. The mean percentage correct was found to be only 29.5% (41.3% after an
    educational intervention).21
    Most recently, the feasibility of assigning levels of
    evidence to abstracts presented at the AAOS Annual
    Meeting was examined. In particular, the levels of evidence assigned by authors, volunteer graders (with access to the abstract only), and session moderators (with
    access to the full paper) were examined. Agreement
    ranged from slight to moderate (kappa 0.16 to 0.46).20
    However, this study did not consider the experience or
    epidemiologic training of the raters in question. The
    study also found that authors tended to grade the level
    of evidence of their own work more favorably than did
    other graders,20 which is a finding deserving of further
    investigation.

    Current Levels of Evidence in the


    Orthopaedic Literature
    Recent studies have been fairly consistent in describing
    the current status of the orthopaedic literature. The
    most common study type is therapeutic (69% to 71%),
    followed by prognostic (20% to 25%), diagnostic (6%
    to 9%), and economic/decision analysis (0% to
    0.5%).16,17 With regard to level of evidence, level IV
    studies comprise 54% to 58% of the orthopaedic literature, whereas level I evidence accounts for only 11%
    to 16%.16-18 Upon closer examination of the level I
    data, many of these studies appear to have shortcomings.22,23
    However, recent studies provide reason to be optimistic regarding levels of evidence in the orthopaedic
    literature. In a 2009 study, 551 articles in The Journal
    of Bone and Joint Surgery: American volume published
    over the past 30 years were examined. The percentage
    of clinical studies providing level I evidence increased
    from 4% to 21% between 1975 and 2005, while the
    percentage of level IV studies decreased from 81% to
    48% over this same period.24 An earlier study found
    that the number of randomized trials published in orthopaedic journals increased substantially between
    1968 and 199925 (Figure 1). Similar trends have been
    observed within the subspecialty field of sports medicine, as a 2005 study documented significant increases
    in the number of randomized controlled trials and prospective cohort studies coupled with a significant decrease in the number of case series and descriptive studies between 1991-1993 and 2001-2003.26
    In recent years, some researchers have sought to investigate the relationship between levels of evidence
    and other factors in orthopaedic research. Manuscripts

    2011 American Academy of Orthopaedic Surgeons

    Chapter 14: Evidence-Based Orthopaedics: Levels of Evidence and Guidelines in Orthopaedic Surgery

    Table 2

    Grades of Recommendation
    Grade

    Overall Quality of
    Evidence

    Good-quality evidence

    More than one level I study with consistent findings for or against recommending
    intervention

    Fair-quality evidence

    More than one level II or III study with consistent findings or a single Level I study
    for or against recommending intervention.

    Poor-quality evidence

    More than one level IV or V study or a single level II or III study for or against
    recommending intervention

    No evidence or conflicting
    evidence

    There is insufficient or conflicting evidence not allowing a recommendation for or


    against intervention.

    Description of Evidence

    1: Principles of Orthopaedics

    Data from Grades of Recommendation for Summaries or Reviews of Orthopaedic Surgical Studies. Rosemont, IL, American Academy of Orthopaedic Surgeons.
    Http://www.aaos.org/research/evidence/gradesofrec.asp. Accessed Nov. 10, 2010.

    submitted to The Journal of Bone and Joint Surgery:


    American volume were studied; studies with a higher
    level of evidence were more likely to be accepted for
    publication.19 Articles published in three prominent
    general orthopaedics journals also were examined, and
    it was found that studies with a higher level of evidence
    were also more likely to be cited following publication.27 The relationship between level of evidence and
    declared funding support was examined in a recent
    study. It was determined that industry-funded studies
    were more likely to provide level IV evidence than were
    studies funded by not-for-profit sources.28 This last association has not been documented previously and is
    certainly deserving of further investigation.

    Using Levels of Evidence in


    Orthopaedic Practice
    The levels of evidence classification system provides a
    rapid assessment of study quality, which may help readers to quickly place studies into context. Because studies of higher level of evidence have greater methodologic safeguards against bias, they may provide better
    information to guide physicians in their care of patients.
    However, it is important to emphasize that a level of
    evidence rating does not tell the whole story with regard to a particular study. Assignment of a particular
    level of evidence represents an assessment of the study
    design as reported by the authors but does not address
    other factors such as quality of data gathering or interpretation.16 This is emphasized in the first footnote in
    Table 1, which states that a complete assessment of
    [the] quality of individual studies requires critical appraisal of all aspects of the study design.29 Levels of
    evidence cannot be used in a blind manner; orthopaedic
    surgeons must always consider all aspects of a given
    study, and integrate these data with their individual
    clinical expertise.

    2011 American Academy of Orthopaedic Surgeons

    Clinical Practice Guidelines

    History and Purpose


    When medical decision making is based largely on
    opinion, wide variation in clinical practice is expected.
    Although variability certainly persists within the
    evidence-based model, large discrepancies in practice
    patterns invite investigation. It was in this context that
    the Institute of Medicine first proposed clinical practice
    guidelines, defined as systematically developed statements to assist practitioner and patient decisions about
    appropriate health care for specific clinical circumstances.30
    Since they were first proposed in 1990,30 the number
    of such guidelines has grown rapidly. By August of
    2010, for example, there were nearly 2,500 guidelines
    listed in the National Guideline Clearinghouse.31
    Over the past few years, AAOS has begun to publish
    clinical practice guidelines on a variety of topics within
    orthopaedic surgery.32 As of August 2010 there were
    nine such guidelines that had been approved by AAOS,
    with several more in various stages of the development
    process.

    Developing Clinical Practice Guidelines


    In the selection of topics for guideline development,
    ideal candidates include common conditions with a
    solid evidence base but wide variation in practice patterns. In these cases, clinical practice guidelines have
    the best opportunity to achieve their objectives of decreasing practice variability, optimizing clinical outcomes, and promoting cost efficiency.
    The backbone of any clinical practice guideline is the
    literature review, which proceeds in a systematic and
    carefully considered manner. Retrospective case reviews
    are excluded, and underpowered studies are not considered (unless used as part of a de novo meta-analysis).

    Orthopaedic Knowledge Update 10

    161

    Section 1: Principles of Orthopaedics

    Table 3

    1: Principles of Orthopaedics

    Sample of Recommendations From a Recent AAOS Clinical Practice Guideline on the Treatment of
    Pediatric Diaphyseal Femur Fractures
    Level of
    Evidence

    Grade of
    Recommendation

    1. We recommend that children younger than 36 months with a diaphyseal femur


    fracture be evaluated for child abuse.

    II

    2. Treatment with a Pavlik harness or a spica cast are options for infants 6 months and
    younger with a diaphyseal femur fracture.

    IV

    3. We suggest early spica casting or traction with delayed spica casting for children age 6
    months to 5 years with a diaphyseal femur fracture with less than 2 cm of shortening.

    II

    8. It is an option for physicians to use flexible intramedullary nailing to treat children age
    5 to 11 years diagnosed with diaphyseal femur fractures.

    III

    9. Rigid trochanteric entry nailing, submuscular plating, and flexible intramedullary


    nailing are treatment options for children age 11 years to skeletal maturity diagnosed
    with diaphyseal femur fractures, but piriformis or near piriformis entry rigid nailing are
    not treatment options.

    IV

    10. We are unable to recommend for or against removal of surgical implants from
    asymptomatic patients after treatment of diaphyseal femur fractures.

    IV

    Inconclusive

    Adapted from American Academy of Orthopaedic Surgeons: Treatment of Pediatric Diaphyseal Femur Fractures: Guideline and Evidence Report. Rosemont, IL, American
    Academy of Orthopaedic Surgeons, 2009.

    On the basis of the best available evidence, recommendations are made regarding the management of patients. Each recommendation carries a level of evidence
    derived from the data underlying the recommendation,
    as well as a grade of recommendation (Table 2). Table
    3 presents a sample of recommendations from a recent
    AAOS Clinical Practice Guideline on the management
    of pediatric diaphyseal femur fractures. Once a guideline has been created, it must undergo peer review and
    finally a thorough approval process. The entire process
    of developing an AAOS clinical practice guideline is
    quite extensive and usually takes 12 to 18 months to
    complete.

    Concerns Regarding Clinical


    Practice Guidelines
    Although clinical practice guidelines have generally
    been welcomed by the evidence-based medicine community, this reception has not been universal. Some argue, for example, that clinical practice guidelines erode
    physician autonomy and run the risk of transforming
    clinical practice into cookbook medicine. Others
    complain that existing guidelines are too comprehensive or too narrowly focused, and quickly become outdated. Still others voice fears that guidelines will be
    used to critique the treatment decisions of physicians in
    legal and pay-for-performance settings.33
    More recently, critics have pointed to the potential
    for bias in the recommendations made by clinical practice guideline authors. In a recent study of physicians
    who authored 44 clinical practice guidelines on common adult diseases, it was found that 87% of the au162

    Orthopaedic Knowledge Update 10

    thors had some form of interaction with the pharmaceutical industry, including 59% who had relationships
    with companies whose products were considered in the
    guideline they authored. However, in only two cases
    were these personal financial interactions specifically
    disclosed in the final published guideline.34 Although
    clinical practice guidelines are meant to be completely
    objective, the development process does involve
    subjective judgments where competing interests could
    come into play. AAOS has taken several steps to
    combat bias in the development of clinical practice
    guidelines, including requiring full conflict of interest
    disclosure from all authors and using well-defined, systematic processes that are transparent and reproducible.35

    Using Clinical Practice Guidelines


    in Orthopaedic Practice
    Like levels of evidence, clinical practice guidelines are
    not instruments to be used blindly. Guidelines provide
    recommendations that are to be carefully evaluated by
    each physician and integrated with his or her clinical
    expertise.36 The Evidence-Based Medicine Working
    Group, writing in the Journal of the American Medical
    Association (JAMA) in 1995, proposed several questions that physicians should consider when using a particular clinical practice guideline.37 In particular, clinicians are urged to evaluate the validity and content of
    the guideline recommendations, as well as their applicability to the patient in question. By following the
    steps outlined in this article, physicians have the best
    opportunity to use clinical practice guidelines in a man-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 14: Evidence-Based Orthopaedics: Levels of Evidence and Guidelines in Orthopaedic Surgery

    ner that will provide the greatest benefit for their patients.

    Davidoff F, Haynes B, Sackett D, Smith R: Evidence


    based medicine. BMJ 1995;310(6987):1085-1086.

    9.

    Sackett DL: Rules of evidence and clinical recommendations on the use of antithrombotic agents. Chest 1986;
    89(2, Suppl):2S-3S.

    10.

    Wright JG, Swiontkowski MF, Heckman JD: Introducing levels of evidence to the journal. J Bone Joint Surg
    Am 2003;85(1):1-3.

    11.

    Lubowitz JH: Understanding evidence-based arthroscopy. Arthroscopy 2004;20(1):1-3.

    12.

    Reider B: Read early and often. Am J Sports Med 2005;


    33(1):21-22.

    13.

    Hentz RV, Meals RA, Stern P, Manske PR: Levels of evidence and the Journal of Hand Surgery. J Hand Surg
    Am 2005;30(5):891-892.

    14.

    Wright JG. Levels of evidence and grades of recommendation. AAOS Bulletin 2005;53(2).

    15.

    Wright JG: A practical guide to assigning levels of evidence. J Bone Joint Surg Am 2007;89(5):1128-1130.
    Practical tips for assigning levels of evidence to orthopaedic articles are provided.

    16.

    Bhandari M, Swiontkowski MF, Einhorn TA, et al: Interobserver agreement in the application of levels of evidence to scientific papers in the American volume of
    the Journal of Bone and Joint Surgery. J Bone Joint Surg
    Am 2004;86(8):1717-1720.

    17.

    Obremskey WT, Pappas N, Attallah-Wasif E, Tornetta P


    III, Bhandari M: Level of evidence in orthopaedic journals. J Bone Joint Surg Am 2005;87(12):2632-2638.

    18.

    Wupperman R, Davis R, Obremskey WT: Level of evidence in Spine compared to other orthopedic journals.
    Spine (Phila Pa 1976) 2007;32(3):388-393.
    In this study of articles published in Spine between January and June 2003, 16.1% were level I, 22.3% level II,
    8.0% level III, and 53.6% level IV. With regard to study
    type, 43.8% were therapeutic, 37.5% prognostic,
    17.9% diagnostic, and 0.9% economic.

    19.

    Okike K, Kocher MS, Mehlman CT, Heckman JD,


    Bhandari M: Publication bias in orthopaedic research:
    An analysis of scientific factors associated with publication in the Journal of Bone and Joint Surgery (American
    Volume). J Bone Joint Surg Am 2008;90(3):595-601.
    In this study of manuscripts submitted to The Journal of
    Bone and Joint Surgery: American volume, studies of
    higher level of evidence were more likely to be accepted
    for publication.

    Summary
    Levels of evidence and clinical practice guidelines are
    tools of the evidence-based medicine movement that can
    help physicians provide better care for their patients.
    They do not represent cookbook instructions to be followed blindly, but rather instruments to be carefully evaluated and integrated with clinical expertise.
    There is reason to be optimistic regarding evidencebased practice in the field of orthopaedic surgery. Levels of evidence are steadily increasing in the orthopaedic literature, and randomized trials are becoming more
    common. Several carefully researched clinical practice
    guidelines have recently been approved by AAOS, and
    others are under development. These advances have the
    potential to not only enhance the orthopaedic evidence
    base but also improve patient care.

    Annotated References
    1.

    Sackett DL, Rosenberg WM, Gray JA, Haynes RB,


    Richardson WS: Evidence based medicine: What it is
    and what it isnt. BMJ 1996;312(7023):71-72.

    2.

    Isaacs D, Fitzgerald D: Seven alternatives to evidence


    based medicine. BMJ 1999;319(7225):1618.

    3.

    Evidence-Based Medicine Working Group: Evidencebased medicine: A new approach to teaching the practice of medicine. JAMA 1992;268(17):2420-2425.

    4.

    Bernstein J: Evidence-based medicine. J Am Acad Orthop Surg 2004;12(2):80-88.

    5.

    Schnemann HJ, Bone L: Evidence-based orthopaedics:


    a primer. Clin Orthop Relat Res 2003;413:117-132.

    6.

    Bhandari M, Tornetta P III: Evidence-based orthopaedics: A paradigm shift. Clin Orthop Relat Res 2003;413:
    9-10.

    7.

    Poolman RW, Sierevelt IN, Farrokhyar F, Mazel JA,


    Blankevoort L, Bhandari M: Perceptions and competence in evidence-based medicine: Are surgeons getting
    better? A questionnaire survey of members of the Dutch
    Orthopaedic Association. J Bone Joint Surg Am 2007;
    89(1):206-215.
    In this survey of Dutch orthopaedic surgeons, evidencebased medicine was welcomed and clinical practice
    guidelines were perceived as the best means of proceeding from opinion-based medicine to evidence-based
    practice.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    8.

    163

    1: Principles of Orthopaedics

    Section 1: Principles of Orthopaedics

    164

    20.

    Schmidt AH, Zhao G, Turkelson C: Levels of evidence


    at the AAOS meeting: Can authors rate their own submissions, and do other raters agree? J Bone Joint Surg
    Am 2009;91(4):867-873.
    In this study of abstracts accepted for presentation at
    the 2007 AAOS Annual Meeting, interrater reliability
    ranged from slight to moderate, and authors were found
    to grade the level of evidence of their own work more
    favorably than did others who graded the abstract.

    21.

    Wolf JM, Athwal GS, Hoang BH, Mehta S, Williams


    AE, Owens BD: Knowledge of levels of evidence criteria
    in orthopedic residents. Orthopedics 2009;32(7):494.
    In this study, orthopaedic residents were able to identify
    the level of evidence of blinded studies only 29.5% of
    the time before an educational intervention, and just
    41.3% of the time posteducation.

    22.

    Bhandari M, Richards RR, Sprague S, Schemitsch EH:


    The quality of reporting of randomized trials in the
    Journal of Bone and Joint Surgery from 1988 through
    2000. J Bone Joint Surg Am 2002;84(3):388-396.

    23.

    Poolman RW, Struijs PA, Krips R, Sierevelt IN, Lutz


    KH, Bhandari M: Does a Level I Evidence rating imply high quality of reporting in orthopaedic randomised
    controlled trials? BMC Med Res Methodol 2006;6:44.

    24.

    Hanzlik S, Mahabir RC, Baynosa RC, Khiabani KT:


    Levels of evidence in research published in The Journal
    of Bone and Joint Surgery (American Volume) over the
    last thirty years. J Bone Joint Surg Am 2009;91(2):425428.
    In this study of articles published in The Journal of
    Bone and Joint Surgery: American volume between
    1975 and 2005, the percentage of level I studies increased from 4% to 21% while the percentage of level
    IV studies decreased from 81% to 48%.

    25.

    Kiter E, Karatosun V, Gnal I: Do orthopaedic journals


    provide high-quality evidence for clinical practice? Arch
    Orthop Trauma Surg 2003;123(2-3):82-85.

    26.

    Brophy RH, Gardner MJ, Saleem O, Marx RG: An assessment of the methodological quality of research published in The American Journal of Sports Medicine. Am
    J Sports Med 2005;33(12):1812-1815.

    27.

    Okike K, Kocher MS, Torpey JL, Nwachukwu BU, Mehlman CT, Bhandari M: Level of evidence and conflict
    of interest disclosure associated with higher citation
    rates in orthopedics. J Clin Epidemiol 2010 Oct 12.
    Epub ahead of print.
    In this study of articles published in three general orthopaedics journals in 2002-2003, factors associated with
    an increased number of citations at 5 years were high
    level of evidence, large sample size, representation from
    multiple institutions, and self-reported disclosure of a
    conflict of interest.

    Orthopaedic Knowledge Update 10

    28.

    Noordin S, Wright JG, Howard A: Relationship between declared funding support and level of evidence.
    J Bone Joint Surg Am 2010;92(7):1647-1651.
    In this study of articles published in J Bone Joint Surg
    Am between 2003 and 2007, studies funded by industry
    were significantly more likely to report level IV evidence
    as compared to studies funded by governments, foundations, or universities.

    29.

    The American Academy of Orthopaedic Surgeons: Levels of evidence for primary research question. http://
    www.aaos.org/Research/Committee/Evidence/
    loetable1.pdf. Accessed August 29, 2010.
    A table summarizing the characteristics of each level of
    evidence as it applies to therapeutic, prognostic, diagnostic, and economic / decision analysis studies is presented.

    30.

    Committee to Advise the Public Health Service on Clinical Practice Guidelines / Institute of Medicine: Clinical
    Practice Guidelines: Directions for a New Program.
    Washington, DC: National Academy Press, 1990.

    31.

    The National Guideline Clearinghouse: The National


    Guideline Clearinghouse. http://www.guideline.gov. Accessed August 29, 2010.
    The National Guideline Clearinghouse is a repository of
    Clinical Practice Guidelines maintained by the Agency
    for Healthcare Research and Quality (AHRQ), a branch
    of the United States Department of Health and Human
    Services. Its stated mission is to provide physicians and
    other health professionals, health care providers, health
    plans, integrated delivery systems, purchasers, and others an accessible mechanism for obtaining objective, detailed information on clinical practice guidelines and to
    further their dissemination, implementation, and use.

    32.

    The American Academy of Orthopaedic Surgeons:


    AAOS Evidence-based Clinical Practice Guidelines.
    http://www.aaos.org/research/guidelines/guide.asp. Accessed August 29, 2010.
    A repository of clinical practice guidelines developed by
    the AAOS is presented.

    33.

    Shaneyfelt TM, Centor RM: Reassessment of clinical


    practice guidelines: Go gently into that good night.
    JAMA 2009;301(8):868-869.
    The authors describe the shortcomings of clinical practice guidelines as they currently exist and argue that
    they should undergo major changes or be abandoned.

    34.

    Choudhry NK, Stelfox HT, Detsky AS: Relationships


    between authors of clinical practice guidelines and the
    pharmaceutical industry. JAMA 2002;287(5):612-617.

    35.

    The American Academy of Orthopaedic Surgeons:


    AAOS Evidence-based Clinical Practice Guidelines Frequently Asked Questions. http://www.aaos.org/
    research/guidelines/Guideline_FAQ.asp. Accessed August 29, 2009.
    A summary of answers to frequently asked questions regarding clinical practice guidelines in orthopaedics.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 14: Evidence-Based Orthopaedics: Levels of Evidence and Guidelines in Orthopaedic Surgery

    36.

    American Academy of Orthopaedic Surgeons: Treatment of Pediatric Diaphyseal Femur Fractures: Guideline and Evidence Report. Rosemont, IL, American
    Academy of Orthopaedic Surgeons, 2009.
    This document, which makes recommendations regarding the management of pediatric diaphyseal femur fractures, represents a typical example of a Clinical Practice
    Guideline.

    37.

    Hayward RS, Wilson MC, Tunis SR, Bass EB, Guyatt


    G: Users guides to the medical literature: VIII. How to
    use clinical practice guidelines: A. Are the recommendations valid? The Evidence-Based Medicine Working
    Group. JAMA 1995;274(7):570-574.

    1: Principles of Orthopaedics

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    165

    Chapter 15

    Orthopaedic Research: Health


    Research Methodology
    Brad A. Petrisor, MSc, MD, FRCSC

    Mohit Bhandari, MD, MSc, FRCSC

    The paradigm of evidence-based surgical practice requires a clear delineation of clinical questions and actions based on the best available evidence. Proficiency
    in health research methods is needed to identify and appraise the best available surgical literature. Surgeons
    must be able to categorize clinical research into a hierarchy of evidence, identify pitfalls in the conduct of
    clinical research, and understand fundamental practical statistics.

    The Language of Research: Common Terms to


    Relay a Treatments Effect
    Surgeons, in general, are interested in the results of
    high-quality clinical studies such as randomized trials.
    These results guide clinical practitioners in making
    treatment decisions and communicating the risks and
    benefits of these treatments to their patients. Results of
    trials are based on the occurrence or nonoccurrence of
    an outcome event. The two main categories of outcomes are dichotomous outcomes and continuous outcomes (or continuous variables).1-3 Dichotomous outcomes (such as death, nonunion, infection, or revision
    surgery) either occur or do not occur. Continuous outcomes can take the form of a scale of values such as

    Dr. Petrisor or an immediate family member is a member


    of a speakers bureau or has made paid presentations
    on behalf of Stryker, Smith & Nephew, and AO; serves as
    a paid consultant to or is a paid employee of Stryker;
    and has received research or institutional support from
    Synthes and Stryker. Dr. Bhandari or an immediate family member is a member of a speakers bureau or has
    made paid presentations on behalf of Stryker, Smith &
    Nephew, and Amgen; serves as a paid consultant to or is
    an employee of Amgen, Pfizer, Baxter, King Pharmaceuticals, Wyeth, Smith & Nephew, and Stryker; and has received research or institutional support from Canadian
    Institutes of Health Research (CIHR), Canadian Orthopedic Foundation, AO, DePuy, National Institutes of Health
    (NIAMS & NICHD), Smith & Nephew, and Stryker.

    2011 American Academy of Orthopaedic Surgeons

    health outcome scores, laboratory values, or range of


    motion measurements. For the purposes of this discussion, the focus will be on dichotomous outcome variables.
    Results of dichotomous outcomes are commonly expressed in the language of proportions (such as relative
    risk, relative risk reduction, or odds ratios) or in terms
    of absolute differences between risks, the absolute risk
    reduction, risk difference, or the number needed to
    treat.1,4 The relative risk is defined as the ratio of the
    risk of an event among an exposed population to the
    risk among an unexposed population1,3 (Table 1). If
    the relative risk is equal to 1, there is no difference between the exposed or unexposed (or experimental and
    control, respectively) populations. If the relative risk is

    1: Principles of Orthopaedics

    Introduction

    Table 1

    Table of Events for a Fictitious Trial With an


    Experimental Group and a Control Group
    Illustrating the Calculation of Different
    Measures of Treatment Effect
    Outcome
    Event

    No Outcome
    Event

    Experimental group
    N = 100

    10

    90

    Control group
    N = 100

    20

    80

    Relative risk

    10/100
    20/100
    = 0.5

    Relative risk reduction

    1 RR
    =50%

    Odds ratio

    10/90
    20/80
    = 0.44

    Absolute risk reduction

    10% - 20%
    = 10%

    Number needed to treat

    1/ARR
    = 10

    RR = relative risk, ARR = absolute risk reduction

    Orthopaedic Knowledge Update 10

    167

    Section 1: Principles of Orthopaedics

    1: Principles of Orthopaedics

    less than 1, then risk is, by convention, given in terms


    of the relative risk reduction or 1 minus the relative risk
    (1 RR). For example, in a hypothetical experiment
    with treatment A versus a control group receiving no
    treatment, if the relative risk of infection with treatment A is 0.5, then an individual is 50% as likely to get
    an infection with treatment A compared with the control. Similarly the relative risk reduction would then be
    1 0.5, or 50%; that is, an individual is 50% less likely
    to have an infection with treatment A compared with
    the control.
    Odds ratios are another way of expressing treatment
    effects. In general, odds ratios are used to approximate
    relative risk in retrospective study designs in which the
    baseline risk or incidence rates are unknown or when
    event rates are very low.1,3 Some researchers believe
    that odds ratios may overestimate or underestimate
    treatment effects if event rates are high, and that clinicians intuitively understand relative risks better than
    odds ratios.5-7 An odds ratio by definition is the ratio
    of the odds of having an event in an exposed group to
    the odds of having an event in a group that is not exposed1 (Table 1). Odds themselves are the ratio of
    events to nonevents.
    Relative risk is a common way to report the treatment effect based on a dichotomous outcome variable;
    however, it can at times be misleading. For instance, in
    the aforementioned example, if treatment A reduces the
    risk of infection by 50% then it stands to reason that
    most people would choose treatment A over control
    (receiving no treatment). However, if the baseline risk
    of infection is 1%, then treatment A would reduce the
    risk of infection to 0.5%, a potentially clinically meaningless reduction in risk. Thus, relative risks do not
    take into account baseline risks. To be truly meaningful, relative risks should be presented along with baseline risks.5,6,8,9 It has been shown that patients prefer to
    have relative risks and baseline risks presented during
    discussions with their physicians.9
    The absolute risk reduction is defined as the absolute difference in the rate of harmful outcomes between
    experimental groups and control groups1,3 (Table 1).
    Thus, if the infection rate in treatment A is 20% and
    the infection rate in the control group is 10%, then the
    absolute risk difference would be 10%. For every 100
    patients treated with treatment A, 10 patients will not
    get an infection. Stated another way, for every 10 patients treated with treatment A, one infection can be
    prevented. This is the number needed to treat and is
    given by 1 divided by the absolute risk reduction
    (1/ARR).1,3,10,11 This is arguably a powerful number to
    clinicians because it helps them to understand the potential clinical relevance of an intervention. Confidence
    intervals should also be provided for all of these results
    to help clinicians understand the precision of the measure of treatment effect. Accuracy can be defined as
    how close the measure of treatment effect is to the
    truth; precision can be defined as how close repeated
    measures of effect are to each other.
    168

    Orthopaedic Knowledge Update 10

    Randomized Controlled Trials


    Within the hierarchy of evidence, randomized controlled trials are considered by many researchers and
    clinicians to provide the highest-quality evidence.4,12
    Randomized controlled trials are experimental study
    designs. In simple terms, patients are randomly allocated to either an experimental group or a control
    group. This study design is considered by many researchers to be the best study design to determine therapeutic efficacy or effectiveness.13,14 The strength of
    randomization, or random allocation, is that patients in
    the study groups are balanced at baseline.1,3,13 That
    is, both the known and unknown prognostic or confounding factors are balanced between groups. Although it is easy to balance for known confounding
    factors or prognostic factors, such as age, sex, or comorbidities, it is not possible to balance for unknown
    prognostic factors except through the act of randomization. Even though randomization is considered the
    best method to evaluate a therapy, this study design
    presents several challenges, especially within the field of
    orthopaedic surgery. Medical randomized trials often
    compare drug A against placebo, or drug A against
    drug B, looking for either superiority or at least equivalence or noninferiority. In surgical situations, sham
    surgery would be equivalent to placebo. However, inducing anesthesia in patients, cutting skin, and not providing treatment presents many ethical issues. Although
    sham surgery has been used successfully in orthopaedic
    trials in the past,15 the significant ethical concerns with
    respect to both the patient and the surgeon can severely
    limit patient recruitment and a surgeons willingness to
    participate. Indeed, it would be difficult to obtain the
    consent of institutional research ethics boards. For this
    reason, randomized trials in orthopaedic surgery tend
    to assess two different treatments of a particular condition, such as total hip implant A compared with total
    hip implant B, and sometimes surgical versus nonsurgical treatment.
    There are several potential barriers to conducting
    randomized controlled trials in orthopaedic surgery.
    Such trials can be very costly to manage and coordinate. A well-managed randomized trial includes a steering committee to oversees the overall conduct of the
    study, an outcome adjudication committee to assess all
    outcome events, a data safety and monitoring committee, a methods center with its associated staff, and individual site investigators.11,16 Because it is often necessary to collaborate with numerous medical centers,
    many surgeons with different levels of expertise in particular procedures must be asked to recruit patients.
    There are also ethical concerns regarding the use of
    new implants or devices. Because surgeons often have a
    preferred technique or their own nuances for a common technique, they may be reluctant to participate in
    a trial or to recruit patients for a trial that uses a different technique. Although such issues are challenging,
    they are not insurmountable. Many randomized trials
    have been conducted and published in the orthopaedic

    2011 American Academy of Orthopaedic Surgeons

    Chapter 15: Orthopaedic Research: Health Research Methodology

    Figure 1

    literature, although there have been far fewer randomized trials compared with the number of observational
    trials.17,18
    Although randomization can balance both known
    and unknown prognostic variables, the prognostic balance can be threatened in several ways. If patient allocation to treatment groups is not concealed, patients
    can be differentially excluded; this leads to prognostically uneven treatment groups. If investigators and outcomes assessors know to which group a patient has
    been allocated (that is, they were not blinded or
    masked), they can affect the way the patient is treated
    throughout the trial. The lack of concealment in allocation and blinding can affect the validity of the
    trial.13,19,20 It has been shown that trials with inadequate concealment of allocation may overestimate the
    effect of interventions by as much as 40%.21,22 In the
    orthopaedic literature, the lack of blinding may be associated with an overestimation of the benefit of some
    treatment effects.19
    Sample size is another important factor in surgical
    trials. Surgical trials are typically significantly smaller
    than trials in other medical specialties such as cardiology. When trials have fewer participants, imbalances
    within groups can occur through random chance. In
    trials with fewer patients, the prognostic balance between groups can be achieved in several ways, including the use of stratified randomization. For example, a
    trial is designed to compare the outcomes of using a
    new type of plate to fix tibial plafond fractures with
    two centers selected to enroll patients. One center is a
    high-volume trauma center and the other is a community hospital in a small town. It is likely that the patients from the trauma center will differ prognostically
    (more high-energy fractures and open wounds) than the
    patients at the community hospital. If the randomization is stratified by center, then the centers will contribute patients to both arms of the study on a fairly equal
    basis. This method will balance the groups for the potential prognostic differences of patients in the two cen-

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    Illustration of a factorial trial design. Patients


    are randomized to either treatment A, treatment B, or control. The red arrows denote analysis 1: treatment A versus control. The blue
    arrows denote analysis 2: Treatment B versus
    control. With this trial design, the same study
    population is used for two interventions and
    analyses.

    ters. However, when stratification is used, blocked randomization also should be incorporated into the
    randomization scheme. Blocking ensures that the
    groups are similar with respect to the number of patients in each group and aids in concealing the randomization scheme. For example, if the block size is four,
    and three patients have been randomized to treatment
    groups (A, A, and B) then the next patient will be randomized to group B. The block sizes can be changed
    from two to four or six (or any size); usually blocks
    will alternate from four to six or eight and back.
    Randomized controlled trials can take several different designs, including the parallel design, crossover design, factorial design, or the expertise-based design.

    Parallel Design
    The parallel design trial is the simplest and most classic
    design for a randomized controlled trial. In this trial
    design, participants are randomized to two or more
    groups of different treatments and each group is exposed to a different intervention and only that intervention.11,13 In medical parallel design trials, one group is
    often given a treatment or an experimental drug and
    the other group receives no treatment or a placebo. In
    an orthopaedic surgical parallel trial, one group may
    receive one type of treatment and the other group a different type of treatment. For example, in a parallel design trial of fracture fixation, one group may be treated
    with intramedullary nail fixation and the other with extramedullary fixation. This trial design produces
    between-group or -participant comparisons. Multiple
    comparisons and interventions can be made depending
    on the number of groups to which patients are randomized. However, increasing the number of groups (or
    arms) in the trial requires a larger sample size to permit
    statistically and clinically meaningful comparisons.

    Crossover Design
    In the crossover design trial, both groups receive both
    interventions over a randomly allocated time period.11,13 This design is easier to implement in medical
    trials. Group A can receive the treatment, and after a
    suitable washout period, can receive the placebo.
    Group B can receive the placebo and later can receive
    the treatment; this produces within-participant comparisons.13 The advantage of a crossover design trial is that
    fewer participants may be needed to produce both statistically and clinically meaningful results compared
    with parallel design trials.13 The crossover design trial
    has a limited role in surgical interventions because it is
    difficult or impossible for patients to receive both treatment interventions, such as plate and nail fixation, or a
    cemented versus an uncemented total hip replacement.

    Factorial Design
    Factorial design trials allow for two interventions to be
    compared within the same study group23 (Figure 1). For
    example, a participant can be randomized to receive
    treatment A, treatment B, or control. This design is
    more easily represented in a two-by-two table with

    Orthopaedic Knowledge Update 10

    169

    Section 1: Principles of Orthopaedics

    tion. However, the expertise-based design may affect


    the generalizability of the results.24 For example, if outcomes are better with treatment A, is it because of the
    treatment or because patients were treated by experts
    in that treatment? How would the results apply to patient care for a surgeon who in the past had primarily
    used treatment B? The outcome would mean that a surgeon would either need to obtain training in treatment
    A or should refer patients to another surgeon who is an
    expert in treatment A.

    1: Principles of Orthopaedics

    Conclusion

    Figure 2

    Illustration of a cohort study design compared


    with a case-control study design. Note that a
    retrospective cohort will ask the study question
    after the outcomes have accrued but will go
    back in time, identify cohorts, and follow the
    groups to determine who developed the outcome of interest. This is in contrast to a casecontrol design, where the researcher identifies
    cases and controls and looks back in time to
    identify associated risk factors.

    those receiving or not receiving treatment A being analyzed, and those receiving treatment B or not receiving
    treatment B being analyzed. Practically, patients are
    randomized to either treatment A and B, treatment A
    or control, treatment B or control, or no treatment. The
    strength of this trial design is that two interventions
    can be assessed with the same study population. Also,
    any interaction between the treatments can be determined11 (for example, does treatment A work differentially when combined with treatment B?)

    Expertise-Based Design
    Another type of randomized controlled trial design is
    the expertise-based trial, or randomizing to a particular
    surgeon with expertise in the treatment.23,24 If the use of
    an intramedullary nail for proximal tibia fractures is to
    be compared with a proximal minimally invasive locking plate, the nonexpertise-based trial would randomize the patients to treatment A or treatment B, and the
    surgeon would perform either treatment A or treatment
    B based on this randomization. The problem with this
    trial design is that the participating surgeons may not
    have equal expertise in performing both types of procedures. A surgeon who does not have significant expertise with intramedullary nailing could choose to use a
    minimally invasive plate, thus creating a protocol deviation that could potentially affect the outcome. Alternatively, the surgeon may elect not to participate in the
    trial. In expertise-based trials, a patient would be randomized to treatment A and surgeon A, who would be
    an expert in intervention A; another patient may be
    randomized to treatment B and surgeon B, an expert in
    the B procedure. This trial design ensures that the intervention is done by the requisite expert in the interven170

    Orthopaedic Knowledge Update 10

    Randomized controlled trials are not appropriate for


    all research questions. Some situations make it unethical to randomize patients for treatment. For example,
    to determine how smoking affects fracture healing or
    bone ingrowth on an implant, it is not ethical to randomize one group of patients to smoking and the other
    group to nonsmoking. In other situations, a condition
    may be too rare to perform a randomized controlled
    trial. For example, without substantial collaboration, it
    would be difficult to randomize patients with infected
    tibial nonunions to treatment with an Ilizarov onestage reconstruction or a two-stage reconstruction because it would take many years to perform such a
    study. For these reasons, it may be necessary to use observational studies.11,25

    Observational Studies
    Observational studies necessarily observe participants
    in groups within the study; these groups are not randomized. There are three main types of observational
    study designs: the cohort study, the case-control study,
    and the case series.

    Cohort Studies
    The cohort study can be done prospectively or retrospectively26 (Figure 2). By nature, the prospective study
    design produces higher-quality evidence than the retrospective design and it is considered level I evidence, or
    the highest level of evidence in studies of a prognostic
    nature.4,27 The prospective cohort study design would
    be similar in every respect to a randomized controlled
    design except that the patients are not randomized to
    the study groups. Patient groups are determined on the
    basis of having received a specific exposure or not
    having received the exposure. For example, in a
    study to determine the effect of smoking on fracture
    nonunion, a prospective cohort design could include
    one group of patients with fractures who smoke and
    one group with fractures who do not smoke. The
    groups can be matched by age, sex, and medical comorbidities. The only known difference between groups
    then would be smoking (the exposure). Thus, the prospective cohort design attempts to match the groups for
    known prognostic variables; however, it is not known if
    unrecognized prognostic variables have also been
    matched. In the analysis of results, researchers must be

    2011 American Academy of Orthopaedic Surgeons

    Chapter 15: Orthopaedic Research: Health Research Methodology

    Case-Control Studies
    The case-control study design is often confused with a
    retrospective cohort design; however, in the casecontrol design, the patients who have an outcome of interest are identified and then matched to a control
    group who did not have the outcome of interest. The
    researcher then proceeds backward in time to identify
    the factors potentially associated with the outcome of
    interest.28,29 The case-control design is necessarily a retrospective study. Although this design produces a lower
    level of evidence, the case-control design can be useful
    for evaluating rare outcomes or diseases.28 Case-control
    studies are often far less expensive to conduct than prospective trials, and are useful for generating a hypothesis. Case-control studies allow the calculation of incidence rates and odds ratios to potentially approximate
    the relative risk.

    Case Series
    A case series is a study of patients receiving a particular
    treatment, often by a single surgeon or at a single institution. The case series can be prospective or retrospective and can be used to determine important information such as the natural history of a disease and
    possible complications of a particular treatment. This
    study design can be used to generate hypotheses for further research. The hallmarks of a well-designed case series include prospective data collection, inclusion of
    each patient who received the treatment, validated outcome measures, the use of independent outcomes assessors and data analysts, and a high follow-up rate.

    Conclusion
    Within the orthopaedic literature, observational studiescase series, case-control designs, and cohort designshave provided most of the information that
    guides clinical practices. Only a small number of orthopaedic studies are randomized controlled trials.17
    There is controversy concerning the relative merits
    of observational study designs versus experimental designs. Some authors have suggested that observational
    studies overestimate or underestimate treatment effects
    or relative risks.25,30 In moving along the hierarchy of
    evidence from cases series to randomized controlled tri-

    2011 American Academy of Orthopaedic Surgeons

    als, increasing safeguards against bias are introduced. It


    can be argued, however, that methodologically superior
    observational trials can result in estimates of effect with
    more accuracy and precision than methodologically
    flawed randomized controlled trials; therefore, it is important to determine the validity of the trial based on
    its methodology.

    Limiting Bias in Clinical Research


    Bias is often defined as a systematic tendency or deviation from the truth, which is different than deviations
    from the truth caused by chance.1,11 The fundamental
    difference between randomized trials and observational
    studies is that observational studies are more prone to
    bias. If a randomized trial was repeated 100 times, the
    results would vary to some degree based on random
    chance. Biases that can encroach on the validity of a
    study include selection, ascertainment, observational,
    and measurement biases.
    In randomized controlled trials, selection bias can
    occur, especially if randomization has not been concealed to the enrolling investigator. However, even if
    randomization is concealed, some patients could be excluded systematically from the trial. Selection bias is
    more readily apparent in an observational trial.
    Ascertainment bias occurs when the outcomes or
    conclusions of a trial are systematically distorted by the
    knowledge of which intervention each participant received.13 This type of bias is combated by the act of
    blinding or masking information from those involved
    in the trial. Blinding differs from concealment of allocation in that blinding attempts to keep those involved in
    the trial unaware of the intervention to which the patient has been randomized. The importance of blinding
    is that it preserves randomization because those involved in the trial (such as surgeons, nurses, physiotherapists, outcomes assessors, data analysts, and patients)
    can affect and influence how someone is treated if they
    have knowledge of the group to which the patient was
    randomized. From a surgical point of view, it is obviously not possible to blind a surgeon to the treatment
    allocated to a patient, nor is it possible to blind the surgical team (residents, fellows, and nursing staff). In
    some instances, however, it may be possible to blind the
    patient, clinic staff, outcomes assessors, and data analysts to the allocated treatment. Trials where outcome
    assessors were unblinded had significantly greater treatment effects than in those trials where outcomes assessors were blinded.19
    Observational and measurement biases can be introduced by those collecting outcome data and, in part, by
    the outcome instruments used. Independent outcomes
    assessors, a team of independent blinded outcomes adjudicators, and valid and reliable outcome measures
    help to limit this type of bias. Biases can result in systematic deviations from the truth that are different
    than deviations resulting from random chance.

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    cognizant of any confounding variables that may as yet


    be unknown. Prospective cohort designs can be powerful studies. They should have strict inclusion and exclusion criteria, validated outcomes that use outcome assessors and data analysts, and high follow-up rates.26
    A retrospective cohort study also can be done using
    a database of information that allows a question in the
    present to be answered by using an already established
    database to identify two cohorts of patients, who are
    followed to determine an outcome of interest. The
    problem with the retrospective study design is that not
    all of the requisite data points may have been determined, treatments could have changed over the course
    of the database, and not all of the important outcomes
    may have been assessed.

    171

    Section 1: Principles of Orthopaedics

    Conducting Subgroup Analyses

    1: Principles of Orthopaedics

    Subgroup analyses are performed to look for important


    differences in treatment effects.11,31 These differences
    can be related to different characteristics of the patients
    (such as older versus younger, male versus female) or to
    aspects of the treatment (such as reaming versus nonreaming of tibial nails, open versus closed fractures, or
    cemented versus uncemented implants). To determine
    when a subgroup effect is believable, certain information must be determined.1,3,32 It is necessary to know if
    the subgroup was determined before or after the study
    began. For example, in a 2008 study to prospectively
    evaluate patients with tibial fractures treated with
    reamed intramedullary nails, the investigators noted a
    potential subgroup effect of open versus closed fractures.33 This factor was discussed as an important subgroup effect before patients were enrolled and before
    the trial started. Investigators who argue against post
    hoc subgroup analyses suggest that this may be a form
    of data dredging and that multiple statistical analyses will by chance alone find a statistically significant
    result.1 Some guidelines have been developed to determine if an identified potential subgroup effect is real
    and some relevant questions have been formulated.1,3,34
    (1) Did the hypothesis precede, rather than follow, the
    analysis? (2) Was the subgroup difference one of the
    small number of hypothesized effects? (3) Is the magnitude of the subgroup difference large? (4) Is the subgroup difference consistent? (5) Was the subgroup difference statistically significant? (6) Does external
    evidence support the hypothesized subgroup difference?
    It is sometimes difficult to determine true and statistically significant subgroup effects in small trials, especially if these trials are underpowered to detect differences in even the primary outcome. Hence, the practice
    of multiple statistical testing on limited data can result
    in spurious-false positive findings of subgroup effects.

    Practical Statistics for Surgeons


    In statistical testing for experimental studies, the initial
    hypothesis must be determined by the investigators. For
    statistical testing, the null hypothesis, which states that
    there is no difference between the two groups being
    studied, is used. In comparison, the alternate hypothesis is that there is a difference between the two groups
    being studied. Two main types of error can occur when
    testing these hypotheses. The first type of error is
    known as the type I error, or error, or a false
    positive.35-37 In statistical terms, this is the rejection of
    the null hypothesis when the hypothesis is true. A difference between study groups is found when there is no
    difference. The second type of error in hypothesis testing is the type II error, or the error, or a false negative, which is the acceptance of the null hypothesis
    when the hypothesis is false. No difference between
    treatment groups is found when there is an actual difference between the groups. The term is given to the
    172

    Orthopaedic Knowledge Update 10

    probability of committing an error, or type I error,


    and is represented by the P value (often set by convention at 0.05). The term represents the probability of
    committing a type II error and is related to the power
    of the trial. The power of a study is the ability of a trial
    to detect a difference when in fact a true difference exists between groups; the power of the test is designated
    as 1 . This is the probability that the study will detect a true difference when one actually exists.

    P Values and Confidence Intervals


    As was previously mentioned, the P value (or ) is the
    probability of committing a type I error, or stated another way, it is the probability of finding a difference
    between groups in a trial when in fact there is no difference. By convention, the P value is set at 0.05. The P
    value by itself indicates if groups in a trial are statistically significantly different. If the P value is less than
    0.05, there is less than a 5% chance that the difference
    between groups is caused by chance. A P value does not
    provide information about the size of the treatment effect or whether the observed effect is clinically significant.38,39 In contrast, confidence intervals (CIs) indicate
    the probability of committing a type I error and provide information on the clinical significance of the results, the precision of the results, and the magnitude of
    the treatment effect.1,35,40,41 By convention, a 95% CI is
    used. This means that if a trial is repeated 100 times,
    95 of 100 times the result will fall within the 95% CI.
    Thus, 5% of the time the result would fall outside of
    the 95% CI and it would erroneously be concluded
    that there was a difference between groups when in fact
    there was no difference. CIs can be used around any
    measure of treatment effect, including relative risk,
    odds ratio, absolute risk reduction, and the number
    needed to treat. The treatment effect of a main study
    outcome is termed a point estimate or the point estimate of effect (that is, the relative risk, odds ratio, or
    risk reduction). With a 95% CI around the point
    estimate of effect, it would depict the true result 95%
    of the time. The CI determines the precision of the estimate of effect; the wider the CI, the less precise is
    the measure of effect.1,40 Several factors, including
    sample size, determine the width of the CI in clinical
    trials. The smaller the sample size, the lower the
    event rate and the more imprecise the measure of effect.
    A small sample size results in a large or wide CI. The
    size of the CI (90%, 95%, or 99%) also affects the CI
    width. Another factor affecting the size of the CI width
    is the actual level of variability within the study
    population. Increasing variability will increase the size
    of the CIs because increasing variability is associated
    with less precision. While indicating the precision
    around the estimate of effect, the CI also represents
    the spread of possible treatment effects. This information helps to determine the clinical significance of the
    treatment effect as well as the statistical significance
    (Figure 3).

    2011 American Academy of Orthopaedic Surgeons

    Chapter 15: Orthopaedic Research: Health Research Methodology

    Figure 3

    Study Power
    Study power, as previously mentioned, relates to the
    ability of the study to find a difference between groups
    if one really exists; study power is given by 1 . The
    larger the sample size for a clinical trial (and some argue, the higher the outcome event rate), the more ability the trial has to determine statistically and clinically
    important differences between groups. The power of
    the study is set conventionally at 0.8, or 80%, meaning
    that there would be an 80% chance that the study
    would detect true differences between groups if there
    was a difference to be found. Consequently, there is a
    20% chance () that the study would find no difference
    if in fact there was a true difference. Study power is
    typically determined before the study begins and in the
    trial design phase.

    Sample Size
    The sample size calculation is an important component
    of the study design. It is suggested that a statistician be
    consulted when calculating the sample size for a study.
    Internet search engines also can help in identifying Web
    sites that provide assistance with sample size calculations.42 The general reasons for doing a sample size calculation relate to issues of hypothesis testing. That is,
    investigators do not want to erroneously say there is a
    difference between study groups when there is no difference ( or type 1 error), nor do they want to say
    there is no difference between study groups when in
    fact there is a difference ( or type 2 error). Thus, sample size helps determine the power (1 ) of the study
    (accurately identifying a difference in groups when in
    fact there is one). Sample size calculations need to take
    into account (usually set at 0.05), (usually set at
    0.2), and the power (usually 0.8). Other factors to consider when calculating sample size are the potential effect size as well as the dropout rate of the trial. Although researchers should strive for 100% follow-up, it
    is not always attainable. Convention suggests that 80%
    follow-up is good; sample size calculations should take
    this into account. The potential effect size should be

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    A forest plot showing two fictitious trials. Both have relative risk reductions of 50% in favor of the experimental
    group. Trial 1 denotes a larger trial with a more precise estimate of treatment effect (the 95% CIs are narrow).
    Trial 2 has fewer patients, fewer events, and is less precise in its measure of treatment effect. The solid vertical line
    denotes a fictitious level of clinical significance (this level can be based on clinical judgment and what surgeons
    believe is a clinically important result). Trial 1 is both clinically and statistically significant. That is, the CI does not
    include either the line indicating clinical significance or 1 (the line of no effect). Trial 2, however, is neither statistically nor clinically significant.

    approximated from previous research or a pilot trial.


    The clinically significant effect size, which can be determined from previous literature as well as survey data
    (such as clinical information gathered from other surgeons), also should be incorporated.

    The Era of Evidence-Based Orthopaedics:


    Critical Appraisal
    The description of evidence-based medicine has evolved
    like medicine itself. In 1991, it was initially described
    as a shift in the medical paradigm, and placed a higher
    value on evidence derived from clinical research and a
    lower value on authority.2 More recent descriptions of
    evidence-based medicine express not only the need for
    a hierarchy of evidence with an understanding of the
    best available evidence, but also the need to combine
    this evidence with discussions of patients values and
    preferences, the pros and cons of particular treatments,
    and clinical experience and acumen.1,14,43,44 The combination of this triumviratebest available evidence, patients values and preferences, and clinical expertise
    encompasses what is construed by many physicians as
    evidence-based practice.1,3,12
    The object of critical appraisal is not to deconstruct
    every study so severely that the study must be completely disregarded, but to understand how well the
    study was constructed methodologically to determine
    its validity (does it answer the question or questions it
    seeks to answer?) and to understand its methodological
    limitations, which can introduce bias into the trial, thus
    systematically deviating the results from the truth. Critical appraisal also aids in understanding the results of a
    particular trial and in applying (if possible) those results to the specific patients who a surgeon is treating.
    When assessing an article on therapy, the surgeon
    should ask several questions (Table 2). (1) Are the results valid? (2) What are the results? (3) How can I apply the results to patient care? For the purposes of explanation, the following discussion focuses on the

    Orthopaedic Knowledge Update 10

    173

    Section 1: Principles of Orthopaedics

    Table 2

    Questions for Assessing a Therapy Trial


    Are the Results Valid?
    Did experimental and control groups begin the study with a
    similar prognosis?
    Were patients randomized?
    Was randomization concealed?
    Were patients analyzed in the groups to which they were
    randomized?
    Were patients in the treatment and control groups similar
    with respect to known prognostic factors?
    1: Principles of Orthopaedics

    Did experimental and control groups retain a similar


    prognosis after the study started?
    Were five important groups (patients, caregivers, collectors
    of outcome data, adjudicators of outcome, data analysts)
    aware of group allocation?
    Aside from the experimental intervention, were groups
    treated equally?
    Was follow-up complete?
    What Are the Results?
    How large was the treatment effect?
    How precise was the treatment effect?
    How Can I Apply the Results to My Patients Care?
    Were the study patients similar to my patient?
    Were all patient-important outcomes considered?
    Can the worth of likely treatment benefits be favorably
    balanced against any potential harms and costs?
    (Reproduced with permission from Guyatt GH, Rennie D: American Medical
    Association: Users Guides to the Medical Literature: A Manual for Evidence-Based
    Clinical Practice, ed 2. Chicago, IL, American Medical Association Press,
    2001.)

    critical appraisal of a therapeutic randomized controlled trial.

    Are the Results Valid?


    In assessing the validity of results, it is first necessary to
    ascertain if the patients start out the trial with the same
    prognosis. It should then be determined if the patients
    were randomized. Randomization can be achieved
    through the generation of random number tables or
    through the use of computer programs that generate a
    randomization sequence. Randomization is the only
    method to obtain balance in prognostic factors, both
    known and unknown. As an extreme example of the
    pitfall of nonrandomization is a trial evaluating the efficacy of intramedullary nail fixation versus plate fixation for a long-bone fracture in which only patients
    with open fractures are placed in the intramedullary
    nail group and only those with closed fractures are assigned to the plate fixation group. This lack of randomization creates a severe prognostic imbalance from the
    trials inception. Because open fractures have a worse
    174

    Orthopaedic Knowledge Update 10

    prognosis, the intramedullary nail group would presumably have significantly poorer outcomes than the
    plate group because of the initial prognostic imbalance
    rather than the treatment. This example, illustrates the
    significance of prognostic balance at the beginning of
    trials. Observational studies that are not randomized
    risk creating prognostic imbalance based not necessarily on the known prognostic variables, which can be
    addressed, but on any potential unknown variables.
    Next, it should be determined if randomization was
    concealed. This is a pivotal factor because a trial investigator may exclude a patient from the trial if it is
    known to which group the patient will be randomized.
    Unconcealed randomization can introduce bias such as
    a selection bias. Some examples of unconcealed randomization include studies using hospital admissions
    on even or odd days, or sealing hospital records in
    opaque envelopes, which can sometimes be brightlighted or opened and resealed.1,45 Clinical trial centers commonly use a remote telephone call-in or
    Internet-based randomization method to preclude the
    possibility of predicting in which group the patient will
    be placed.11
    A third factor in assessing the validity of results is to
    determine if the patients in the study group were similar with respect to known prognostic factors. This typically includes an assessment of patient demographic
    data within each group. This demographic assessment
    will let the reader know how well randomization was
    working. If there are significant imbalances in known
    prognostic factors, such as age, sex, or medical comorbidities, it may indicate that randomization was not
    working properly.
    Next, it should be determined if prognostic balance
    was maintained as the study progressed. The best
    method to maintain prognostic balance and maintain
    randomization is to blind as many people as possible to
    study information that may lead to bias; therefore, it is
    important to determine who was blinded in the trial
    (investigators, patients, outcomes assessors, research
    associates, data analysts, the writing committee). Individual subjective biases can be introduced throughout
    the course of the trial if it is known to which group the
    patients have been randomized. Treatment effects can
    be underestimated or overestimated in unblinded trials
    compared with those that are blinded.19 It is important
    not to think of randomized trials based on terms such
    as double-blinded or triple-blinded, but to consider the
    principle that everyone should be blinded who can possibly be blinded.
    Maintaining prognostic balance at the studys completion is another important consideration. It is necessary to determine if follow-up was complete, if the patients were analyzed in the groups to which they were
    randomized, and if the trial was stopped early.
    Follow-up is clearly important because a differential
    loss to follow-up between groups can lead to biased results. For example, the end-of-study prognostic balance
    can be affected if a group of patients with specific prognostic characteristics dropped out of one arm of a
    study. Although 80% follow-up is considered good, re-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 15: Orthopaedic Research: Health Research Methodology

    What Are the Results?


    The discussion of the results should ascertain the size
    and precision of the treatment effect. The presentation
    of treatment effects has been previously described in
    this chapter as well as the estimation of the precision
    around this effect (CIs). Treatment effects for continuous variables, such as those for outcome scores, can be
    presented as mean differences or standardized mean
    differences between groups. CIs around this estimate
    also can be presented.

    patient care refers to the external validity of the trial.


    One method that physicians can use to assess the
    generalizability of a trial is to determine if their patients
    would have been included in the study. Evaluating inclusion and exclusion criteria is important in determining the applicability of the results. Physicians also can
    assess if described outcomes of the trial would be important to their patients. For example, if a randomized
    controlled trial on hip implant A versus hip implant B
    reports on surgical time, this arguably is less important
    to the patient than the risk of infection, the need for
    transfusion, or the functional outcome following the
    treatment. If a trial does not report important outcomes, it is difficult to apply the results to a patient. If
    the trial results are discussed, described, and found to
    be applicable to a patient, it is necessary to determine if
    the recommended treatment fits with a particular patients values and preferences. What are the pros and
    cons and the risks and benefits for the patient? For example, in a trial of treatment A compared with treatment B for femoral shaft fractures, treatment A results
    in quicker weight bearing but treatment B has a decreased transfusion requirement; both result in good
    function. Some patients may value quicker weight bearing whereas others may chose delayed weight bearing
    with a decreased risk of a blood transfusion.

    Summary
    Evidence-based medicine requires a knowledge and appraisal of the literature, sound clinical judgment, and a
    discussion with patients to incorporate their values and
    preferences when making treatment decisions. This necessarily entails obtaining information from the patient,
    obtaining relevant treatment data, and assessing evidence and results to formulate a plan that will achieve
    an optimal outcome for the patient. Thus, evidencebased medicine begins and ends with the patient.

    Annotated References
    1.

    Guyatt GH, Rennie D: American Medical Association:


    Users Guides to the Medical Literature: A Manual for
    Evidence-Based Clinical Practice, ed 2. Chicago, IL,
    American Medical Association Press, 2001.

    2.

    Haynes B, Sackett DL, Guyatt GH, Tugwell P: Clinical


    Epidemiology: How to Do Clinical Practice Research.
    Philadelphia, PA, Lippincott Williams and Wilkins,
    2006.

    3.

    Guyatt GH, Rennie D, Meade M, Cook DJ: American


    Medical Association: Users Guides to the Medical Literature: A Manual for Evidence-Based Clinical Practice,
    ed 2. Chicago, IL, American Medical Association Press,
    2008.
    This book highlights critical appraisal of study designs
    and how to incorporate evidence-based medicine into
    practice.

    How Can the Results Be


    Applied to Particular Patients?
    The final aspect in the critical appraisal of a trial is the
    determination of the applicability of the therapy to particular patients. Physicians must determine if the study
    patients are similar to their own patients, if all important patient outcomes were considered, and if the
    worth of likely treatment benefits can be favorably balanced against any potential harms and costs. The methodology of the trial write-up refers to its internal validity, whereas extrapolating or generalizing the results to

    2011 American Academy of Orthopaedic Surgeons

    1: Principles of Orthopaedics

    searchers should strive for 100% follow-up. To help


    determine if the loss to follow-up is significant, a
    worst-case scenario can be calculated. If all patients
    who are lost to follow-up in each group are assigned a
    poor outcome or a worst-case outcome and the results
    do not change significantly, follow-up can be considered sufficient. Several strategies have been devised for
    researchers to obtain follow-up goals, including collecting information on the patients family, obtaining multiple contact numbers, obtaining contact information
    for the patients family doctors, and confirming future
    follow-up commitments at each visit.
    Analyzing patients in the groups to which they were
    randomized is termed an intention-to-treat analysis. If
    two groups receive different treatments, it is intuitive to
    believe that a patient who crossed over to another
    group should be analyzed in the group to which they
    crossed over. Analyzing patients based on the treatment
    they received is called a per-protocol analysis. The
    power of intention-to-treat analysis is that it preserves
    randomization. If there were several patients who
    crossed over in a particular trial, there may be some
    prognostic difference between those patients and the
    other patients in the trial; therefore, the prognostic balance can be affected at the completion if the trial. Some
    trials will conduct both an intention-to-treat analysis
    and a per-protocol analysis, presenting both analyses in
    the trial write-up.
    After the methodology of a particular therapeutic
    randomized trial has been discussed, it is often a good
    exercise for those involved in the critical appraisal to
    rate the validity of the trial. This rating sets the stage
    for further discussions of the results as well as the application of the results. If the methodology of the trial
    is significantly weak, caution would be appropriate
    when discussing the applicability of the trial to patient
    care.

    Orthopaedic Knowledge Update 10

    175

    Section 1: Principles of Orthopaedics

    Poolman RW, Struijs PA, Krips R, Sierevelt IN, Lutz


    KH, Bhandari M: Does a Level I Evidence rating imply high quality of reporting in orthopaedic randomised
    controlled trials? BMC Med Res Methodol 2006;6:44.

    Gigerenzer G, Edwards A: Simple tools for understanding risks: From innumeracy to insight. BMJ 2003;
    327(7417):741-744.

    18.

    Gigerenzer G, Hertwig R, van den Broek E, Fasolo B,


    Katsikopoulos KV: A 30% chance of rain tomorrow:
    How does the public understand probabilistic weather
    forecasts? Risk Anal 2005;25(3):623-629.

    Bhandari M, Richards RR, Sprague S, Schemitsch EH:


    The quality of reporting of randomized trials in the
    Journal of Bone and Joint Surgery from 1988 through
    2000. J Bone Joint Surg Am 2002;84(3):388-396.

    19.

    Poolman RW, Struijs PA, Krips R, et al: Reporting of


    outcomes in orthopaedic randomized trials: Does blinding of outcome assessors matter? J Bone Joint Surg Am
    2007;89(3):550-558.
    This study highlights the differences in treatment effects
    seen in unblinded and blinded trials.

    20.

    Jadad AR, Moore RA, Carroll D, et al: Assessing the


    quality of reports of randomized clinical trials: Is blinding necessary? Control Clin Trials 1996;17(1):1-12.

    21.

    Schulz KF: Subverting randomization in controlled trials. JAMA 1995;274(18):1456-1458.

    22.

    Schulz KF, Chalmers I, Hayes RJ, Altman DG: Empirical evidence of bias. Dimensions of methodological
    quality associated with estimates of treatment effects in
    controlled trials. JAMA 1995;273(5):408-412.

    23.

    Bhandari M, Pape HC, Giannoudis PV: Issues in the


    planning and conduct of randomised trials. Injury 2006;
    37(4):349-354.

    Sackett DL, Haynes RB, Guyatt GH, Tugwell P: Clinical


    Epidemiology: A Basic Science for Clinical Medicine, ed
    2. Boston, MA, Little, Brown, and Company, 1991.

    5.

    6.

    7.
    1: Principles of Orthopaedics

    17.

    4.

    Grimes DA, Schulz KF: Making sense of odds and odds


    ratios. Obstet Gynecol 2008;111(2 Pt 1):423-426.
    This article discusses the advantages and disadvantages
    of using odds ratios.

    8.

    Citrome L: Relative vs. absolute measures of benefit and


    risk: Whats the difference? Acta Psychiatr Scand 2010;
    121(2):94-102.
    This article provides a review of relative measures of effect in comparison with absolute measures of effect.

    9.

    Edwards AG, Evans R, Dundon J, Haigh S, Hood K, Elwyn GJ: Personalised risk communication for informed
    decision making about taking screening tests. Cochrane
    Database Syst Rev 2006;4:CD001865.

    10.

    Cook RJ, Sackett DL: The number needed to treat: A


    clinically useful measure of treatment effect. BMJ 1995;
    310(6977):452-454.

    11.

    Bhandari M, Joensson A: Clinical Research for Surgeons. Stuttgart, Germany, Georg Thieme Verlag, 2009.
    This book highlights theoretical and practical techniques for designing and understanding clinical trials.

    25.

    Hoppe DJ, Schemitsch EH, Morshed S, Tornetta P III,


    Bhandari M: Hierarchy of evidence: Where observational studies fit in and why we need them. J Bone Joint
    Surg Am 2009;91(Suppl 3): 2-9.
    This study provides a review of observational studies.

    12.

    Sackett DL, Rosenberg WM, Gray JA, Haynes RB,


    Richardson WS: Evidence based medicine: What it is
    and what it isnt. BMJ 1996;312(7023):71-72.

    13.

    Jadad AR, Enkin MW: Randomized Controlled Trials:


    Questions, Answers and Musings. Malden, MA, Blackwell Publishing, 2007.
    This book provides an excellent discussion of the different types of randomized trials, methodology, critical appraisal, and interpretation of results.

    26.

    Grimes DA, Schulz KF: Cohort studies: Marching towards outcomes. Lancet 2002;359(9303):341-345.

    27.

    Sackett DL: Rules of evidence and clinical recommendations on the use of antithrombotic agents. Chest 1986;
    89(2, suppl)2S-3S.

    Bhandari M, Guyatt GH, Swiontkowski MF: Users


    guide to the orthopaedic literature: How to use an article about a surgical therapy. J Bone Joint Surg Am
    2001;83(6):916-926.

    28.

    Grimes DA, Schulz KF: Compared to what? Finding


    controls for case-control studies. Lancet 2005;
    365(9468):1429-1433.

    29.

    Schulz KF, Grimes DA: Case-control studies: Research


    in reverse. Lancet 2002;359(9304):431-434.

    30.

    Grimes DA, Schulz KF: Bias and causal associations in


    observational research. Lancet 2002;359(9302):248252.

    14.

    15.

    16.

    176

    24. Devereaux PJ, Bhandari M, Clarke M, et al: Need for


    expertise based randomised controlled trials. BMJ 2005;
    330(7482):88.

    Moseley JB, OMalley K, Petersen NJ, et al: A controlled trial of arthroscopic surgery for osteoarthritis of
    the knee. N Engl J Med 2002;347(2):81-88.
    Hulley SB, Cummings S, Browner WS, Grady DG,
    Newman T: Designing Clinical Research, ed 3. Philadelphia, PA, Lippincott Williams and Wilkins, 2006.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 15: Orthopaedic Research: Health Research Methodology

    Schulz KF, Grimes DA: Multiplicity in randomised trials


    II: Subgroup and interim analyses. Lancet 2005;
    365(9471):1657-1661.

    39.

    Hoffrage U, Lindsey S, Hertwig R, Gigerenzer G: Medicine. Communicating statistical information. Science


    2000;290(5500):2261-2262.

    32.

    Bhandari M, Devereaux PJ, Li P, et al: Misuse of baseline comparison tests and subgroup analyses in surgical
    trials. Clin Orthop Relat Res 2006;447:247-251.

    40.

    Altman DG: Why we need confidence intervals. World J


    Surg 2005;29(5):554-556.

    33.

    Bjandari M, Guyatt G, Tornetta P III, et al; SPRINT Investigators: Study to prospectively evaluate reamed intramedually nails in patients with tibial fractures
    (S.P.R.I.N.T.): Study rationale and design. BMC Musculoskelet Disord 2008;9:91.
    This study is the largest orthopaedic randomized controlled trial comparing reamed and unreamed intramedullary tibial nails.

    41.

    Grimes DA, Schulz KF: An overview of clinical research: The lay of the land. Lancet 2002;359(9300):5761.

    42.

    Power and sample size programs. University of California, San Francisco, Web site. http://www.epibiostat.
    ucsf.edu/biostat/sampsize.html. Accessed March 4,
    2010.
    A program used to calculate treatment effects is presented.

    43.

    Haynes RB, Sackett DL, Gray JM, Cook DJ, Guyatt


    GH: Transferring evidence from research into practice:
    1. The role of clinical care research evidence in clinical
    decisions. ACP J Club 1996;125(3):A14-A16.

    44.

    Haynes RB, Sackett DL, Gray JA, Cook DL, Guyatt


    GH: Transferring evidence from research into practice:
    2. Getting the evidence straight. ACP J Club 1997;
    126(1):A14-A16.

    45.

    Schulz KF, Grimes DA: Allocation concealment in randomised trials: Defending against deciphering. Lancet
    2002;359(9306):614-618.

    34.

    35.

    Bhandari M, Whang W, Kuo JC, Devereaux PJ, Sprague


    S, Tornetta P III: The risk of false-positive results in orthopaedic surgical trials. Clin Orthop Relat Res 2003;
    413:63-69.
    Lang TA, Secic M: How to Report Statistics in Medicine, ed 2. Philadelphia, PA, American College of Physicians, 2006.

    36.

    Altman DG: Practical Statistics for Medical Research.


    London, England, Chapman and Hall, 1991.

    37.

    Petrie A: Statistics in orthopaedic papers. J Bone Joint


    Surg Br 2006;88(9):1121-1136.

    38.

    Goodman SN: Toward evidence-based medical statistics. 1: The P value fallacy. Ann Intern Med 1999;
    130(12):995-1004.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    1: Principles of Orthopaedics

    31.

    177

    Chapter 16

    Bone Metabolism and Metabolic


    Bone Disease
    Hue H. Luu, MD

    Introduction

    2: Systemic Disorders

    The skeleton is one of a few organs with tremendous


    regenerative capacity. For bone formation, a complex
    and regulated series of events is needed that leads to the
    net result of a structure that has the ability to continually repair and remodel throughout life. The human
    skeleton has multiple functions aside from providing
    structural support. These functions often include other
    organ systems such as the hematopoietic and endocrine
    systems. Fundamental in the cascade of bone formation
    is the highly controlled process of osteoblastic differentiation. This process is essential for the normal development of bone, physiologic remodeling, and fracture repair. Over the past 5 to 10 years, researchers have
    begun to understand the important regulatory elements
    of osteoblastic differentiation and bone formation.
    These key factors include morphogens, signal transduction proteins, and transcription factors. Mutations
    and/or deletions in key regulatory genes lead to several
    musculoskeletal disorders. As a better understanding is
    gained concerning the normal processes of osteogenesis
    and bone metabolism, researchers may potentially identify new therapies for regeneration of injured or diseased bone and bone loss caused by aging.

    osteoprogenitor cells. Several transcription factors are


    turned on, differentiating the cells into preosteoblasts
    and eventually mature osteoblasts. Some of the osteo-

    Osteoblastogenesis and Bone Formation

    Osteoblastic Differentiation
    Bone formation is a complex sequence of events that
    begins with the stimulation of mesenchymal stem cells
    to differentiate into mature osteoblasts, and eventually
    osteocytes. The mesenchymal stem cells have the capacity to differentiate into multiple lineages, including osteoblastic, myogenic, adipogenic, and chondrogenic
    lines (Figure 1). The lineage down which mesenchymal
    stem cells differentiate depends on the stimuli received. In osteoblastic differentiation, for example, the
    mesenchymal stem cells receive stimuli to become

    The University of Chicago Section of Orthopaedic Surgery has received royalties from Biomet.

    2011 American Academy of Orthopaedic Surgeons

    Figure 1

    Diagram showing osteoblastic and osteoclastic


    differentiation. Osteoblasts and other mesenchymal lineages are derived from mesenchymal
    stem cells. BMPs are potent stimulators of osteoblastic differentiation. Osteoclasts are derived from pluripotent stem cells that have been
    stimulated by M-CSF to become hematopoietic
    mononuclear cells and subsequently into
    preosteoclasts. The preosteoclasts differentiate
    into mature osteoclasts when activated by the
    RANKL pathway. OPG is secreted by osteoblasts
    and stromal cells to inhibit osteoclastic maturation. BMP=bone morphogenetic protein;
    OPG=osteoprotegerin; M-CFS=macrophagecolony-stimulating factor; PTH = parathyroid
    hormone; RANKL=receptor activator of nuclear
    factor -B ligand.

    Orthopaedic Knowledge Update 10

    181

    Section 2: Systemic Disorders

    2: Systemic Disorders

    blasts become osteocytes within a bony matrix; these


    ostecytes serve as mechanoreceptors and regulate calcium homeostasis.
    Many growth factors, transcription factors, and sex
    hormones that stimulate osteoblastic differentiation
    have been identified. Among these, bone morphogenetic
    proteins (BMPs) have been intensely studied and clinically applied during the past decade. BMPs are potent
    osteoinductive factors that promote osteoblastic differentiation and eventual bone formation. BMPs are secreted proteins, are found abundantly in bone, and are
    part of the transforming growth factor-beta (TGF-) superfamily.1 The discovery of these proteins was first reported in the 1960s when the introduction of demineralized bone matrix was observed to be capable of
    inducing bone formation in animal models. From the
    demineralized bone matrix, BMPS were purified and
    identified.2 Although not all BMPs are osteogenic, at
    least 20 members of this protein family have been identified. Both BMP-2 and BMP-7 are used clinically to promote bone formation in procedures such as spinal fusions, fracture care, and maxillofacial reconstructions.
    Both BMPs and TGF- are potent stimulators of osteoblastic differentiation and share a common signaling
    pathway. The BMP and TGF- ligands bind to their respective tetrameric receptor complexes of two pairs of
    transmembrane proteins. Upon binding, the activated
    receptors phosphorylate the receptor-regulated SMADs
    (R-SMADs). SMADs are intracellular proteins that help
    in transduction of the BMP or TGF- signal to the nucleus. The R-SMADs then dimerize with SMAD-4, also
    known as co-SMAD, and the dimer translocates into
    the nucleus. Once in the nucleus, the SMAD complex
    acts as a transcription factor to regulate several downstream genes, such as RUNX2. These genes then stimulate the mesenchymal stem cells down a path of differentiation toward mature osteoblasts. The osteoblasts
    then secrete an osteoid matrix that eventually becomes
    mature bone.
    As with any signaling pathway, BMP signaling can be
    modulated at multiple levels. Bone formation involves
    the balanced coordination of stimulus signals, such as
    BMPs and BMP antagonists. In the extracellular compartment, several BMP antagonists, such as noggin,
    have been identified. Many of these antagonists work
    by binding to the BMP ligand to prevent the binding of
    the BMPs to their receptors. In the cytoplasmic compartment, inhibitor-SMADs (I-SMADs) are inhibitors of
    BMP and TGF- signaling and compete with the
    R-SMADs for binding to the type I BMP receptor, thereby inhibiting transduction of the BMP signal.1 Several
    human skeletal diseases have been linked to defects in
    the signaling pathway for osteoblastic differentiation.
    These diseases include fibrodysplasia ossificans progressiva (FOP), which is linked to mutations in the BMP receptor; cleidocranial dysplasia, which is linked to mutations in RUNX2; and Camurati-Engelmann disease,
    which is linked to mutations in TGFB1.
    182

    Orthopaedic Knowledge Update 10

    Diseases Caused by Defects


    in Osteoblastic Function

    Fibrodysplasia Ossificans Progressiva


    Fibrodysplasia Ossificans Progressiva is a rare disabling
    genetic disease that results in multiple skeletal malformations with progressive heterotopic ossification. The
    prevalence of FOP is approximately 1 in 2 million individuals worldwide, with no apparent ethnic, racial, sex,
    or geographic predisposition.3 Recently, the etiology of
    this disease has been associated with abnormal BMP
    signaling and has been specifically linked to the type I
    BMP receptor (activin receptor 1A [ACVR1], also
    known as activin-like kinase 2 [ALK2]).4 The molecular
    pathogenesis is an activating mutation of the type I
    BMP receptors on the cell membrane. Although BMP-4
    has been shown to bind to this receptor and have increased signaling in patients with FOP, other BMPs also
    have the potential to bind to this receptor. The net result is hyperactivation of the BMP signaling pathway.
    There are two clinical hallmarks of this diseaseprogressively extensive heterotopic bone formation
    throughout the body (Figure 2, A) and deformities of
    the great toes bilaterally (Figure 2, B).
    During the first decade of life, areas of painful and
    highly inflammatory swelling develop in patients with
    FOP; heterotopic bone may eventually form at these
    sites.3 Minor traumas, such as falls, intramuscular injections for immunization, or nerve blocks for procedures, can lead to heterotopic bone formation. Systemic
    illness such as influenza can trigger a flare-up and also
    lead to progressive systemic heterotopic bone formation. The heterotopic bone can form in skeletal muscles
    and other connective tissue, such as fascia, ligaments,
    tendons, and aponeuroses. There is a characteristic spatial and temporal pattern of heterotopic bone formation that mimics the pattern of normal embryonic skeletal formation. Contracted joints often develop in the
    extremities.
    Interestingly, several skeletal muscles, such as the diaphragm, tongue, and extraocular muscles, are spared.3
    Cardiac and smooth muscles also are spared. Most patients are confined to a wheelchair by the third decade
    of life and die at a median age of 45 years. Death is
    typically caused by pulmonary complications related to
    thoracic insufficiency syndrome.
    Treatment for these patients involves management of
    symptoms. Surgical releases of joint contractures are
    usually unsuccessful and can induce formation of more
    heterotopic bone.3 General anesthesia in a patient with
    FOP is challenging; awake, fiberoptic intubation is often required because of ankylosis of the temporomandibular joints. Fall prevention is essential. Anecdotal
    use of corticosteroids, cyclooxygenase-2 inhibitors, leukotriene inhibitors, and mast cell stabilizers has been
    reported.3 To date, there is no proven therapy that will
    halt or reverse the natural progression of FOP. Bone
    marrow transplant has been investigated as an option
    for treatment, but results have not been promising.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 16: Bone Metabolism and Metabolic Bone Disease

    Figure 2

    The characteristic features of FOP are diffuse heterotopic bone formation and great toe deformities. A, CT scan with
    three-dimensional reconstruction shows diffuse heterotopic bone in the soft tissues in a patient with FOP. B, AP
    radiograph of the feet shows bilateral great toe deformities. (Reproduced with permission from Shore EM, Xu M,
    Feldman GJ, et al: A recurrent mutation in the BMP type I receptor ACVR1 causes inherited and sporadic fibrodysplasia ossificans progressiva. Nat Genet 2006;38(5):525-527.)

    Cleidocranial Dysplasia

    2011 American Academy of Orthopaedic Surgeons

    clavicles. Absence of the clavicle allows for hypermobility of the shoulders; the patient can bring the two humeral heads in near contact with each other anteriorly
    (Figure 3, B). Treatment is primarily symptomatic.
    Coxa vara may develop in up to 50% of patients but
    often resolves spontaneously with growth and may not
    require surgery. In rare cases, coxa valga can develop.
    The femoral head has been described as having a
    chefs hat appearance in patients with cleidocranial
    dysplasia.7 Osteotomy is not recommended until the
    Hilgenreiner epiphyseal angle exceeds 60.8 In a study
    with few patients, it was reported that a femoral valgus
    derotational osteotomy resulted in good outcomes with
    no recurrences.8

    2: Systemic Disorders

    Cleidocranial dysplasia is an autosomal dominant skeletal disorder resulting from a mutation in the RUNX2
    gene.5 RUNX2 (also known as CBFA1 or OSF2) is a
    transcription factor and master regulator of osteoblastic
    differentiation. RUNX2 is one of several key genes that
    is turned on with BMP stimulation of mesenchymal
    stem cells into mature osteoblasts. The estimated prevalence of cleidocranial dysplasia is approximately 1 in 1
    million individuals; however, the disease may be more
    common and underdiagnosed because of the relatively
    low rate of musculoskeletal symptoms occurring in patients with mild forms of the disease.6 Cleidocranial
    dysplasia has been reported in all ethnic groups and has
    no sex predilection. Patients with cleidocranial dysplasia have several craniofacial abnormalities, including
    frontal bossing, wormian bones (extra bones within
    cranial sutures), delayed ossification of the fontanelle
    caused by delayed closure of the sutures, depression at
    the base of the nose, and supernumerary and late erupting teeth (Figure 3, A). Other radiographic findings include hypoplasia of the sphenoid and maxilla, as well as
    delayed closure of the mandibular symphysis.
    In addition to the craniofacial abnormalities, patients with cleidocranial dysplasia often have several orthopaedic abnormalities, including short stature, rudimentary or absent clavicles, a wide pubic symphysis,
    peripheral joint laxity, progressive coxa vara, joint dislocations, scoliosis, and kyphosis.6 Although the severity of the disease varies widely, the characteristic feature of this disease is the hypoplastic or absent

    Osteoclastogenesis and Bone Turnover

    Osteoclastic Differentiation
    Bone resorption is an essential step in the normal repair
    and remodeling of the skeleton. Osteoclasts are responsible for the degradation of bone in the Howship lacunae. Osteoclasts are derived from pluripotent stem cells
    that have differentiated into hematopoietic monocytes
    and eventually into multinucleated osteoclasts9 (Figure
    1). The initial stimulus for pluripotent stem cells to expand and differentiate into hematopoietic monocytes is
    mediated by macrophage-colony stimulating factor (MCSF). Hematopoietic monocytes are stimulated directly
    or indirectly to differentiate into osteoclast precursor
    cells by several factors, including interleukin-1, para-

    Orthopaedic Knowledge Update 10

    183

    Section 2: Systemic Disorders

    Figure 3

    Patients with cleidocranial dysplasia characteristically have hypoplastic or absent clavicles as well as several craniofacial abnormalities. A, Supernumerary teeth and tooth germs are commonly present. B, Absence of the clavicle allows for hypermobility of the shoulders. (Reproduced with permission from Suba Z, Balaton G, Gyulai-Gal S, Balaton P, Barabs J, Tarjn I: Cleidocranial dysplasia: Diagnostic criteria and combined treatment. J Craniofac Surg
    2005;16(6):1122-1126.)

    2: Systemic Disorders

    thyroid hormone (PTH), and 1,25-dihydroxyvitamin


    D. Essential to the terminal differentiation of osteoclasts is the stimulation by receptor activator of nuclear
    factor- B ligand (RANKL). The preosteoclasts express
    receptor activator of nuclear factor- B (RANK) on
    their cell surfaces. This stimulation is antagonized by
    osteoprotegerin (OPG), which is secreted by stromal
    cells and osteoblasts. OPG is a decoy receptor that
    binds RANKL and prevents its binding to RANK on
    preosteoclasts. This pathway is the target of many investigational drugs for several human conditions, including osteoporosis, osteolysis, and other metabolic
    disorders.
    When stimulated, osteoclasts secrete enzymes from
    their lysosomes into the extracellular matrix. The cells
    form the distinctive ruffled border at the interface between themselves and the bone matrix. In this low pH
    environment, the calcium of mineralized bone is hydrolyzed to essentially dissolve the bone matrix. The acidic
    environment is mediated by the combined functions of
    several proteins, including carbonic anhydrase II, vacuolar H+-adenosine triphosphatase, and chloride channel
    ion pumps.10 The degraded bone matrix undergoes endocytosis by the osteoclasts, is transported to the opposite membrane, and released. This allows the osteoclasts to continually remove bone degradation products
    without releasing the sealing zone on the bone. This
    sealing zone is dynamic, mediated by cell adhesion molecules, and moves with the cell as the osteoclasts migrate along the bone surface. Dysfunction of this low
    pH microenvironment, as well as other osteoclastic
    functions, can lead to several human diseases.

    184

    Orthopaedic Knowledge Update 10

    Diseases Caused by Defects in


    Osteoclastic Function

    Osteopetrosis
    Osteopetrosis is a rare metabolic bone disease in which
    there is inadequate bone resorption and the continual
    accumulation of bone deposition by osteoblasts. The
    clinical course of osteopetrosis can range from mild
    with no symptoms to severe. Even within the same family, there is heterogeneity of manifestations, which suggests that the disease exhibits variable penetrance. Several genetic defects have been identified in osteopetrosis
    (Table 1), and many involve the inability to resorb
    bone at the ruffled border. Some of the described examples include CAII (carbonic anhydrase II) mutations,
    RANKL loss of function, CLCN7 (chloride channel 7)
    loss of function, and OSTM1 (a protein associated with
    the chloride channel) loss of function.10,11
    The genetic inheritance of osteopetrosis includes autosomal dominant osteopetrosis (ADO), autosomal recessive osteopetrosis, and X-linked osteopetrosis.10 The
    prevalence of osteopetrosis is variable and depends on
    the type.12 For example, one form of the autosomal dominant variant of osteopetrosis (ADO II) has a prevalence
    of 5.5 per 100,000 individuals, whereas the second autosomal dominant variant (ADO I) has been reported
    only in three families. The autosomal recessive variant is
    estimated to occur in 1 in 200,000 individuals. The severity of the disease can be variable and can include diffuse sclerosis in nearly all bones, as seen in the severe
    forms of the disease. The characteristic radiographic feature of osteopetrosis is the alternating pattern of lucent
    bands with denser bands. This feature is commonly de-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 16: Bone Metabolism and Metabolic Bone Disease

    Table 1

    Known Mutations in Osteopetrosis


    Inheritance Pattern

    Gene

    Severity

    Autosomal dominant

    CLCN7 (dominant negative)


    LRP5 (N-term mutation)
    PLEHKM1 (missense mutation)

    Ranges from asymptomatic to lethal


    Mild
    Mild

    Autosomal recessive

    Carbonic anhydrase II (loss of function)


    TCIRG1 (several mutations)
    OSTM1 (loss of function)
    RANKL (loss of function)
    ITGB3
    PLEHKM1 (loss of function)
    CLCN7 (missense mutation)

    Intermediate with brain calcifications


    Severe with replacement of marrow
    Severe with neural and eye involvement
    Severe
    Severe with Glanzmann thrombasthenia
    Intermediate
    Severe with retinal and optic nerve involvement

    X-linked

    NEMO

    Severe with immunodeficiency and lymphedema

    2: Systemic Disorders

    Figure 4

    A, Sclerosis in nearly all bones with the characteristic Erlenmeyer flask appearance of the distal femur can develop
    in patients with osteopetrosis. B and C, Radiographs of the spine often demonstrate a rugger jersey appearance.

    scribed as a bone in bone pattern. Radiographs of the


    patients spine can show the rugger jersey spine sign resulting from focal sclerosis; the characteristic Erlenmeyer
    flask appearance often develops in the distal femur (Figure 4). Although there is increased bone mineral density
    (BMD), the bone is prone to fracture because of the fragile and poorly organized bone matrix that is commonly
    described as brittle marble bones.

    2011 American Academy of Orthopaedic Surgeons

    In patients with severe osteopetrosis, sclerotic bone


    can replace normal marrow; life-threatening disorders
    such as anemia and pancytopenia can develop. Osteomyelitis and sepsis may also occur because of poorly developed bone marrow and an impaired hematopoietic
    system. In these patients, secondary hematopoiesis in
    the spleen and liver occurs with resultant hypertrophy
    in these organs. Blindness and deafness also may devel-

    Orthopaedic Knowledge Update 10

    185

    Section 2: Systemic Disorders

    op as a result of nerve compression by the rapidly growing sclerotic bone. Patients with osteopetrosis may also
    have tooth eruption defects and severe dental caries.
    The treatment of patients with osteopetrosis centers
    on managing disorders resulting from the bone fragility.
    Patients often require multiple open reduction and internal fixation procedures for recurrent fractures and
    deformity correction. Some patients eventually are
    treated with joint arthroplasties. Patients with osteopetrosis have a high rate of surgical complications, including iatrogenic fractures, infection, implant loosening,
    and nonunions.

    Paget Disease

    2: Systemic Disorders

    Paget disease of bone was first described in 1877. This


    bone disorder is believed to be an osteoclastic disease
    and is marked by focally increased skeletal remodeling
    within the axial or appendicular skeleton. There is an
    initial wave of osteoclast-mediated bone resorption,
    followed by the second phase of disorganized skeletal
    repair. This process leads to excessively disorganized
    woven bone and lamellar bone, characterized by osteosclerosis and hyperostosis, respectively, and results in
    the characteristic findings of cement lines seen histologically. The disorganized bone is weaker and prone to
    fractures. The final phase of the disease is the quiescent
    phase in which there is little bone turnover. Radiographically, Paget disease can involve only one bone or
    multiple bones, and is further characterized by coarse
    trabeculae. The risk of malignant degeneration to Paget
    sarcoma of bone is rare but has been well described.
    Although the etiology of Paget disease remains uncertain, there is increasing evidence of a genetic cause.
    Many scientists believe that Paget disease is caused, in
    part, by a paramyxoviral infection due to the presence
    of inclusion bodies seen microscopically. However, to
    date, no intact virus has ever been recovered from patients with this disease. It is unknown why people from
    certain geographic origins, such as northern Europeans,
    are more likely to have Paget disease, because
    paramyxoviral infections (such as measles) are common
    worldwide. This factor leads scientists to believe that
    genetic factors play an important role in the etiology of
    or susceptibility to Paget disease of bone.
    Recent studies have strengthened the theory of a genetic etiology for Paget disease.13,14 Four genes
    (SQSTM1, RANK, OPG, and VCP) have been associated with Paget disease.13 Recent studies have linked a
    subset of patients with Paget disease to mutations on
    the SQSTM1 gene located on chromosome 5. Approximately 26% of familial and 9% of sporadic Paget
    cases were linked to SQSTM1 mutations.14 The
    SQSTM1 gene product (also known as p62) binds indirectly to the cytoplasmic portion of RANK in the nuclear factor B signaling pathway. The differentiation
    of osteoclasts relies on RANK, which is expressed on
    preosteoclasts. Similarly, mutations in VCP (also know
    as p97) have also been linked to Paget disease. Like
    SQSTM1, VCP indirectly binds to the cytoplasmic portion of RANK to regulate osteoclastic differentiation.13
    186

    Orthopaedic Knowledge Update 10

    Additionally, the early onset form of Paget disease has


    been linked to an activating mutation in RANK itself.
    Mutations in the OPG gene have recently been identified as a cause of the rare juvenile form of Paget disease. OPG is a decoy ligand to RANK and acts to inhibit osteoclastic differentiation. Taken together, there
    is increasing evidence that at least one third of Paget
    disease cases may be caused by mutations in genes important in osteoclastic differentiation. Although other
    regulatory genes for osteoclastic differentiation may be
    involved, they remain to be identified.
    The treatment of Paget disease has changed significantly with the advent of bisphosphonates (such as pamidronate, alendronate, and zoledronic acid).13 Bisphosphonates act to inhibit osteoclasts at the ruffled border
    where active bone resorption occurs. The bisphosphonates serve to prevent complications (such as fracture)
    caused by the disease. Bisphosphonates are commonly
    used to treat postmenopausal osteoporosis and Paget
    disease. Calcitonin also is used to treat Paget disease.
    Nonsteroidal anti-inflammatory medications can help
    relieve pain related to active Paget disease. In some instances, patients are treated with orthopaedic procedures such as fracture care and joint arthroplasty. Operating on pagetoid bone is associated with increased
    bleeding and a longer time to union in patients treated
    with osteotomies or fracture care.13 Knee replacement
    in patients with pagetoid bone is characteristically challenging, with a greater incidence of suboptimal alignment.

    Hormonal and Steroid Regulation of Bone


    Bone serves as a major reservoir for calcium. The release of calcium from bone is highly regulated by several hormones and steroid derivatives. Calcium has
    many important roles in the human body, such as functioning as a second messenger for cell signaling and
    nerve conduction and as a mediator of muscle cell contraction. Calcium in the serum exists in three separate
    fractions: 45% protein bound, 45% ionized, and 10%
    complex calcium bound to various anions.15 The serum
    level of calcium (ranging from 8.5 to 10 mg/dL) is fairly
    stable and relies on tight hormonal regulation.
    Each day, approximately 200 to 300 mg of calcium
    is absorbed in the adult digestive tract based on the recommended daily intake of 1,000 mg for middle-aged
    adults.15 Most of the calcium is absorbed by active
    transport in the duodenum and jejunum. The recommended intake of calcium varies with age and depends
    on the relative need for calcium for skeletal maintenance and growth (Table 2). Calcium intake should be
    higher during periods of growth, lactation in women,
    and in older individuals because of increased bone resorption. The excretion of calcium is approximately
    150 to 200 mg/day through renal and fecal losses. The
    absorption of calcium from the digestive tract, resorption from bone, and excretion of calcium is well controlled by several hormones.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 16: Bone Metabolism and Metabolic Bone Disease

    PTH and Parathyroid


    Hormone-Related Protein

    Table 2

    PTH regulates the serum levels of calcium and phosphate in the body by altering the resorption of bone by
    osteoclasts and the excretion of calcium and phosphate
    in the kidneys. There are receptors for PTH on osteoblasts and stromal cells, which stimulate the expression
    of osteoclastic stimulatory factors, such as M-CSF and
    RANKL, to induce preosteoclasts to terminally differentiate and resorb bone.14 PTH acts to stimulate the reabsorption of calcium and inhibit the reabsorption of
    phosphate in the glomerular filtrate. PTH indirectly
    stimulates the intestinal absorption of calcium by stimulating the production of 1,25-dihydroxyvitamin D in
    the kidney. The net effect of PTH stimulation is to increase serum calcium and decrease serum phosphate
    levels. As a feedback loop, elevated levels of calcium
    will inhibit the secretion of PTH by the parathyroid
    cells.
    Although the net effect of PTH on bone is an increase in osteoclast number and activity, osteoclasts
    paradoxically do not express the receptor for PTH.
    Stimulation through the osteoblasts or stromal cells
    drives the mononuclear osteoclast precursors to mature
    into multinucleated osteoclasts. This functional linkage
    of osteoblasts and osteoclasts explains the abundance
    of both cell types in the brown tumor in hyperparathyroidism. As will be described later in the chapter, PTH
    is the target of recent novel therapies in osteoporosis
    and fracture prevention.
    Parathyroid hormone-related protein (PTHrP) is a
    recently discovered second member of the PTH family.15 PTHrP was first identified as the cause of hypercalcemia in malignancy. This disorder is characterized
    by both hypercalcemia and hypophosphatemia. Interestingly, because PTH levels were noted to be low in
    these cancer patients, this finding led to the search for
    and identification of PTHrP. This protein has since
    been found in normal physiologic conditions. There is
    high sequence homology in the N-terminal region of
    PTHrP and PTH. PTHrP binds to the same receptor as
    PTH on osteoblasts and renal cells. The effects of
    PTHrP are similar to those of PTH in that preosteoclasts are stimulated to differentiate, and the production of 1,25-dihydroxyvitamin D is accelerated in the
    kidneys. The serum level of PTHrP is considerably
    lower than PTH and likely has a less significant role in
    regulating calcium.

    Recommended Daily Calcium Intake

    Calcitonin is a 32amino-acid hormone that is primarily secreted by C cells in the thyroid gland. The effect of
    calcitonin on bone is to inhibit osteoclasts. Within minutes of calcitonin administration, osteoclasts begin to
    shrink in size and decrease their bone resorptive activity.15 Recombinant calcitonin is approved by the Food
    and Drug Administration (FDA) for use in subcutaneous, intramuscular, and nasal spray formulations. Calcitonin is used to treat Paget disease, osteoporosis, and
    hypercalcemia in malignancy. Clearance of calcitonin

    2011 American Academy of Orthopaedic Surgeons

    Amount (mg/day)

    Up to 6 months

    210

    6 to 12 months

    270

    1 to 3 years

    500

    4 to 8 years

    800

    9 to 18 years

    1,300

    19 to 50 years

    1,000

    Older than 50 years

    1,200

    Pregnant and Lactating Women


    14 to 18 years

    1,300

    19 to 50 years

    1,000

    (Data from the Office of Dietary Supplements, Bethesda, MD, National Institutes
    of Health. http://ods.od.nih.gov/.)

    occurs within minutes and is primarily mediated by the


    kidneys. Calcitonin also can be secreted by medullary
    thyroid carcinoma and multiple endocrine neoplasia
    type II tumors.

    Sex Hormones and Steroids


    Both estrogen and testosterone have anabolic effects on
    bone. It is evident that women begin to have dramatic
    bone loss after menopause. This is caused by the decrease in estrogen levels and the fact that there are estrogen receptors on osteoblasts and osteoclasts. The net
    effect of estrogen is to stimulate bone production. Soon
    after menopause, annual bone loss is 2% to 3% for the
    first 6 to 8 years as a result of the abrupt drop in estrogen levels.15
    It has been well recognized that glucocorticoids induce bone loss since Cushing described the effects of
    hypercortisolism on the human skeleton. Systemic corticosteroids are currently used to treat several human
    diseases, such as autoimmune disease and asthma. Interestingly, glucocorticoids have a greater effect on trabecular bone than cortical bone. Therefore, fractures
    are more likely to occur in vertebrae, ribs, and the
    metaphyseal regions of long bones. Bone loss, as determined by BMD, is very rapid in the first year of highdose steroid treatment.15 For example, the administration of prednisolone exceeding 2.5 mg/day can cause
    significant trabecular bone loss and increase the risk of
    vertebral fractures. Glucocorticoids appear to have an
    inhibitory effect on osteoblastic proliferation and differentiation. A much lower physiologic concentration
    of glucocorticoid is essential for terminal differentiation
    of osteoblasts; however, the doses used to treat several
    human conditions far exceed these physiologic requirements. Glucocorticoids inhibit pituitary secretion of gonadotropins, which stimulate the production of sex
    hormones. This further promotes accelerated bone loss
    because of the loss of the anabolic effects of the sex
    hormones.

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    Calcitonin

    Age

    187

    Section 2: Systemic Disorders

    Table 3

    Criteria for Osteoporosis


    Normal

    BMD within 1 SD of the young adult


    reference mean

    Osteopenia

    BMD between 1.0 to 2.5 SD of the


    young adult reference mean

    Osteoporosis

    BMD 2.5 SD below the young adult


    reference mean

    BMD = bone mineral density; SD = standard deviation


    (Data from the World Health Organization, Geneva, Switzerland.
    http://www.who.int.)

    Vitamin D

    2: Systemic Disorders

    Vitamin D is a secosteroid that is made by the skin


    when exposed to sunlight. The active metabolite, 1,25dihydroxyvitamin D, is formed by two successive hydroxylations in the liver and in the kidney, respectively.15 The major role of 1,25-dihydroxyvitamin D is
    to maintain a normal serum calcium level. Although
    1,25-dihydroxyvitamin D stimulates the terminal differentiation of osteoclasts, it also stimulates the intestinal
    absorption of calcium. When osteoclasts have matured,
    however, they lose their ability to respond to 1,25dihydroxyvitamin D and rely on osteoblasts to release
    cytokines for stimulation. Important to the skeleton,
    1,25-dihydroxyvitamin D promotes the mineralization
    of osteoid matrix laid down by osteoblasts. This is
    done by maintaining the extracellular calcium and
    phosphate concentrations within normal limits, which
    helps in the deposition of calcium hydroxyapatite in the
    bone matrix.
    Recently, there has been an increase in the number of
    patients with vitamin D deficiency.16 This is believed to
    be caused by less time spent outside in the sun. Vitamin
    D deficiency is on the rise in all children because of less
    time playing outdoors; however, it is particularly prevalent in black children because darker skin blocks
    much of the ultraviolet light necessary for the production of vitamin D. The amount of time outside needed
    to maintain normal vitamin D levels depends on the
    geographic latitude because latitude determines the intensity of sunlight. Sun exposure through glass or Plexiglas is ineffective because the light does not contain the
    ultraviolet band that is necessary for the production of
    vitamin D.

    Osteoporosis
    There are two broad categories of metabolic bone disease: (1) osteoporosis, in which there is decreased bone
    mass; and (2) osteomalacia or rickets, in which there
    are defects in mineralization of bone. Osteoporosis is
    the most common metabolic bone disease and is highly
    prevalent in postmenopausal women. Osteoporosis is
    characterized by decreased bone mass, with loss of the
    microarchitecture of bone, leading to increased fragility
    and an increased risk of fractures. Osteoporosis is de188

    Orthopaedic Knowledge Update 10

    fined by a BMD that is 2.5 or more standard deviations


    below that of normal young adults (Table 3). In the
    United States, an estimated 4 to 6 million women and 1
    to 2 million men older than 50 years have osteoporosis,
    whereas an additional 13 to 17 million women and 8 to
    13 million men have osteopenia.17 Osteopenia is defined by a BMD between 1.0 up to 2.5 standard deviations below the mean of normal young adults. The etiology of osteoporosis is multifactorial, and several
    medical conditions are associated with an increased
    risk of osteoporosis.
    In 2005, the cost for treating osteoporotic fractures
    in the United States was $17 billion, and it is expected
    to increase by 50% by 2025.17 Therefore, screening for
    and treating osteoporosis is essential for decreasing the
    overall cost of health care. Most osteoporotic fractures
    involve cancellous bone and often occur in vertebrae,
    ribs, the distal radius, and the proximal femur. The
    treatment of long-bone osteoporotic fractures follows
    principles similar to the treatment of fractures resulting
    from trauma. However, it is essential that orthopaedic
    surgeons refer patients with osteoporosis to specialists
    who will initiate laboratory tests and medical therapies
    to prevent future fractures. Often, presentation to an
    orthopaedic surgeon for treatment of a fracture is the
    first indication that a patient has osteoporosis.

    Novel Treatments
    Recently, there has been controversy regarding the surgical treatment of vertebral compression fractures in
    patients with osteoporosis. Vertebroplasty and kyphoplasty have gained popularity over the past decade,
    with the principal goal of more rapid pain reduction.
    However, two recent randomized controlled trials comparing vertebroplasty to placebo demonstrated no improvement in reducing overall pain or activity-related
    pain in patients with osteoporotic vertebral compression fractures.18,19 However, the authors of a recent randomized controlled trial reported improvement in pain
    and function in patients with vertebral compression
    fractures treated with kyphoplasty compared with nonsurgical treatment.20 The advantage of kyphoplasty is
    that it has the potential to correct kyphotic deformities
    caused by a compression fracture. Theoretically, this is
    only possible if the kyphoplasty is performed relatively
    soon after the fracture occurs and before bone healing.

    Pharmacologic Treatment
    The development of bisphosphonates has revolutionized the treatment of osteoporosis. In addition to calcium and vitamin D, a few antiresorptive agents, such
    as bisphosphonates, calcitonin, estrogen, and teriparatide (PTH peptide), have been used to treat osteoporosis.
    Bisphosphonates
    Bisphosphonates have gained popularity in part because of their ease of administration and favorable tolerability. There are several different bisphosphonates
    with varying dosing regimens. A relatively new bispho-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 16: Bone Metabolism and Metabolic Bone Disease

    sphonate, zoledronic acid, is appealing to patients because it is administered intravenously only once every
    12 months. Bisphosphonates decrease osteoclastmediated bone resorption by promoting apoptosis and
    inhibiting enzymes in the cholesterol synthesis (mevalonate) pathway. The molecular mechanism of bisphosphonates depends on the presence of a nitrogen
    atom on the alkyl chain.15 Nonnitrogen-containing
    bisphosphonates (such as etidronate, clodronate, and tiludronate) are taken up by the osteoclasts and cause the
    production of toxic adenosine triphosphate analogues
    that lead to premature death in these cells. Nitrogencontaining bisphosphonates (such as pamidronate, alendronate, risedronate, and zoledronate) are taken up by
    osteoclasts and inhibit farnesyl pyrophosphate synthase, an enzyme in the mevalonate pathway.15 Exposure of osteoclasts to bisphosphonates results in the loss
    of cytoskeletal integrity at the ruffled border. This leads
    to reduced resorptive activity and accelerated apoptosis
    of osteoclasts. Bisphosphonates also have been shown
    to inhibit the maturation of osteoclasts. Interestingly,
    bisphosphonate therapy has been linked to osteonecrosis of the jaw and subtrochanteric stress fractures in rare
    instances.

    Calcitonin
    Calcitonin, like estrogen, inhibits bone resorption, decreases the rate of bone loss, and is used as another
    mode of therapy for osteoporosis. The beneficial effect
    of calcitonin is observed as long as it is given in intermittent pulse regimens. Calcitonin also has analgesic
    properties, likely related to its concomitant function as
    a neurotransmitter. The main adverse effects are flushing, nausea, vomiting, and diarrhea. These adverse effects are virtually eliminated with the nasal spray formulation.
    Teriparatide (PTH Peptide)
    Over the past few years, there has been an increase in
    the use of human recombinant PTH peptide (teriparatide) in the treatment of osteoporosis. Teriparatide
    is a recombinant peptide that contains the first 34
    amino acids of PTH, and was approved by the FDA in
    2002. Although continuous administration of teriparatide leads to net bone loss, intermittent administration of teriparatide has an anabolic effect on bone and
    stimulates bone formation. A strong positive effect of
    teriparatide has been demonstrated in postmenopausal

    2011 American Academy of Orthopaedic Surgeons

    Rickets and Osteomalacia


    2: Systemic Disorders

    Estrogen
    Estrogen therapy is also classified as an antiresorptive
    agent because it inhibits bone resorption by decreasing
    the frequency of activation of the bone remodeling cycle. There are estrogen receptors in both osteoclasts
    and osteoblasts.15 The ability of estrogen to affect gains
    in bone mass is limited to an annual increase of approximately 2% to 4% for the first 2 years of therapy.
    Estrogen therapy has several important disadvantages,
    including increased risk of endometrial hyperplasia,
    breast cancer, and thromboembolic events.

    women and osteoporotic men in randomized controlled


    studies.21,22 In postmenopausal women, there was an increase in BMD and a reduction in vertebral and nonvertebral fractures. In men, there was an increase in
    BMD in the spine and hip and a trend toward fracture
    reduction.22 Combination treatment with bisphosphonates and teriparatide also has been shown to have a
    strong positive effect in both men and women.23 A second recombinant PTH protein, hrPTH 1-84 (H05AA03
    or preotact), has been reported to have positive results
    in Europe but has not yet received FDA approval in the
    United States.
    Although the anabolic effects of teriparatide have
    been beneficial, there is a potential risk for the development of osteosarcoma based on the observation that
    osteosarcoma developed in approximately 45% of rats
    who received the highest tested dose of teriparatide.24
    As a result, the FDA has mandated a black-box
    warning and a company-sponsored surveillance program. Since its approval in 2002 by the FDA, more
    than 430,000 patients have received teriparatide; osteosarcoma developed in 2 patients. It is noteworthy that
    both of these patients also received radiation for the local treatment of breast or prostate cancer. After teriparatide, osteosarcoma developed in the rib and pubic
    ramus (the radiated fields), respectively. It remains uncertain whether osteosarcoma was caused by the radiation, teriparatide, or both. Clinicians must consider this
    risk when contemplating the use of teriparatide.

    In addition to osteoporosis, rickets and osteomalacia


    combined are the second broad category of metabolic
    bone disease. The principal abnormality in both rickets
    and osteomalacia is a defect in the mineralization of the
    osteoid matrix. The difference between the two diseases
    is that rickets is used to describe the condition before
    closure of the physis, whereas osteomalacia occurs after
    physeal closure. The mineralization defect is caused by
    inadequate calcium and phosphate deposition in the
    matrix. Deficiencies in vitamin D, calcium, or phosphorus caused by inadequate intake or malabsorption can
    result in rickets or osteomalacia. Additionally, drugs resulting in hypocalcemia or hypophosphatemia can lead
    to rickets or osteomalacia (Table 4).
    Several genetic disorders result in rickets, including
    vitamin D-dependent rickets and hypophosphatemic vitamin D-resistant rickets.15 Vitamin D-dependent rickets is caused by a mutation in the renal tubular 25hydroxyvitamin D1 hydrolase. This enzyme is required
    for the second of the two successive hydroxylations of
    vitamin D to form the active metabolite 1,25dihydroxyvitamin D. These patients are easily treated
    with 1,25-dihydroxyvitamin D or 1-alphahydroxyvitamin D3. In hypophosphatemic vitamin D-resistant
    rickets there is a mutation in the PEX gene, which codes
    for a membrane bound endopeptidase. This gene is located on the X chromosome and, to date, there have
    been more than 180 different mutations identified on

    Orthopaedic Knowledge Update 10

    189

    Section 2: Systemic Disorders

    Table 4

    Factors Causing Osteomalacia or Rickets


    Substances Associated With Vitamin D Deficiency
    Cadmium
    Cholestyramine

    differentiation of osteoclasts. Activation and function


    of osteoclasts is an important aspect of osteoporosis
    and is also the target of novel therapies. As the complex
    mechanism of bone metabolism is further studied and
    understood, new strategies or therapies to treat bonerelated diseases may emerge along with new techniques
    to stimulate bone regeneration.

    Glucocorticoids
    Phenobarbital
    Phenytoin
    Rifampin

    Annotated References
    1.

    Deng ZL, Sharff KA, Tang N, et al: Regulation of osteogenic differentiation during skeletal development. Front
    Biosci 2008;13:2001-2021.
    Osteoblastic differentiation is a complex cascade of
    events controlled by multiple genes. This article reviews
    the highly regulated process of osteoblastic differentiation and bone formation.

    2.

    Urist MR: Bone: formation by autoinduction. Science


    1965;150(698):893-899.

    3.

    Kaplan FS, Le Merrer M, Glaser DL, et al: Fibrodysplasia ossificans progressiva. Best Pract Res Clin Rheumatol 2008;22(1):191-205.
    The authors review the clinical findings and treatment
    options for patients with FOP.

    4.

    Shore EM, Xu M, Feldman GJ, et al: A recurrent mutation in the BMP type I receptor ACVR1 causes inherited
    and sporadic fibrodysplasia ossificans progressiva. Nat
    Genet 2006;38(5):525-527.

    5.

    Cohen MM Jr: The new bone biology: pathologic, molecular, and clinical correlates. Am J Med Genet A
    2006;140(23):2646-2706.

    6.

    Cooper SC, Flaitz CM, Johnston DA, Lee B, Hecht JT:


    A natural history of cleidocranial dysplasia. Am J Med
    Genet 2001;104(1):1-6.

    7.

    Aktas S, Wheeler D, Sussman MD: The chefs hat appearance of the femoral head in cleidocranial dysplasia.
    J Bone Joint Surg Br 2000;82(3):404-408.

    8.

    Trigui M, Pannier S, Finidori G, Padovani JP, Glorion


    C: Coxa vara in chondrodysplasia: Prognosis study of
    35 hips in 19 children. J Pediatr Orthop 2008;28(6):
    599-606.
    The authors report on the results of a retrospective
    study examining 35 surgically treated hips in patients
    with coxa vara secondary to chondrodysplasia. Some
    patients in the study had cleidocranial dysplasia. Those
    patients were treated with femoral varus derotational
    osteotomies and had excellent outcomes and no recurrences.

    9.

    Duplomb L, Dagouassat M, Jourdon P, Heymann D:


    Concise review: Embryonic stem cells: A new tool to
    study osteoblast and osteoclast differentiation. Stem
    Cells 2007;25(3):544-552.

    Sunscreen
    Substances Affecting Phosphate Homeostasis
    Aluminum-based antacids
    Cadmium
    Ifosfamide
    Saccharated ferric oxide
    Substances Affecting Bone Mineralization
    Aluminum
    Etidronate
    Fluoride

    2: Systemic Disorders

    this gene. PEX is needed for phosphate transport in the


    proximal renal tubules. Patients with X-linked hypophosphatemic vitamin D-resistant rickets are treated
    with high doses of 1,25-dihydroxyvitamin D.
    In rare circumstances, certain tumorous conditions,
    ranging from benign tumors (such as a nonossifying fibroma) to malignant tumors (such as an osteosarcoma)
    can induce rickets or osteomalacia.15 These tumors are
    not restricted to bone but also can be soft-tissue tumors
    or carcinomas. The pathophysiology of tumor-induced
    osteomalacia remains unknown; however, it is speculated that it may result from humoral factors that may
    affect multiple functions of the proximal renal tubules.

    Summary
    At the core of bone metabolism are the steps in bone
    formation and the sequence necessary for bone resorption. Bone formation and regeneration is a complex
    and well-regulated cascade of events involving cells of
    mesodermal origin. The mesenchymal stem cells are recruited and stimulated to differentiate by several secreted factors such as BMPs. Defects in this highly controlled process can lead to several human diseases.
    Once bone has formed, it is continually remodeled and
    regulated by several hormones and metabolites, including sex hormones, PTH, PTHrP, calcitonin, corticosteroids, and vitamin D.
    Bone resorption also involves the well-coordinated
    stimulation of pluripotent stem cells to differentiate
    into monocytes and eventually into osteoclasts. Critical
    in this process is the RANKL pathway in the terminal
    190

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 16: Bone Metabolism and Metabolic Bone Disease

    tic vertebral fractures. N Engl J Med 2009;361(6):


    557-568.

    The development of osteoblasts and osteoclasts from


    stem cells is reviewed in this article, along with a discussion of the conditions needed for differentiation of stem
    cells into osteoblasts and osteoclasts in vitro.
    10.

    Del Fattore A, Cappariello A, Teti A: Genetics, pathogenesis and complications of osteopetrosis. Bone 2008;
    42(1):19-29.
    The authors present a comprehensive review of genetic
    mutations that lead to the development of osteopetrosis.
    There are multiple mutations that can lead to osteopetrosis, and many are discussed in this article. The clinical
    manifestations of osteopetrosis also are reviewed.

    11.

    Pangrazio A, Poliani PL, Megarbane A, et al: Mutations


    in OSTM1 (grey lethal) define a particularly severe form
    of autosomal recessive osteopetrosis with neural involvement. J Bone Miner Res 2006;21(7):1098-1105.

    12.

    Helfrich MH: Osteoclast diseases. Microsc Res Tech


    2003;61(6):514-532.

    13.

    Ralston SH, Langston AL, Reid IR: Pathogenesis and


    management of Pagets disease of bone. Lancet 2008;
    372(9633):155-163.
    Mutations in SQSTM1, RANK, OPG, and VCP have
    been linked to Paget disease. This article reviews the
    mechanistic consequences of these mutations as well as
    the clinical management of Paget disease.
    Hocking LJ, Lucas GJ, Daroszewska A, et al: Domainspecific mutations in sequestosome 1 (SQSTM1) cause
    familial and sporadic Pagets disease. Hum Mol Genet
    2002;11(22):2735-2739.

    15.

    Rosen CJ, ed: Primer on the Metabolic Bone Diseases


    and Disorders of Mineral Metabolism, ed 7. Washington, DC, American Society for Bone and Mineral Research, 2008.
    This textbook, written by experts in the field, presents
    an overview of bone metabolism and metabolic bone
    diseases.

    16.

    17.

    18.

    Prentice A: Vitamin D deficiency: A global perspective.


    Nutr Rev 2008;66(10, Suppl 2):S153-S164.
    Vitamin D deficiency is common in many parts of the
    world, and recently there has been a resurgence of rickets in children. This article reviews the risk and prevalence of vitamin D deficiency in different ethnic groups
    globally.
    Lim LS, Horksema LJ, Sherin K; ACPM Prevention
    Practice Committee: Screening for osteoporosis in the
    adult U.S. population: ACPM position statement on preventive practice. Am J Prev Med 2009;36(4):366-375.
    Osteoporosis is the most common metabolic bone disease. This article reviews the prevalence of osteoporosis
    in the United States and discusses the role of screening.
    Risk assessment tools to identify patients who may have
    osteoporosis are also discussed.
    Buchbinder R, Osborne RH, Ebeling PR, et al: A randomized trial of vertebroplasty for painful osteoporo-

    2011 American Academy of Orthopaedic Surgeons

    19.

    Kallmes DF, Comstock BA, Heagerty PJ, et al: A randomized trial of vertebroplasty for osteoporotic spinal
    fractures. N Engl J Med 2009;361(6):569-579.
    This multicenter, randomized, placebo-controlled trial
    examined the benefit of vertebroplasty in patients with
    osteoporotic vertebral fractures. The authors concluded
    there are no benefits of vertebroplasty with respect to
    pain and pain-related disabilities. Level of evidence: I.

    20.

    Wardlaw D, Cummings SR, Van Meirhaeghe J, et al: Efficacy and safety of balloon kyphoplasty compared with
    non-surgical care for vertebral compression fracture
    (FREE): a randomised controlled trial. Lancet 2009;
    373(9668):1016-1024.
    The authors present the findings of a randomized controlled trial examining the efficacy and safety of balloon
    kyphoplasty versus nonsurgical care in 300 patients.
    There was a significant difference in the Medical Outcomes Study 36-Item Short Form scores between the
    two groups, with no difference in adverse events. The
    authors concluded that kyphoplasty is safe and effective
    in treating acute vertebral compression fractures. Level
    of evidence: I.

    21.

    2: Systemic Disorders

    14.

    The authors present the findings of a multicenter, randomized, double-blind, placebo-controlled trial examining the role of vertebroplasty in the treatment of vertebral compression fractures. The study did not show any
    benefit of vertebroplasty with respect to pain relief,
    functional benefits, quality of life, and perceived improvement. Level of evidence: I.

    Bouxsein ML, Chen P, Glass EV, Kallmes DF, Delmas


    PD, Mitlak BH: Teriparatide and raloxifene reduce the
    risk of new adjacent vertebral fractures in postmenopausal women with osteoporosis. Results from two randomized controlled trials. J Bone Joint Surg Am 2009;
    91(6):1329-1338.
    The findings of a randomized, controlled, double-blind
    trial examining the effects of teriparatide and raloxifene
    on the risk of subsequent vertebral fractures are presented. Both teriparatide and raloxifene can reduce the
    risks of new vertebral fractures. Level of evidence: I.

    22.

    Geusens P, Sambrook P, Lems W: Fracture prevention in


    men. Nat Rev Rheumatol 2009;5(9):497-504.
    Although there is substantial literature on osteoporosis
    in women, much less is written about osteoporosis in
    men. This article reviews epidemiology, the differences
    in the pathophysiology of bone loss between men and
    women, fracture prevention, and treatment options for
    men with osteoporosis.

    23.

    Pleiner-Duxneuner J, Zwettler E, Paschalis E, Roschger


    P, Nell-Duxneuner V, Klaushofer K: Treatment of osteoporosis with parathyroid hormone and teriparatide.
    Calcif Tissue Int 2009;84(3):159-170.
    Teriparatide has recently emerged as a treatment option
    for osteoporosis in the United States. The authors review the pharmacokinetic and clinical experience in us-

    Orthopaedic Knowledge Update 10

    191

    Section 2: Systemic Disorders

    ing PTH and teriparatide to treat patients with osteoporosis.


    Subbiah V, Madsen VS, Raymond AK, Benjamin RS,
    Ludwig JA: Of mice and men: Divergent risks of
    teriparatide-induced osteosarcoma [published online
    ahead of print July 14, 2009]. Osteoporos Int. PMID:
    19597911.

    2: Systemic Disorders

    24.

    This article analyzed the risk of osteosarcoma in rats


    that received the highest tested dose of teriparatide in
    preclinical studies. Additionally, surveillance data on
    430,000 patients who received teriparatide revealed that
    osteosarcoma developed in 2 patients. Both patients had
    received radiation for cancer treatment in the area
    where the osteosarcoma developed.

    192

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 17

    Musculoskeletal Oncology
    Kevin B. Jones, MD

    Basic Principles

    Population Science

    Molecular Biology
    Sarcomas can be grouped into those with abundant cytogenetic and genetic perturbations and those with bal-

    Neither Dr. Jones nor any immediate family member has


    received anything of value from or owns stock in a commercial company or institution related directly or indirectly to the subject of this chapter.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    Cancer is a common disease, newly affecting more than


    1 million Americans each year; however, neoplasms
    that primarily affect musculoskeletal tissues are relatively rare. According to the Surveillance, Epidemiology, and End Results (SEER) database, an estimated
    2,570 individuals were diagnosed with bone sarcomas,
    with 1,470 deaths in 2008. Soft-tissue sarcomas were
    more common, with 10,660 diagnoses and 3,820
    deaths in 2008.1
    Recent reviews of the SEER database have elucidated several epidemiologic facts about specific sarcoma subtypes. Osteosarcoma was confirmed to have a
    bimodal distribution in age of onset, arising as a primary malignancy in adolescents and young adults but
    as a secondary cancer or complication of Paget disease
    of bone in elderly patients.2 Osteosarcoma survival
    rates have not improved over the past 20 years. Anatomic location, age, and stage at presentation are each
    critical for prognosis.
    Ewing sarcoma was found to be more prevalent in
    Caucasians than in persons of African or Asian descent.3 It also was found that chondrosarcoma survival
    rates have not improved; tumor grade and stage of disease remain the only independent predictors of survival.4 For soft-tissue sarcomas in general, age, surgical
    resection, use of radiation, and tumor grade and size
    each correlated with survival.5 Synovial sarcomas present across a range of ages but have a better prognosis in
    younger patients.6 For patients with clear cell sarcomas,
    nodal as opposed to distant metastasis results in a dramatically better prognosis.7 Age younger than 16 years
    and disease that is localized, surgically resectable, and
    does not involve the lymph nodes are predictive factors
    of long-term survival in patients with epithelioid sarcomas.8

    anced, reciprocal translocations. The biologic understanding of representative tumors in each group is
    progressing rapidly but has produced only minimal impact on therapeutic treatments.
    Osteosarcoma and pleomorphic soft-tissue sarcomas
    are prototype, complex, genotype sarcomas. Insights
    into their pathophysiology have arisen from their increased incidence in hereditary cancer syndromes such
    as Li Fraumeni (from p53 disrupting mutations), congenital retinoblastoma, and Rothmund-Thomson syndrome (from truncating mutations in the RECQL4 helicase.) Mouse models of these sarcomas, using targeted
    disruption of varied tumor suppressor genes, have recently been described. Combined disruption of both
    p53 and pRb in preosteoblasts generated osteosarcomas that mimic the human disease.9 Disruption of Kras
    and either Ink4a-Arf or p53 in the muscles of limbs
    generated pleomorphic soft-tissue sarcomas.10
    Subtype-specific diagnoses have improved dramatically for translocation-associated sarcomas (Table 1).
    Molecular methods, such as spectral karyotyping, fluorescent in situ hybridization, and real-time reverse transcription polymerase chain reaction for fusion transcripts are becoming more widely available to
    diagnostic laboratories. Mouse models have confirmed
    the causative relationship between the translocationgenerated fusion protein and the sarcoma for three specific types: myxoid liposarcoma, alveolar rhabdomyosarcoma, and synovial sarcoma.11-13
    Other sarcomas also have discernible genetic backgrounds (Table 2). Patients with neurofibromatosis
    type I, from inherited mutation in the NF1 gene, are
    predisposed to the development of malignant peripheral nerve sheath tumors. Patients with Ollier disease or
    Maffucci syndrome have multiple enchondromas with
    a high rate of malignant transformation to chondrosarcomas. Mouse models of Ollier disease, which use a variety of genetic derangements to effect increased Indian
    hedgehog signaling, have been used to study the progression to chondrosarcoma.14 Patients with multiple
    osteochondromas, bearing germline mutations in EXT1
    or EXT2, develop numerous metaphyseal osteochondromas and rarely a surface chondrosarcoma (1% to
    3% lifetime risk per patient).15
    The neoplastic character of two lesions, whose clonality has long been questioned, has recently been settled. Pigmented villonodular synovitis and aneurysmal
    bone cysts both share a unique pathophysiology characterized by a small amount (usually less than 10%) of
    193

    Section 2: Systemic Disorders

    Table 1

    Sarcoma Translocations
    Sarcoma

    Chromosome Translocation

    Fusion Gene

    Alveolar rhabdomyosarcoma

    t(2;13)(q35;q14)

    PAX3-FKHR

    t(1;13)(q36;q14)

    PAX7-FKHR

    Alveolar soft-part sarcoma

    t(X;17)(p11;q25)

    TFE3-ASPL

    Aneurysmal bone cyst

    17p3 rearrangement

    USP6 increase

    Clear cell sarcoma

    t(12;22)(q13;q12)

    EWS-ATF1

    Congenital fibrosarcoma

    t(12;15)(p13;q25)

    ETV6-NTRK3

    Dermatofibrosarcoma protuberans

    t(17;22)(q22;q13)

    COL1A1-PDGFB

    Desmoplastic small round cell tumor

    t(11;22)(p13;q11)

    EWS-WT1

    Extraskeletal myxoid chondrosarcoma

    t(9;22)(q22;q12)

    EWS-CHN

    t(9;17)(q22;q11)

    TAF2N-CHN

    t(11;22)(q24;q12)

    EWS-FLI1

    t(21;22)(q22;q12)

    EWS-ERG

    t(7;22)(p22;q12)

    EWS-ETV1

    t(2;22)(q33;q12)

    EWS-E1AF

    2: Systemic Disorders

    Ewing sarcoma family of tumors

    t(17;22)(q12;q12)

    EWS-FEV

    Fibromyxoid sarcoma, low-grade

    t(7;16)(q33;p11)

    FUS-CREB3L2

    t(11;16)(p11;p11)

    FUS-CREB3L1

    Inflammatory myofibroblastic tumor

    t(1;2)(q22;p23)

    TPM3-ALK

    t(2;19)(p23;p13)

    TPM4-ALK

    Myxoid liposarcoma

    t(12;16)(q13;p11)

    FUS-DDIT3

    t(12;22)(q13;q12)

    EWS-DDIT3

    Pigmented villonodular synovitis

    5q33 rearrangement

    CSF1 increase

    Synovial sarcoma

    t(X;18)(p11;q11)

    SYT-SSX1
    SYT-SSX2
    SYT-SSX4

    Table 2

    Sarcomas Associated With Genetic Predispositions to Cancer

    194

    Heritable Syndrome

    Gene(s) Involved

    Associated Musculoskeletal Neoplasm

    Li Fraumeni

    p53

    Osteosarcoma, pleiomorphic rhabdomyosarcoma,


    pleiomorphic undifferentiated sarcoma

    Congenital bilateral retinoblastoma RB1

    Osteosarcoma

    Rothmund-Thomson

    RECQL4

    Osteosarcoma

    Multiple hereditary exostoses

    EXT1, EXT2

    Osteochondroma, secondary chondrosarcoma

    Neurofibromatosis (type I)

    NF1

    Neurofibroma, malignant peripheral nerve sheath tumor

    McCune-Albright

    GNAS1

    Fibrous dysplasia

    Ollier disease

    PTHR1 in minority

    Enchondromas

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 17: Musculoskeletal Oncology

    cells in the tumor volume composed of neoplastic cells


    bearing specific chromosomal translocations: CSF-1
    gene rearrangements16 and chromosome 17p3, USP6
    gene rearrangements,17 respectively. The remaining cells
    in the lesion are not neoplastic, but are recruited to the
    neoplasm to create what is termed a landscape effect.

    For example, a patient who presents with a fracture


    through a lesion who had experienced antecedent pain
    raises suspicion of different diagnoses than a patient
    whose fracture occurred through a previously asymptomatic lesion.

    Clinical Evaluation
    Clinical Research Paradigms

    When taking the patients history, there should be a


    critical focus on discerning the patterns of typical orthopaedic diagnoses. Specifically, the history of pain
    over time is crucial. Pain at rest or at night is indicative
    of biologic pain from the growth of a lesion in a bone.
    Pain with weight bearing or activity raises the suspicion
    of mechanical pain from poor structural integrity in the
    bone. Pain after activity is more indicative of an inflammatory phenomenon than a neoplasm. The pace of disease over time also can be informative. A mass that is
    present for years is unlikely to be an aggressive malignancy unless there has been a recent change in the pace
    of the disease process. A lytic lesion causing bone pain
    that evolves over hours or days is more likely infectious
    than neoplastic, whereas lesional pain evolving over
    weeks or months is more likely to indicate a neoplasm.
    The physical examination should be focused on ruling out alternate orthopaedic diagnoses. Identifying the
    precise location of the pain is critical. If pain does not
    colocalize with the mass or bone lesion identified with
    imaging, it should be determined if the pain fits typical
    referred pain locations, a radicular distribution, or a
    peripheral nerve distribution.
    Few laboratory tests provide useful diagnostic information. Important exceptions are inflammatory markers in the setting of possible infections, lactate dehydrogenase in the setting of possible lymphoma of bone,
    serum and urine protein electrophoreses when there is
    concern about myeloma, alkaline phosphatase as a
    prognosticator for osteosarcoma, and specific tumor
    markers in the workup of metastatic carcinoma such as
    prostate-specific antigen.

    2: Systemic Disorders

    Surgically-related clinical research is focused on improving the quality and longevity of functional outcomes following limb-sparing resection of tumors. The
    previous standard outcomes instruments were the 1987
    and 1993 Musculoskeletal Tumor Society outcome
    scores. Often, both scores are used in tandem. The former score is joint specific and the latter score is more
    generalized. Both instruments use a physician-focused
    rather than a patient-focused approach. The Toronto
    Extremity Salvage Score is a patient- and functionfocused outcome score that also is generalized and is
    not joint or limb specific.
    Most surgical studies in the literature related to sarcoma come from single centers or ad hoc collaborations between a few centers. There have been a few
    cross-Canadian and cross-European collaborative studies, but more are needed. The study of sarcoma began
    with one of the first national collaborative registries,
    called the Bone Tumor Registry, which focused on musculoskeletal neoplasms. This registry was in operation
    from the 1920s through 1953, when data collection
    ceased. The current medicolegal environment and requirements of the Health Insurance Portability and Accountability Act (HIPAA) make it very unlikely that a
    similar contemporary registry will be established in the
    United States.
    There are collaborative groups that continue to
    study sarcoma, including the Childrens Oncology
    Group, Sarcoma Alliance for Research through Collaboration, and the Radiation Therapy Oncology Group;
    however, these groups rarely conduct studies regarding
    surgical techniques or outcomes.

    Imaging
    Bone Lesions

    Patient Presentations
    Musculoskeletal neoplasms and lesions that mimic such
    neoplasms come to the attention of medical caregivers
    when a patient presents for treatment because of pain,
    a detected mass, a fracture, or when an imaging abnormality is noted during the evaluation for an unrelated
    disorder. This last group of incidentally noted lesions
    requires diligent management; however patience and
    serial imaging may confirm the latency of such lesions
    without the anxiety or expense created by investigations using more complex modalities. Each of these
    four categoric presentations can overlap. Even incidentally noted lesions may be found to be symptomatic
    when the patient is probed with specific questions.
    These overlaps in the reason the patient seeks treatment
    can guide the development of a differential diagnosis.

    2011 American Academy of Orthopaedic Surgeons

    Plain radiography remains the diagnostic imaging modality of choice for nearly all skeletal neoplasia. For lesions located in areas that would be difficult to visualize with plain radiography, such as the sacrum and the
    scapulae, CT is the first alternative. These x-raybased
    modalities demonstrate the matrix formed by the lesion
    and the zone of transition between the lesional tissue
    and host bone. Matrix types include bone (appearing as
    smooth mineralization), cartilage (appearing as stippled
    mineralization in rings and arcs), and fibro-osseous matrix (ground-glass appearance).
    The classic categorization of zones of transition between lesion and host tissue was first described in
    1980.18 Three such categories are in current use: latent
    lesions surrounded by a reactive cortical rim; active lesions with an abrupt, easily discernible transition but
    no reactive rind (Figure 1); and aggressive lesions, with
    a broad, infiltrating border with the host. These classifications reflect the lesions presumed activity over

    Orthopaedic Knowledge Update 10

    195

    2: Systemic Disorders

    Section 2: Systemic Disorders

    Figure 1

    A 35-year-old woman delayed seeking medical attention until she felt a pop and could not bear weight on her right
    knee. AP (A) and lateral (B) radiographs of the knee show a lytic lesion with a narrow zone of transition, but no
    reactive rind of cortical bone. Such a lesion-host interface is called an active border and is given a Lodwick A2 rating. Lesions with active borders are usually in the category of benign aggressive bone lesions. C and D, MRI scans
    (T1-weighted coronal and T2-weighted axial, respectively) show a mass filling the proximal tibia, with subchondral
    fracture and tibial tubercle compromise. Incisional biopsy was consistent with giant cell tumor of bone. High-speed
    burr-enhanced intralesional excision was performed, followed by allograft reconstruction of the bone defect and
    reinforcement of the extensor mechanism.

    time, but serial imaging remains the most definitive assessment of lesional behavior. There are few, if any,
    bone lesions that do not require at least a second set of
    imaging studies, separated in time by months, to confirm latency.
    The location of the lesion in the bone also guides the
    differential diagnosis (Table 3). Most, but not all, lesions have a predilection for the metaphyses near major
    growth centers of the skeleton. There are few differential diagnoses for entirely epiphyseal lesions or those lo196

    Orthopaedic Knowledge Update 10

    cated in the small bones of the wrists and ankles. Similarly, few lesions will affect the diaphysis and spare the
    metaphysis.
    Staging is also performed by imaging, but requires
    distinct modalities. Local staging is achieved with MRI,
    which can best identify and localize any soft-tissue extension of the lesion. Although some lesions, such as giant cell tumor of bone, have characteristic appearances
    on MRI, this modality is primarily used for staging
    rather than diagnosis. For malignancies, systemic stag-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 17: Musculoskeletal Oncology

    Table 3

    Bone Tumor Location Within the Bone Defines the Differential Diagnosis
    Epiphysis

    Metaphysis

    Diaphysis

    Chondroblastoma
    Clear cell chondrosarcoma
    Extension of giant cell tumor of bone
    Osteochondromas in Trevor disease

    Most common site for most bone


    neoplasms, primary or metastatic

    Fibrous dysplasia
    Ewing sarcoma
    Langerhans cell histiocytosis
    Osteoid osteoma
    Osteoblastoma
    Osteofibrous dysplasia/adamantinoma
    Lymphoma
    Metastatic carcinoma
    Myeloma

    Table 4

    American Joint Committee on Cancer Staging System


    Stage

    Histologic
    Grade

    Size

    Location (Relative to Fascia)

    Systemic/Metastatic
    Disease Present

    IA

    Low

    < 5 cm

    Superficial or deep

    No

    IB

    Low

    5 cm

    Superficial

    No

    IIA

    Low

    5 cm

    Deep

    No

    IIB

    High

    < 5 cm

    Superficial or deep

    No

    IIC

    High

    5 cm

    Superficial

    No

    III

    High

    5 cm

    Deep

    No

    IV

    Any

    Any

    Any

    Yes

    2011 American Academy of Orthopaedic Surgeons

    2: Systemic Disorders

    ing is required and usually includes a technetium Tc


    99m total body bone scan and noncontrast CT of the
    chest to seek potential sites of metastasis. High suspicion must be maintained for false-negative bone scans
    in the setting of multiple myeloma or diffusely metastatic prostate carcinoma; the former for its lack of detection by bone scan, the latter because evenly increased uptake throughout whole sections of the
    skeleton can create a superscan effect, which can be averaged to appear negative. For myeloma, specifically, a
    skeletal survey is the preferred method for screening the
    skeleton.
    Benign bone tumors are often staged according to
    the Campanacci19 radiographic system, which was
    adapted from the Enneking clinical system. Each system includes grade 1 tumors, which are latent and surrounded by a reactive rind; grade 2 tumors, which are
    active but contained within at least a neocortex, if not
    the original cortex of the host bone; and grade 3 tumors, which include soft-tissue masses extending beyond the cortex and not contained by the neocortex.
    Malignant bone neoplasms are often staged using the
    Enneking system, as adapted by the Musculoskeletal
    Tumor Society.20 Stage I are low-grade lesions, stage II
    are intermediate- or high-grade lesions, and stage III are
    lesions with demonstrable metastatic disease. For stage
    I and II lesions, an intracompartmental, A, or extra-

    compartmental, B, designation relating to the local extent of the disease is applied. The more formal staging
    system of the American Joint Committee on Cancer
    (Table 4) is increasingly used as an alternative or adjunct to the Enneking-Musculoskeletal Tumor Society
    staging system and is recommended for communication
    with oncologists and for central registry data entry.
    Iliac crest bone marrow biopsy also is included in
    the disease-specific staging systems for myeloma and
    the Ewing sarcoma family of tumors. Surgeons can facilitate the use of this evaluation tool if the biopsy is
    performed with the patient under general anesthesia.

    Biopsy
    The purpose of biopsy is to obtain diagnostic tissue as
    well as specimens for tissue-banking and research. Diagnostic tissue can be procured by fine-needle aspiration, core needle biopsy, incisional biopsy, or excisional
    biopsy and may be timed concurrent with the definitive
    surgery or long before it, depending on the clinical scenario. Biopsies are best performed by a team prepared
    to provide definitive treatment. Such interdisciplinary
    teams can best judge which lesions require biopsy and
    which biopsy method will be best suited to the patients
    potential diagnoses.21,22 Although few scenarios are
    safely managed with intraoperative frozen section diagnosis followed by definitive management, obtaining

    Orthopaedic Knowledge Update 10

    197

    Section 2: Systemic Disorders

    2: Systemic Disorders

    frozen sections to confirm the adequacy of tissue is critical to the performance of surgical incisional biopsies
    and thus requires a musculoskeletal pathologist. Biopsies performed without considering definitive surgical
    options can have severe consequences caused by poor
    placement of the incision, violation of otherwise noncontaminated tissue compartments, or by spreading tumor cells by hematoma formation.21,22
    Not all lesions should be biopsied. Asymptomatic,
    latent-appearing bone lesions that represent no significant risk of pathologic fracture based on their size and
    location should be monitored with serial imaging to
    confirm latency, rather than exposing patients to the
    risks of biopsy. Cartilaginous lesions should be biopsied
    only with the intent of confirming their cartilaginous
    character if aggressive treatments are indicated because
    grading of such lesions has been shown to be unsatisfactory, even among skilled pathologists.23
    Hematoxylin and eosin staining is the pathologists
    primary diagnostic tool for bone neoplasms. Although
    immunohistochemical stains are used in specific scenarios, such as for small, round, blue cell-appearing lesions, no specific diagnostic tests are available for most
    bone neoplasms. This situation places increased emphasis on the experience of the interpreting pathologist.
    For small, round, blue cell tumors, several markers are
    used to identify the Ewing sarcoma family of tumors,
    such as immunohistochemistry against CD99 or FLI1,
    and molecular testing for the t(11;22) translocation or
    its fusion products (Figure 2). Other markers, such as
    CD45, as well as flow cytometry may be used to assess
    for or rule out lymphoma. For metastatic carcinomas,
    immunohistochemistry may guide identification of the
    tumors origin; however, it is successful at identifying
    the primary disease type only in a minority of cases in
    which primary tumor tissue is not available or detectable.24 The staging workup and serum markers help to
    identify the primary carcinoma in situations with less
    characteristic pathology.

    ing neoadjuvant chemotherapy. Alternatively, even with


    fixation, diaphyseal fractures may not heal before definitive surgical treatment. Any placed fixation devices,
    along with all tissues contacted during placement, must
    be resectable en bloc with the tumor.
    Once metastatic carcinoma is diagnostically confirmed in a fractured or impending fracture lesion, decision making is refocused on restoring structural integrity. The contribution of two different types of pain
    must be delineated. Pain caused by tumor growth in the
    bone occurs primarily when the patient is at rest and is
    often well managed by radiotherapy. Functional pain
    from an impending fracture is usually not well managed by radiation alone and may require surgical stabilization. The Mirels criteria assign points for pain, location, character, and size of the lesion.25 These criteria
    were developed, and are therefore only validly applied,
    using plain radiography. Lesions that are large and destructive on MRI or CT alone, but involve little cortical
    bone, may not be well characterized by the Mirels criteria. Case-by-case judgment is required.
    One exception to the rule of fracture stabilization in
    metastatic carcinoma involves renal cell and thyroid
    carcinomas, which can occasionally be oligometastatic.
    Although controversial, some retrospective evidence
    suggests a survival benefit for removing metastatic renal cell foci in the presence of minimal to no visceral
    disease.26 This may result from the poor radiosensitivity
    or the relative chemoresistance of the skeletal foci of
    disease. Such treatment has been applied to thyroid
    cancer as well, but with fewer data to support or refute
    the practice.
    Benign Latent Lesions
    With or without a diagnosis, asymptomatic lesions
    with proven latency and minimal risk for pathologic
    fracture based on size and location should receive no
    further treatment (Table 5). The serial observation of
    such lesions in growing children until skeletal maturity
    remains controversial.

    Management Paradigms
    Pathologic Fracture or Impending Fracture
    on Presentation
    A patient presenting with a pathologic fracture or an
    impending pathologic fracture must be assessed with
    two urgent competing goals in mind. First, the diagnosis must precede any definitive surgical treatment, especially any surgery that could compromise the future
    possibility for margin-negative resection. Second, the
    fracture must be stabilized for the patients comfort and
    to prevent the mechanical distribution of tumor cells
    into previously uncompromised compartments by hematoma or further displacement. The only situation in
    which a destructive bone lesion may be definitively
    fixed without a lesion-specific tissue diagnosis is when
    a tissue-confirmed skeletal metastatic carcinoma or
    multiple myeloma has already been diagnosed.
    For pathologic fractures that raise the suspicion for
    sarcoma, fixation is controversial. Minimally displaced
    metaphyseal fractures often heal without fixation dur198

    Orthopaedic Knowledge Update 10

    Benign Aggressive Lesions


    Lesions may be aggressive anatomically or biologically.
    Osteoid osteoma, for example, which usually is subcentimeter in size, is rarely anatomically aggressive. Nonetheless, it can cause severe symptoms requiring ablative
    treatments. Fibrous dysplasia may be biologically
    nearly latent, but by its size may compromise the structural integrity of the host bone, requiring stabilization
    to prevent fracture. The classic lesions treated by the
    benign-aggressive paradigm are giant cell tumors of
    bone, osteoblastomas, chondroblastomas, chondromyxoid fibromas, and aneurysmal bone cysts. Each of
    these lesions has a known predilection toward local recurrence, which should be a treatment consideration.
    Any small, benign, aggressive lesion may be treated
    with percutaneous methods such as radiofrequency ablation. Larger lesions require aggressive intralesional
    excision or resection. Benign aggressive lesions arising
    in expendable bones, such as the proximal fibula, are

    2011 American Academy of Orthopaedic Surgeons

    Chapter 17: Musculoskeletal Oncology

    2: Systemic Disorders

    Figure 2

    A 16-year-old girl had a pathologic fracture to the left femur after being kicked during a dance class. She reported
    experiencing antecedent proximal thigh pain for nearly 1 year, with multiple failed attempts at diagnostic imaging
    of the hip. A, AP radiograph of the fractured femur. Incisional biopsy pathology showed small, round blue cells
    with infiltrating bands of fibrous tissue on hematoxylin and eosin histology (B). Immunohistochemistry for CD99
    (also called O13) showed cytoplasmic staining (C) and fluorescent in situ hybridization confirmed the presence of
    an 11;22 chromosomal translocation, consistent with a diagnosis of Ewing sarcoma. After neoadjuvant chemotherapy, the patient was treated with a limb-sparing intercalary femur resection and endoprosthetic reconstruction. AP
    plain radiographs of the proximal (D) and distal (E) femur show this reconstruction.

    best managed with resection, whereas most arising in


    nonexpendable bones are removed by curettage. Curettage alone produces frequent local recurrences. Recurrence rates are greatly reduced by the use of a highspeed burr and a wide cortical window to permit full

    2011 American Academy of Orthopaedic Surgeons

    visualization of all tumor surfaces.27,28 Additional


    chemical adjuvants such as phenol, ethanol, peroxide,
    cryotherapy, and argon beam coagulation may provide
    additional reductions in the rates of local recurrence,
    but no supporting large comparative studies have been

    Orthopaedic Knowledge Update 10

    199

    Section 2: Systemic Disorders

    Table 5

    Bone Neoplasms
    Tissue Group
    Fibrous

    Cartilaginous

    2: Systemic Disorders

    Osseous

    Giant cell rich

    Round blue cell

    Neoplasm

    Age (decades)

    Location

    Nonossifying fibroma

    First through third

    Metaphysis; eccentric; long bones

    Fibrous dysplasia

    First through fourth

    Anywhere in long bones

    Osteofibrous dysplasia

    First through fourth

    Anterior tibial cortex

    Adamantinoma

    Second through fourth

    Anterior tibia

    Malignant fibrous histiocytoma


    (nonosteogenic spindle cell)

    Any

    Metaphysis; long bones or pelvis

    Enchondroma

    Any

    Metaphysis; central; hand; femur;


    humerus

    Osteochondroma

    First through third

    Metaphysis; long bones; pelvis; scapula

    Periosteal chondroma

    Second through fourth

    Metaphysis; long bones

    Chondromyxoid fibroma

    Second through fourth

    Metaphysis, long bones

    Chondroblastoma

    Second through fourth

    Epiphysis; long bones; hindfoot, wrist

    Low-grade chondrosarcoma

    Third through seventh

    Metaphysis; central; long bones; pelvis

    Peripheral chondrosarcoma

    Third through fifth

    Metaphysis; long bones; pelvis; scapula

    High-grade chondrosarcoma

    Fourth through seventh

    Metaphysis; central; long bones; pelvis,


    scapula

    Dedifferentiated
    chondrosarcoma

    Fourth through seventh

    Metaphysis; long bones; pelvis; scapula

    Chondroblastic osteosarcoma

    First through fourth

    Diaphyseal surface or central


    metaphyseal; long bones; pelvis

    Osteoid osteoma

    First through third

    Anywhere, spine posterior elements

    Osteoblastoma

    Second through fourth

    Anywhere; spine posterior elements

    Parosteal osteosarcoma

    Second through fourth

    Metaphysis; long bones; posterior distal


    femur

    Conventional osteosarcoma

    Second through fourth

    Metaphysis; long bones; femur; tibia;


    humerus

    Secondary osteosarcoma

    Fifth through eighth

    Anywhere

    Giant cell tumor

    Second through fifth

    Metaphysis into epiphysis; long bones

    Aneurysmal bone cyst

    First through fourth

    Metaphysis; long bones; spine

    Langerhans cell histiocytosis

    First through third

    Anywhere

    Multiple myeloma

    Fifth through eighth

    Anywhere

    Lymphoma

    Fifth through seventh

    Long bones; pelvis

    Ewing sarcoma family of tumors Second through third


    Metastatic carcinoma Breast carcinoma

    Fifth through eighth

    Anywhere
    Spine; pelvis; femur, humerus

    Prostate carcinoma

    Fifth through eighth

    Spine; pelvis; femur, humerus

    Lung carcinoma

    Sixth through eighth

    Anywhere

    Renal cell carcinoma

    Fifth through seventh

    Spine; pelvis; femur/ humerus

    Thyroid carcinoma

    Fourth through eighth

    Spine; pelvis; femur/humerus

    NSAIDs = nonsteroidal anti-inflammatory drugs, SPEP/UPEP = serum protein electrophoresis/urine protein electrophoresis
    Green = surgery only necessary if bone is structurally compromised; yellow = lesion extirpation necessary, usually by curettage with adjuvant burring;
    orange = treated by wide resection without systemic adjuvants; red = treated by wide resection with systemic treatments; blue = surgery is aimed only at
    stabilization and prevention of fractures
    (continued on next page)

    200

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 17: Musculoskeletal Oncology

    Table 5

    Bone Neoplasms (continued)


    Pathology

    Special Notes

    Giant cells, histiocytes, hemosiderin

    Misnomer, often ossifies

    Disconnected trabeculae in fibrous stroma; no rimming


    osteoblasts

    G-coupled protein receptor mutations; difficult to eradicate

    Disconnected trabeculae in fibrous stroma with rimming


    osteoblasts

    Extremely rare

    Biphasic; fibrous stroma and epithelial rests

    Extremely rare

    Variable; fibrous stroma; histiocytes

    Treated on osteosarcoma protocols

    Hyaline cartilage within bone

    Avoid surgery

    Loosely organize physis on osseous stalk

    Cortical and medullary continuity

    Hyaline cartilage at bone surface

    Can be painful

    Stellate chondrocytes in myxoid background

    Can be painful

    Round, plump chondroblasts; giant cells; calcifications

    Even with cortical rind, can be painful


    Beware of curettage when in pelvis
    Usually secondary, usually low- to intermediate-grade

    Cellular cartilage, losing hyaline features; pronounced atypia

    No good treatments for high rate of metastatic disease

    Tandem presence of low-grade hyaline cartilage and high-grade


    spindle cell neoplasm

    Deadly with any treatment regimen

    May be predominantly cartilage; osteoid generated by


    malignant cells somewhere

    Periosteal osteosarcoma is intermediate grade

    Variably mineralized woven bone

    Treated by NSAIDs or radiofrequency ablation

    Variably mineralized woven bone

    Larger than 1.5 to 2 cm

    Spindle cell, fibrous background, woven bone, low-grade atypia

    Has long-term low metastatic potential

    Malignant spindle cells making osteoid; telangiectatic areas and


    giant cells common

    Key is systemic therapy to prevent death from metastasis, but


    local control is also critical

    Malignant spindle cells making osteoid

    Underlying Paget disease or prior radiation

    Multinucleated giant cells in stromal background with matched


    nuclei

    Many other lesions have giant cells: nonossifying fibroma,


    chondroblastoma, and osteosarcoma

    Multinucleated giant cells, vascular spaces, peripheral woven


    bone

    Landscape effect from minority neoplastic population

    Histiocytes, multilineage inflammatory cells, prominent


    eosinophils

    The great mimicker; always consider with Ewing sarcoma


    family of tumors and infection; may be self-limited

    Abundant plasma cells with perinuclear hof

    Can be diagnosed by SPEP/UPEP

    Large round blue cells, poorly cohesive

    Can cause hypercalcemia

    Cohesive large round blue cells

    Surgery is adjuvant to chemotherapy

    Epithelial rests; strong cytokeratin staining

    Long survival often possible

    Epithelial rests; strong cytokeratin staining

    Often blastic, less frequently surgical

    Epithelial rests; strong cytokeratin staining

    Often short survival

    Epithelial rests; strong cytokeratin staining

    Beware of hemorrhage, radiosensitive, consider excision

    Epithelial rests; strong cytokeratin staining

    Beware of hemorrhage

    2: Systemic Disorders

    Cellular hyaline cartilage; binucleated lacunae; bone invasion


    Osteochondroma cap greater than 1.5 cm; hyaline cartilage

    NSAIDs = nonsteroidal anti-inflammatory drugs, SPEP/UPEP = serum protein electrophoresis/urine protein electrophoresis

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    201

    Section 2: Systemic Disorders

    Figure 3

    A, Preoperative AP radiograph of a femur fracture in a 48-year-old man who was injured while gardening in the sitting position shows an infiltrative lesion. Lymphoma of bone that was diagnosed on biopsy requires no aggressive
    resection. AP (B) and lateral (C) radiographs of the femur demonstrate stabilization of the fracture, preparatory to
    definitive chemotherapy and radiation.

    2: Systemic Disorders

    published to support this hypothesis. Wide resection


    should be considered for some especially destructive benign aggressive neoplasms; however, intra-articular
    pathologic fractures through giant cell tumors of bone,
    although once believed to be a categoric indication for
    wide resection, can be managed with joint-sparing, intralesional techniques if fastidious attention is paid to
    complete excision.29
    Treatment of the defect following excision also is
    controversial. Although filling the defect with cement
    with or without pin or screw augmentation is most
    commonly used in the United States, allograft filling
    and even no filling of the defect have proven safe and
    effective.28
    Primary Low-Grade Malignant Neoplasms
    Although primary low-grade malignant neoplasms represent a small group of tumors, separate consideration
    is deserved because their treatment is unique and controversial. Some low-grade malignant neoplasms of
    bone, such as adamantinoma and parosteal osteosarcoma, are treated with wide resections that are not surgically different from those used to treat high-grade
    neoplasms, other than the fact that some can be managed with hemicortical resection rather than full segmental resections. The treatment of low-grade chondrosarcoma, however, has recently trended toward less
    aggressive approaches.30 Given its very low metastatic
    202

    Orthopaedic Knowledge Update 10

    potential, low-grade chondrosarcoma is increasingly


    managed more like a benign aggressive neoplasm, with
    adjuvant-enhanced intralesional excision. This approach has been challenged because local recurrences
    can be more aggressive than the primary tumor, requiring more extensive surgery; however, the spared morbidity of en bloc wide resections is advantageous for
    many patients. This approach may not be safely applied in the pelvis.
    Primary High-Grade Malignant Neoplasms
    A critical consideration in the management of malignant
    primary bone neoplasms derives from their sensitivity to
    available adjuvant treatments. Few malignant neoplasms
    primary to bone are radiosensitive, other than myeloma,
    the Ewing sarcoma family of tumors, and lymphoma of
    bone (Figure 3). From a surgical perspective, conventional osteosarcoma, the Ewing sarcoma family of tumors, and nonosteogenic spindle cell sarcomas of bone
    are all identically managed with biopsy, neoadjuvant
    chemotherapy, definitive surgical resection, and adjuvant
    chemotherapy (Figure 4). Although there are few data to
    support neoadjuvant chemotherapy over adjuvant chemotherapy, it permits a measurement of the effects of
    chemotherapy at the time of resection and remains almost universally preferred by surgeons and medical oncologists treating these disorders.
    Chondrosarcoma (Figure 5) is not considered sensi-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 17: Musculoskeletal Oncology

    Figure 5

    Figure 4

    tive to adjuvant treatments, but studies using radiotherapy as definitive treatment of unresectable chondrosarcomas of the spine have reported promising short-term
    local control.31
    The goals of surgical resection are complete extirpation of the neoplasm with minimal functional compromise. Wide, negative margins are ideal. Even if very
    narrow, margins including fascia, epineurium, or vascular sheath are considered adequate; however, muscle or
    adipose tissue margins should be more generous in
    thickness. Bone marrow margins in the diaphysis
    should be generous in length, when possible. Margin

    2011 American Academy of Orthopaedic Surgeons

    depth is controversial in metaphyseal and periphyseal


    areas.
    In instances in which wide margins are not otherwise
    possible, neurovascular structures are sacrificed or bypassed. Limb salvage must always be measured against
    amputation and cannot be pursued if it significantly
    compromises either local control or ultimate function.
    Reconstructive options for major skeletal defects
    present both short- and long-term challenges. In the
    short term, allografts and endoprostheses are prone to
    infections because they are implanted into massive dead
    spaces in immunocompromised hosts. Long-term challenges include late infections, loosening, and fractures.
    In the United States, trends have moved toward allograft reconstruction for intercalary resections within
    a bone, and endoprosthetic reconstructions of bone
    ends including the adjacent joints.32
    The pelvis and shoulder girdle also present challenges to reconstruction. Most major resections of the
    proximal humerus and scapula require resection of too
    much muscle to permit useful shoulder elevation. Most
    shoulder reconstructions, therefore, result in a hanging
    arm in which the functional result is more dependent
    on the neuromuscular function of the elbow and hand
    than the shoulder itself. There has been an increase in
    the number of reports of satisfactory functional results
    of resection without reconstruction of portions of the
    pelvis.33 Complication rates must be considered when
    deciding if reconstruction is the appropriate treatment
    (Figures 6 and 7).

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    A 15-year-old boy presented with a lump in his


    distal thigh and reported pain waking him
    nightly for 3 months. The AP (A) and lateral (B)
    radiographs alone render a fairly confident diagnosis of osteosarcoma, with a clear Codman
    triangle and sunburst periosteal reaction. C, An
    axial T2-weighted MRI shows that much of the
    soft-tissue component was telangiectatic in
    character, with fluid-fluid levels marking vascular spaces. Incisional biopsy confirmed the diagnosis of conventional osteosarcoma. D, The photomicrograph of a hematoxylin and eosin
    stained section from the biopsy shows lacy osteoid formation by malignant-appearing osteoblasts with severe pleiomorphic features and
    nuclear atypia.

    A 41-year-old man presented with a distal


    anteromedial thigh mass and reported a deep
    ache nightly. Classic imaging features of highgrade chondrosarcoma of bone were found. A,
    AP plain radiograph shows a destructive lesion
    making a cartilaginous matrix. B, T2-weighted
    MRI shows the lobular tissue structure, typical
    of cartilaginous neoplasms.

    203

    Section 2: Systemic Disorders

    A 45-year-old male athlete reported worsening pain during activity that persisted through rest and woke him at
    night. A, AP radiograph shows an intermediate-grade chondrosarcoma in the periacetabular periarticular bone of
    the pelvis. B, Axial CT scan through the hip shows the lesion where it has eroded into the hip joint through the
    acetabulum. The CT scan also demonstrates that the posterior column is free of tumor. This anatomy was exploited
    by an extra-articular resection that spared the posterior column, enabling the solid acetabular component for the
    reconstructive total hip arthroplasty, shown in the AP pelvis postoperative radiograph (C).

    Figure 7

    An 80-year-old man presented with worsening sciatica. The axial T2-weighted MRI scan (A) shows the large
    iliosacral mass causing the sciatica. A nonosteogenic spindle sarcoma of bone was noted on biopsy. Because the
    patient wanted to return to walking and golf, he was treated with resection of most of the ilium and sacral ala
    without reconstruction, shown in the postoperative AP pelvis radiograph (B).

    2: Systemic Disorders

    Figure 6

    Soft-Tissue Masses

    Patient Presentations
    The lump or bump noticed by a patient or family member may or may not be painful or changing over time.
    The pace of disease is critical to understanding softtissue masses. Occasionally, large, rapidly growing,
    high-grade soft-tissue sarcomas will produce mild pain,
    but most painful soft-tissue masses tend to be inflammatory and benign in character. Similarly, a lesion that
    waxes and wanes in size over time reduces the concern
    for malignancy. Most worrisome is a lump that inexorably and insidiously expands over time.
    204

    Orthopaedic Knowledge Update 10

    Physical examination of the mass should characterize the depth of the mass by assessing skin involvement,
    as well as mobility from fascia, muscle, and underlying
    bone.34 Superficial masses are easier to remove and less
    likely to be malignant. Mass size also matters, with
    larger masses more predictive of malignancy. The palpable consistency of the mass is instructive, with fluctuant masses rarely representing true neoplasms. It is paramount to correlate the physical examination with the
    patient history (Figure 8). Some patients may fail to recall a traumatic event, but without the involvement of
    anticoagulation or hemophilia, there is no such entity
    as an atraumatic hematoma. Hemorrhagic sarcomas
    exist and suspicion for them should be high when eval-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 17: Musculoskeletal Oncology

    Figure 8

    A 21-year-old woman presented with a fluctuant mass. The axial T2-weighted MRI of the proximal thigh (A) was interpreted radiologically to be a hematoma with an associated muscle tear. No history of trauma was elicited. B,
    Histologic section (hematoxylin and eosin stain) from an open biopsy showed a spindle cell neoplasm; it was also
    positive for the (X:18) SYT-SSX1 translocation product on fluorescent in situ hybridization.

    Imaging
    MRI is the primary imaging modality used for the diagnosis and local staging of soft-tissue neoplasms. The diagnosis of some soft-tissue cysts that do not transilluminate may be confirmed by ultrasound. Plain
    radiographs of the mass preceding or following MRI
    can reveal calcification or ossification within the mass,
    which can suggest or confirm a diagnosis such as hemangioma (from phleboliths) or myositis ossificans
    (Figure 9). MRI alone can be nearly diagnostic for a
    few neoplasms such as lipomatous lesions, hemangioma, pigmented villonodular synovitis, schwannoma,
    and intramuscular myxoma. Gadolinium contrast can
    help to distinguish solid masses from cysts by measuring the depth of enhancement in the lesion. However,
    for most masses, MRI defines the anatomic location
    and surrounding involved structures rather than providing a diagnosis.
    Systemic staging is achieved with technetium Tc
    99m total body bone scanning and noncontrast chest

    2011 American Academy of Orthopaedic Surgeons

    CT; however, certain mass subtypes require additional


    imaging. Myxoid or round cell liposarcomas can metastasize to unusual soft-tissue sites, necessitating evaluation of the retroperitoneum with contrast-enhanced
    CT. Alveolar soft-part sarcoma metastasizes early to
    the brain, usually prompting the need for a brain MRI
    at the time of staging.35
    Positron emission tomography has been used in sarcoma care but usually serves as an adjunctive measure
    of the treatment effect of chemotherapy rather than for
    staging.36 Most sarcomas are PET-avid, or detectable
    using positron emission tomography, but such an expensive imaging modality should be reserved for scenarios in which it serves a unique evidence-based purpose, such as in the staging of metastatic melanoma.

    2: Systemic Disorders

    uating any large deep hematoma for which no history


    of trauma can be elicited.
    Careful examination of the distal neurovascular status also is critical. Direct nerve or vessel involvement is
    rare but has a significant impact on treatment when
    present. Although nodal metastasis is rare in sarcomas,
    regional lymph nodes should be palpated to identify
    mimicking lesions such as metastatic melanoma and
    specific subtypes of soft-tissue sarcoma that can lymphatically spread, including epithelioid sarcoma, clear
    cell sarcoma, rhabdomyosarcoma, angiosarcoma, and
    synovial sarcoma.

    Biopsy
    The goals, methods, and hazards of biopsy for softtissue neoplasms are similar to those for bone lesions.
    Fine-needle aspirations and core needle biopsies are
    more commonly performed for soft-tissue masses but
    require a pathologist who is experienced and comfortable with their interpretation. Excisional biopsy is also
    more frequently performed for soft-tissue neoplasms. If
    lesions are small (< 5 cm), superficial, and free from
    fascia, excisional biopsy is a reasonable choice but
    must not compromise the potential for margin-negative
    wide resection of the entire area of contamination. Excisional biopsy must avoid violation of the deep fascia
    and the development of unnecessary tissue planes.
    One serious complication of biopsy is an incorrect
    diagnosis. As with bone lesions, there are some softtissue neoplasms that should not be biopsied before ex-

    Orthopaedic Knowledge Update 10

    205

    2: Systemic Disorders

    Section 2: Systemic Disorders

    Figure 9

    A 16-year-old male soccer player presented with an exquisitely painful mass of 4 weeks duration. The patient reported receiving a hard kick to the thigh approximately 1 month prior to the onset of symptoms. Imaging studies
    obtained at presentation show disorganized, slight calcification on the axial CT scan (A), bright T2-weighted MRI
    signal (B), and dark T1-weighted MRI signal (C), shown in these coronal images. These imaging features fit several
    potential diagnoses, including synovial sarcoma and soft-tissue osteosarcoma; however, the patients history did
    not fit with these diagnoses. Instead of biopsy, the patients history prompted follow-up imaging 6 weeks later. By
    that time, the pain was beginning to abate and both the plain AP radiograph (D) and axial CT scan (E) showed
    well-circumscribed peripheral ossification confirmatory of myositis ossificans circumscripta.

    cision. Biopsy of lipomatous neoplasms with consistent


    subcutaneous fat signal characteristics throughout present a major challenge because of sampling error. The
    differential diagnosis for these neoplasms includes two
    entities, lipoma and well-differentiated lipoma-like liposarcoma, which are treated identically even though
    they have different propensities for local recurrence.
    The pathologic interpretation of myositis ossificans
    can be difficult and can lead to inappropriate treat206

    Orthopaedic Knowledge Update 10

    ments. Painful masses associated with any history of


    trauma, which are otherwise suspicious for myositis,
    are often best managed with close follow-up and serial
    imaging rather than biopsy so as to avoid the incorrect
    diagnosis of soft-tissue osteosarcoma.
    The pathologic interpretation of soft-tissue neoplasms requires significant knowledge and experience.
    Patterns of cellular growth in bundles, fascicles, or in a
    storiform pattern; the production of myxoid matrix;

    2011 American Academy of Orthopaedic Surgeons

    Chapter 17: Musculoskeletal Oncology

    Figure 10

    A 54-year-old man presented with worsening unilateral stocking foot neuropathy and a palpably enlarging mass in
    his posterior thigh. Core needle biopsy confirmed the diagnosis of myxoid liposarcoma, both histologically and by
    fluorescent in situ hybridization showing the FUS-CHOP rearrangement. Axial (A) and sagittal (B) images from a
    proton-density MRI scan show the sciatic nerve surrounded by the tumor (arrow). During preoperative radiotherapy, the tumor shrank away to a position abutting but no longer surrounding the nerve, permitting nervesparing resection.

    Management Paradigms
    Benign lesions without aggressive behavior usually can
    be managed conservatively (Table 6). Some patients
    elect excision for cosmetic reasons, but this choice must

    2011 American Academy of Orthopaedic Surgeons

    be weighed against the risks involved. Elective resection


    of certain neoplasms should be avoided; popliteal cysts
    and intramuscular hemangiomas both require extensive
    surgeries but result in high rates of local recurrence.
    Benign aggressive lesions with risk for local recurrence are challenging to treat. The prototype of this
    category is the extra-abdominal desmoid tumor or fibromatosis. Although lacking metastatic potential, its
    infiltrative growth pattern leads to high rates of local
    recurrence. Nonetheless, the use of adjuvant therapies
    remains controversial because of their adverse side effects.
    Local control of soft-tissue sarcomas is primarily
    surgical, with adjuvant radiation used when multidisciplinary evaluation determines that achievable margins
    are insufficiently wide. When surgery either precedes or
    follows radiation, wide margins are the goal of resection. An exception is made for the salvage of critical
    structures such as nerves, vessels, and bones, which
    may be displaced or encroached on by the sarcoma
    (Figure 10). Microscopically planned positive margins
    along such structures do not significantly increase the
    rate of local recurrence when radiation is also used.38
    Such planned positive margins must be distinguished
    from positive margins inadvertently obtained from a
    poorly planned or executed resection, or by tumor infiltration beyond that apparent on imaging, which
    greatly increase recurrence rates. For involved vessels,
    resection and bypass reconstruction are used. For sar-

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    the presence of necrosis; and the dominant cell type of


    small, round blue or spindled cells can quickly narrow
    the differential diagnosis based on hematoxylin and eosin staining alone; however, immunohistochemistry is
    the main modality for diagnosis of soft-tissue masses.
    Immunohistochemical stains against cytokeratin are
    primarily used to rule out the presence of metastatic
    carcinoma, but epithelioid and synovial sarcoma will
    lightly stain. Endothelial markers CD31 and CD34 are
    used to detect vascular differentiation. S100 will stain
    nerve-derived tissues specifically but also stains several
    other sarcoma types and melanomas. TLE1 is a specific
    marker for synovial sarcoma because it is a target of
    SYT-SSX transcriptional amplification.37 Markers of
    smooth muscle, such as smooth muscle actin, and striated muscle can be used to identify submorphologic
    differentiation suggestive of leiomyosarcoma or rhabdomyosarcoma.
    Molecular diagnostics have revolutionized the analysis of soft-tissue neoplasms over the past decade. The
    dogma is increasing that the presence of subtypespecific molecular clues trump other histologic information when discrepancies arise.

    207

    Section 2: Systemic Disorders

    Table 6

    Soft-Tissue Masses
    Tissue Group
    Fibrous

    Lipomatous

    Cartilaginous

    2: Systemic Disorders

    Osseous

    Vascular

    Neurogenic

    Myogenic

    Giant cell rich

    Other

    Name

    Age

    Fibroma

    Very young and adolescents

    Desmoid or fibromatosis

    Young adult and middle aged

    Dermatofibroma protuberans

    Middle age to older

    Myxofibrous sarcoma

    Middle age to older

    Pleiomorphic undifferentiated sarcoma

    Middle age to older

    Lipoma

    Middle age

    Hibernoma

    Young to middle age

    Lipoblastoma

    Very young

    Well-differentiated lipoma-like liposarcoma

    Middle age to older

    Myxoid liposarcoma

    Young adults to middle age

    Round cell liposarcoma

    Young adults to middle age

    Pleiomorphic liposarcoma

    Middle age to older

    Chondroma

    Middle age to older

    Synovial chondromatosis

    Middle age to older

    Extraskeletal myxoid chondrosarcoma

    Young adults to middle age

    Myositis ossificans

    Any age

    Metaplastic bone

    Any age

    Soft-tissue osteosarcoma

    Older adults

    Arteriovenous malformation

    Adolescents through middle age

    Hemangioma

    Adolescents through middle age

    Hemangiopericytoma

    Middle age to older

    Epithelioid sarcoma

    Young adults through older

    Angiosarcoma

    Middle age to older

    Schwannoma

    Any age

    Neurofibroma

    Adolescents through middle age

    Malignant peripheral nerve sheath tumor

    Young adults through middle age

    Embryonal rhabdomyosarcoma

    Very young

    Alveolar rhabdomyosarcoma

    Adolescents

    Pleiomorphic rhabdomyosarcoma

    Middle age to older

    Leiomyosarcoma

    Middle age to older

    Pigmented villonodular synovitis

    Young adults to middle age

    Tenosynovial giant cell tumor

    Young adults to middle age

    Myxoma

    Any age

    Synovial sarcoma

    Young adults to middle age

    Green = Surgery is a last resort; yellow = Marginal excision is indicated; orange = Wide resection without adjuvants, unless recurrent; red = Wide resection with adjuvant
    radiation chemotherapy
    (continued on next page)

    208

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 17: Musculoskeletal Oncology

    Table 6

    Soft-Tissue Masses (continued)


    Pathology

    Special Notes

    Bland fibrous tissue, low cellularity

    Common on digits; recurrence common

    Dense fascicles of collagen

    Recurrence is a major challenge

    Low-grade spindle cell neoplasm

    Skin sarcoma; Moh surgery

    Intermediate-grade fibrous lesion with histiocytes and


    myxoid features

    More commonly superficial, but can have spreading growth pattern

    Variable high-grade spindle cell neoplasm

    Most common soft-tissue sarcoma, previously know as malignant


    fibrous histiocytoma

    Normal adipose

    Can be superficial or intramuscular

    Brown adipose tissue

    Rare neoplasm

    Lipoblasts at variable stages of maturation

    Rare and potentially self-limited

    Mostly normal adipose with some lipoblasts and fibrous


    septae

    Treated the same as intramuscular lipoma, but more recurrences

    Intermediate-grade adipose/myxoid tissue, translocation

    Especially radiosensitive

    High-grade version of myxoid liposarcoma

    Believed to be chemosensitive

    High-grade spindle cell neoplasm with some lipoblasts

    Second most common soft-tissue sarcoma

    Hyaline cartilage

    Very rare neoplasm

    Hyaline cartilage undergoing endochondral ossification

    Always intra-articular; behaves as low-grade malignant

    Myxoid neoplasm with stellate chondrocytes,


    translocation

    Treated on standard soft-tissue sarcoma protocols

    Organized layers of ossification

    Try to avoid biopsy when suspected

    Woven bone area in other tumor

    Can occur in synovial sarcoma, liposarcoma, and malignant


    peripheral nerve sheath tumors
    Debate on whether this should get osteosarcoma chemotherapy
    Try to avoid surgery

    Variably sized bland vascular channels

    Consider sclerotherapy or embolization

    Round cells with fried egg appearance

    Low, but not zero, metastatic potential; often treated as sarcoma

    Round cells, forming nests

    Often small on hands and feet

    High-grade round cells forming vessel vestiges

    Dreaded subtype, regionally progressive

    Myxoid and spindled Schwann cells

    Can be marginally excised sparing the nerve, usually

    Fibrous and spindled cells

    Nerve sparing is difficult

    High-grade spindle cell neoplasm

    Difficult to manage, radioresistant, chemoresistant

    Round blue cells

    Very chemosensitive

    Round blue cells with stunted myogenic differentiation

    Chemosensitive, surgery is adjuvant

    High-grade spindle or round blue cells with striated


    muscle markers

    Chemoresistant

    High-grade spindle cells with smooth muscle markers

    Extrauterine sites are treated the same as other sarcomas

    Multinucleated giant cells on stromal background,


    hemosiderin

    Complete intralesional excision is challenging, CSF1 gene


    rearrangement

    Multinucleated giant cells on stromal background,


    hemosiderin

    CSF1 gene rearrangement

    Paucicellular myxoid matrix

    Marginal excision usually successful

    High-grade spindle cell, or biphasic with epithelial test, or


    round blue cell

    No relationship whatsoever with synovium

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    High-grade spindle cells making osteoid matrix


    Large venous channels, bland

    209

    Section 2: Systemic Disorders

    comas with single nerve involvements, nerve resection


    and limb salvage may provide adequate, although compromised, function.
    The timing of radiotherapy has been studied in a
    randomized controlled trial. Postoperative radiotherapy requires higher doses and larger treatment volumes, which increase the adverse side effects of radiation. Preoperative radiotherapy minimizes the longterm complications of radiotherapy but increases the
    rate of early postoperative wound-healing complications.
    The role of chemotherapy in the management of
    soft-tissue sarcomas remains controversial, with strong
    proponents and opponents among the experts. Survival
    benefits have not been demonstrated in large collective
    trials; however, some subtypes such as synovial sarcoma and round cell liposarcoma are believed to be
    more sensitive to chemotherapy.

    with patients of African descent. Localized disease,


    smaller tumors, and appendicular skeletal location portend a good prognosis.
    4.

    Giuffrida AY, Burgueno JE, Koniaris LG, Gutierrez JC,


    Duncan R, Scully SP: Chondrosarcoma in the United
    States (1973 to 2003): an analysis of 2890 cases from
    the SEER database. J Bone Joint Surg Am 2009;91(5):
    1063-1072.
    This analysis of 2,890 cases from the SEER database includes the largest number of patients in any single study
    of chondrosarcoma. The authors confirm that only the
    grade and stage of the tumors are predictive of survival
    on multivariate analysis, and that no improvement in
    treatment success has been observed over recent decades.

    5.

    Gadgeel SM, Harlan LC, Zeruto CA, Osswald M,


    Schwartz AG: Patterns of care in a population-based
    sample of soft tissue sarcoma patients in the United
    States. Cancer 2009;115(12):2744-2754.
    This population evaluation study of soft-tissue sarcoma
    treatments confirmed the use of adjuvant radiation for
    survival and introduced the interesting observation that
    care of extremity sarcomas follows accepted guidelines
    more commonly than sarcomas at other anatomic sites.

    6.

    Sultan I, Rodriguez-Galino C, Saab R, Yasir S, Casanova M, Ferrari A: Comparing children and adults with
    synovial sarcoma in the Surveillance, Epidemiology, and
    End Results program, 1983 to 2005: an analysis of
    1268 patients. Cancer 2009;115(15 ):3537-3547.
    Children and adults with synovial sarcoma have similar
    presentations but different outcomes, which may indicate that historic treatments differed between these
    groups or that the underlying tumor biology changes in
    older patients.

    7.

    Blazer DG III, Lazar AJ, Xing Y, et al: Clinical outcomes of molecularly confirmed clear cell sarcoma from
    a single institution and in comparison with data from
    the Surveillance, Epidemiology, and End Results registry. Cancer 2009;115(13):2971-2979.
    This single-institution review of patients with molecularly confirmed clear cell sarcomas was enhanced by
    consideration of the population-based, albeit less detailed data from the SEER database. The review confirmed that nodal metastasis is prognostically distinct
    from distant metastasis.

    8.

    Jawad MU, Extein J, Min ES, Scully SP: Prognostic factors for survival in patients with epithelioid sarcoma:
    441 cases from the SEER database. Clin Orthop Relat
    Res 2009;467(11):2939-2948.
    By far the largest study of epithelioid sarcoma available,
    this SEER database review showed an increasing incidence in diagnosis (likely resulting from improved recognition of the rare entity), but no improvement in
    treatment success, which was dependent entirely on surgical success and tumor stage.

    9.

    Walkley CR, Qudsi R, Sankaran VG, et al: Conditional


    mouse osteosarcoma, dependent on p53 loss and poten-

    Summary

    2: Systemic Disorders

    Advances in population science, molecular biology, and


    clinical research methods have improved the understanding and accurate diagnosis of musculoskeletal
    neoplasia in recent years. Nonetheless, treatment protocols for this varied group of bone lesions and soft-tissue
    masses have remained fairly consistent over the past
    two decades. It is important to review the basic principles of current understanding and the clinical approach
    to and treatment of bone and soft-tissue neoplastic conditions, emphasizing recent modifications to longstanding accepted standards.

    Annotated References
    1.

    http://seer.cancer.gov. Accessed August 30, 2010.


    The SEER program of the National Cancer Institute
    provides detailed information on cancer incidence and
    survival data in the United States.

    2.

    Mirabello L, Troisi RJ, Savage SA: Osteosarcoma incidence and survival rates from 1973 to 2004: data from
    the Surveillance, Epidemiology, and End Results Program. Cancer 2009;115(7):1531-1543.
    This SEER database study confirmed that osteosarcoma
    is bimodal in adolescents and those older than 60 years,
    with the latter group usually associated with underlying
    Paget disease or prior radiation. Treatment success has
    not improved in 20 years.

    3.

    210

    Jawad MU, Cheung MC, Min ES, Schneiderbauer MM,


    Koniaris LG, Scully SP: Ewing sarcoma demonstrates
    racial disparities in incidence-related and sex-related differences in outcome: an analysis of 1631 cases from the
    SEER database, 1973-2005. Cancer 2009;115(15):
    3526-3536.
    This sampling of patients with Ewing sarcoma from the
    SEER database showed a ninefold increased incidence
    but no difference in survival for Caucasians compared

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 17: Musculoskeletal Oncology

    tiated by loss of Rb, mimics the human disease. Genes


    Dev 2008;22(12):1662-1676.
    This mouse model of osteosarcoma formation is generated from conditional ablation of the p53 and Rb1
    tumor-suppressors, noted to be frequently disrupted in
    human osteosarcomas. Morphologically and molecularly (with wild chromosomal aberrations) this model
    matches the human disease.
    10.

    11.

    12.

    13.

    Riggi N, Cironi L, Provero P, et al: Expression of the


    FUS-CHOP fusion protein in primary mesenchymal
    progenitor cells gives rise to a model of myxoid liposarcoma. Cancer Res 2006;66(14):7016-7023.
    Keller C, Arenkiel BR, Coffin CM, El-Bardeesy N, DePinho RA, Capecchi MR: Alveolar rhabdomyosarcomas
    in conditional Pax3:Fkhr mice: cooperativity of Ink4a/
    ARF and Trp53 loss of function. Genes Dev 2004;
    18(21):2614-2626.
    Haldar M, Hancock JD, Coffin CM, Lessnick SL,
    Capecchi MR: A conditional mouse model of synovial
    sarcoma: insights into a myogenic origin. Cancer Cell
    2007;11(4):375-388.
    The authors describe a mouse model of synovial sarcoma, generated by the expression of one of the human
    fusion transcripts, SYT-SSX2, in mouse myoblasts. This
    confirms that the fusion oncoprotein is sarcomagenic
    and specific for the synovial histologic subtype in the tumors generated.
    Mau E, Whetstone H, Yu C, Hopyan S, Wunder JS, Alman BA: PTHrP regulates growth plate chondrocyte differentiation and proliferation in a Gli3 dependent manner utilizing hedgehog ligand dependent and
    independent mechanisms. Dev Biol 2007;305(1):28-39.
    The authors follow up on a mouse model of Ollier disease using a mutated form of PTHR1 from a patient.
    Additional mouse models of enchondromatosis were
    generated using downstream members of the same pathway.

    15.

    Bove JV: Multiple osteochondromas. Orphanet J Rare


    Dis 2008;3:3.
    The author presents an up-to-date review of the clinical
    manifestations, therapeutic challenges, and remaining
    molecular quandaries of multiple hereditary exostoses
    and solitary osteochondroma formation. Level of evidence: V.

    16.

    West RB, Rubin BP, Miller MA, et al: A landscape effect


    in tenosynovial giant-cell tumor from activation of
    CSF1 expression by a translocation in a minority of tu-

    2011 American Academy of Orthopaedic Surgeons

    17.

    Oliveira AM, Perez-Atayde AR, Inwards CY, et al:


    USP6 and CDH11 oncogenes identify the neoplastic cell
    in primary aneurysmal bone cysts and are absent in socalled secondary aneurysmal bone cysts. Am J Pathol
    2004;165(5):1773-1780.

    18.

    Lodwick GS, Wilson AJ, Farrell C, Virtama P, Dittrich


    F: Determining growth rates of focal lesions of bone
    from radiographs. Radiology 1980;134(3):577-583.

    19.

    Campanacci M: Giant-cell tumor and chondrosarcomas: grading, treatment and results (studies of 209 and
    131 cases). Recent Results Cancer Res 1976;54:257261.

    20.

    Enneking WF, Spanier SS, Goodman MA: A system for


    the surgical staging of musculoskeletal sarcoma. Clin
    Orthop Relat Res 1980;153:106-120.

    21.

    Mankin HJ, Lange TA, Spanier SS: The hazards of biopsy in patients with malignant primary bone and softtissue tumors. J Bone Joint Surg Am 1982;64(8):11211127.

    22.

    Mankin HJ, Mankin CJ, Simon MA; Members of the


    Musculoskeletal Tumor Society: The hazards of the biopsy, revisited. J Bone Joint Surg Am 1996;78(5):656663.

    23.

    Skeletal Lesions Interobserver Correlation among Expert Diagnosticians (SLICED) Study Group: Reliability
    of histopathologic and radiologic grading of cartilaginous neoplasms in long bones. J Bone Joint Surg Am
    2007;89(10):2113-2123.
    The poor reliability of grading appendicular cartilage
    masses as benign, low-grade, or high-grade malignancies
    is confirmed even among recognized experts in bone tumor pathology and radiology. Level of evidence: II.

    24.

    Rougraff BT: Evaluation of the patient with carcinoma


    of unknown origin metastatic to bone. Clin Orthop
    Relat Res 2003;(415, Suppl):S105-S109.

    2: Systemic Disorders

    14.

    Kirsch DG, Dinulescu DM, Miller JB, et al: A spatially


    and temporally restricted mouse model of soft tissue
    sarcoma. Nat Med 2007;13(8):992-997.
    This mouse model of pleiomorphic undifferentiated
    soft-tissue sarcoma (formerly known as malignant fibrous histiocytoma) was generated from conditional ablation of Kras with either p53 or CDKN2a. The ablation was activated by the administration of a virus
    containing Cre-recombinase.

    mor cells. Proc Natl Acad Sci U S A 2006;103(3):690695.

    25. Mirels H: Metastatic disease in long bones: A proposed


    scoring system for diagnosing impending pathologic
    fractures. Clin Orthop Relat Res 1989;249:256-264.
    26.

    Lin PP, Mirza AN, Lewis VO, et al: Patient survival after surgery for osseous metastases from renal cell carcinoma. J Bone Joint Surg Am 2007;89(8):1794-1801.
    The authors provide an analysis of the largest series of
    patients treated for skeletal metastasis of renal cell carcinoma. They emphasize the use of tumor excision, even
    if intralesional, and question the use of adjuvant radiation in the same patients. Level of evidence: IV.

    27.

    Blackley HR, Wunder JS, Davis AM, White LM, Kandel


    R, Bell RS: Treatment of giant-cell tumors of long bones
    with curettage and bone-grafting. J Bone Joint Surg Am
    1999;81(6):811-820.

    Orthopaedic Knowledge Update 10

    211

    Section 2: Systemic Disorders

    28.

    Prosser GH, Baloch KG, Tillman RM, Carter SR,


    Grimer RJ: Does curettage without adjuvant therapy
    provide low recurrence rates in giant-cell tumors of
    bone? Clin Orthop Relat Res 2005;435:211-218.

    29.

    Deheshi BM, Jaffer SN, Griffin AM, Ferguson PC, Bell


    RS, Wunder JS: Joint salvage for pathologic fracture of
    giant cell tumor of the lower extremity. Clin Orthop
    Relat Res 2007;459:96-104.
    Intra-articular fractures secondary to locally advanced
    giant cell tumor of bone have been considered an indication for wide resection and endoprosthetic reconstruction in many centers. This study challenges that dogma
    with a successful series of patients treated with jointsalvage surgery. Level of evidence: III.

    30.

    31.

    2: Systemic Disorders

    32.

    212

    Hanna SA, Whittingham-Jones P, Sewell MD, et al:


    Outcome of intralesional curettage for low-grade chondrosarcoma of long bones. Eur J Surg Oncol 2009;
    35(12):1343-1347.
    This is the largest and most recent of several studies reporting results from the technique of intralesional curettage for grade I chondrosarcoma, which is growing in
    popularity. Level of evidence: IV.
    Nguyen QN, Chang EL: Emerging role of proton beam
    radiation therapy for chordoma and chondrosarcoma of
    the skull base. Curr Oncol Rep 2008;10(4):338-343.
    The recently burgeoning data for proton beam and
    other high-dose radiation technologies as isolated treatments for surgically unresectable chondrosarcomas and
    chordomas of the axial skeleton are discussed. Level of
    evidence: V.
    Zimel MN, Cizik AM, Rapp TB, Weisstein JS, Conrad
    EU III: Megaprosthesis versus Condyle-sparing intercalary allograft: distal femoral sarcoma. Clin Orthop
    Relat Res 2009;467(11):2813-2824.
    This is the most recent of many studies evaluating outcomes of limb salvage with endoprosthetic or allograft

    Orthopaedic Knowledge Update 10

    reconstruction. The authors emphasize a specific technique to expand the indications for intercalary allograft
    reconstruction to very thin residual epiphyses. Level of
    evidence: IV.
    33.

    Scwartz AJ, Kiatisevi P, Eilber FC, Eilber FR, Eckardt JJ:


    The Friedman-Eilber resection arthroplasty of the pelvis. Clin Orthop Relat Res 2009;467(11):2825-2830.
    This article reviews the very positive functional results
    of a large consecutive study of patients treated with pelvic resections, including resection of the hip joint without fusion, endoprosthetic reconstruction, and allograft
    reconstruction. Level of evidence: IV.

    34.

    Eilber FC, Brennan MF, Eilber FR, Dry SM, Singer S,


    Kattan MW: Validation of the postoperative nomogram
    for 12-year sarcoma-specific mortality. Cancer 2004;
    101(10):2270-2275.

    35.

    Ogose A, Morita T, Hotta T, et al: Brain metastases in


    musculoskeletal sarcomas. Jpn J Clin Oncol 1999;29(5):
    245-247.

    36.

    Schuetze SM, Rubin BP, Vernon C, et al: Use of positron


    emission tomography in localized extremity soft tissue
    sarcoma treated with neoadjuvant chemotherapy. Cancer 2005;103(2):339-348.

    37.

    Terry J, Saito T, Subramanian S, et al: TLE1 as a diagnostic immunohistochemical marker for synovial sarcoma emerging from gene expression profiling studies.
    Am J Surg Pathol 2007;31(2):240-246.
    The authors describe TLE1 as both a transcriptional target of the SYT-SSX fusion oncoproteins and a unique
    immunohistochemical marker for synovial sarcoma.

    38.

    Clarkson PW, Griffin AM, Catton CN, et al: Epineural


    dissection is a safe technique that facilitates limb salvage
    surgery. Clin Orthop Relat Res 2005;438:92-96.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 18

    Arthritis
    SM Javad Mortazavi, MD

    Javad Parvizi, MD, FRCS

    Introduction
    Joint disorders or arthritis affect 21% of the US population (69.9 million people) according to recent surveys
    by the Centers for Disease Control and Prevention.1 Arthritis has been traditionally categorized as either inflammatory or noninflammatory, depending on the underlying pathologic processes. Inflammatory arthritis
    may be infectious (septic arthritis), crystal-induced
    (gout or pseudogout), immune-related (rheumatoid arthritis [RA]), or reactive (Reiter syndrome). Osteoarthritis (OA) is considered the prototype for noninflammatory arthritis, although in recent years the
    noninflammatory nature of OA has been disputed. An
    orthopaedic surgeon should be familiar with different
    types of arthritis because an accurate diagnosis is essential for planning an appropriate treatment strategy.

    Osteoarthritis

    Neither Dr. Mortazavi nor an immediate family member


    has received anything of value from or holds stock in a
    commercial company or institution related directly or indirectly to the subject of this chapter. Dr. Parvizi or an
    immediate family member serves as a board member,
    owner, officer, or committee member of the American
    Association of Hip and Knee Surgeons, American Board
    of Orthopaedic Surgery, British Orthopaedic Association,
    Orthopaedic Research and Education Foundation, and
    SmartTech; serves as a paid consultant to or an employee of Stryker; and has received research or institutional support from KCI, Medtronic, the Musculoskeletal
    Transplant Foundation, Smith & Nephew, and Stryker.

    2011 American Academy of Orthopaedic Surgeons

    Pathophysiology
    OA is essentially joint failure because all structures of the
    joint undergo pathologic changes. Traditionally, OA was
    considered to be a disease of articular cartilage, with loss
    of cartilage considered the essential pathologic process
    for OA. In recent years, however, it has been realized that
    OA affects the entire joint structure, including synovium,
    ligaments, and subchondral bone, along with the articular cartilage.8 Each structure in the joint plays an important and unique role in the daily function of the joint.
    Articular cartilage, with its compressive stiffness and
    smooth surface; synovial fluid, which provides a smooth
    and frictionless surface for movement; the joint capsule
    and the ligaments, which protect the joint from excessive excursions; the periarticular muscles, which minimize focal stresses across the joint by appropriate muscle contractions; the sensory fibers, which provide
    feedback for muscles and tendons; and the subchondral
    bone, with its mechanical strength and shock-absorbing
    function all interact in an intricate manner to provide optimal function for the joint. Destruction of any of these
    structures or a disruption in the balance between them
    leads to the process of arthritis.
    The earliest changes in OA usually appear in the hyaline articular cartilage. The cartilage matrix consists of
    two important macromolecules: type II collagen and
    aggrecan (a proteoglycan macromolecule with highly
    negatively charged glycosaminoglycans). Chondrocytes
    produce all the elements of the cartilage matrix as well
    as the enzymes that break down the matrix, cytokines,
    and growth factors. In OA, chondrocytes produce abnormally high quantities of inflammatory cytokines
    such as interleukin (IL)1- and tumor necrosis factor-
    (TNF-), which in turn decrease collagen synthesis and
    increase degradative proteases (including matrix metalloproteinases and other inflammatory mediators, such
    as IL-6, IL-8, prostaglandin E2, nitric oxide, and bone
    morphogenetic protein-2).8,9 It is now clear that OA is
    also an inflammatory process initiated and propagated

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    OA or degenerative joint disease continues to be the


    leading cause of disability and impaired quality of life
    in developed countries.2 It is the most common of all
    joint diseases that imparts substantial economic burden
    on health care systems and society, and it is the single
    greatest cause of lost work days.3 The chronic use of
    analgesics and anti-inflammatory drugs and the need
    for surgical treatment result in additional costs. Moreover, as the baby-boomer generation ages, it is expected
    that the prevalence of OA will increase 66% to 100%
    by the year 2030.4 Currently, approximately 800,000
    total knee and total hip arthroplasties are performed in

    the United States annually, with the number expected


    to exceed 1.2 million by the year 2020.5 Symptomatic
    OA of the knee (defined as the presence of knee pain on
    most days of a recent month plus radiographic evidence
    of OA in the same knee) occurs in 12% of adults age
    60 years or older in the United States and in 6% of all
    adults age 30 years or older.6 Symptomatic OA of the
    hip is approximately one third as common as OA in the
    knee.7

    213

    Section 2: Systemic Disorders

    2: Systemic Disorders

    by inflammatory mediators that lead to the demise of


    the articular cartilage first and damage to other structures over time.10 The production of these mediators
    leads to an increase in the metabolic activity of articular cartilage, a tissue that usually has low activity. As
    OA progresses, the cartilage undergoes a gradual depletion of aggrecan and collagen type II; the tightly woven
    collagen type II then begins to unfurl. As a result, the
    cartilage loses its compressive stiffness and becomes
    more vulnerable to further injury.
    The classification of OA as a noninflammatory arthritis is, in part, based on the fact that the leukocyte
    count in the synovial fluid of OA patients is typically
    less than 2,000 cells/L. There is no question that lowgrade synovial inflammation contributes to the pathogenesis of this disease. In contrast to RA, synovial inflammation in OA is mostly confined to the area
    adjacent to the affected cartilage and bone.
    The initiation of inflammation sets up a vicious cycle
    whereby further inflammatory mediators, such as proteinases and cytokines, are released from the synovium
    and can accelerate the destruction of the nearby cartilage. In turn, cartilage breakdown products, resulting
    from mechanical or enzymatic destruction, can provoke
    the release of collagenase and other hydrolytic enzymes
    from synovial cells, which can lead to vascular hyperplasia in synovial membranes. This cascade sequentially
    results in the induction of IL-1 and TNF-, which enhance the inflammatory process. This cytokine storm
    is more likely to occur in the earlier stages of OA.10
    Investigations have shown that the production of reactive oxygen species plays an important role in the initiation and propagation of OA.11 The by-products of
    reactive oxygen species were detected during early OA
    and may be used as biomarkers for detecting this condition early in the process. Future directions for treating OA will likely be based on the discovery of new
    biomarkers for OA, further information about the enzymatic pathways active in the disease, and the development of disease-modifying OA drugs.

    Risk Factors
    Several risk factors for OA have been identified. These
    factors either result in disruption of the protective
    mechanisms of the joint, rendering them dysfunctional,
    or cause excessive forces across the joint, which overload otherwise competent structures. The risk factors
    can be categorized into two groups based on the location of their effect (systemic or local).
    Systemic Risk Factors
    Advancing Age
    Advancing age is perhaps the most important risk factor for OA because it increases the vulnerability of
    joints through several mechanisms.12 With advancing
    age, cartilage becomes less responsive to dynamic loading and is slower to regenerate; as a result, older patients have thinner cartilage, which is more sensitive to
    shear stresses and is at significantly greater risk for
    damage. Advancing age also increases the risk of failure
    214

    Orthopaedic Knowledge Update 10

    in other joint protectors. Muscles become weaker, ligaments stretch and are less able to absorb stresses, and
    sensory input slows. It is important to note that OA is
    not an inevitable consequence of aging; it is not a simple wearing out of the joint. Age-related changes in the
    joint can be distinguished from those caused by disease.
    The ability of aging chondrocytes to produce and repair the extracellular matrix is compromised because of
    a decline in growth factor activity. This appears to be
    related to both a decline in the local availability of
    growth factors, including BMP-7 and TGF-, as well as
    a decline in the response of chondrocytes to growth
    factors such as insulin-like growth factor-I.13 Chondrocyte senescence, which is marked by shortened telomeres, increased levels of B-galactosidases, and decreased adenosine triphosphate production caused by
    mitochondrial dysfunction, has a key role in the development and progression of age-related impairments in
    cartilage repair. Telomere erosion and oxidative damage are the two main mechanisms for chondrocyte senescence. In the telomere erosion hypothesis, cell aging
    is regulated by an intrinsic genetic clock associated
    with the erosion of telomeres. Oxidative stress, another
    important cause of age-related chondrocyte senescence,
    is explained by the age-related degeneration of mitochondria. Mitochondria provide metabolic energy via
    respiration and protect cells from the toxic effects of
    oxygen and its free-radical derivatives; therefore, the
    damage to mitochondria limits energy production and
    exposes cells to oxidative damage.14
    Gender
    A variety of studies have reported that women are more
    at risk for developing OA. In addition, women have a
    greater number of involved joints and are more likely
    to have OA that affects the knees and the hands. Although the exact reason for the higher incidence of OA
    in women is not known, loss of estrogen over time is
    believed to be an important contributing factor.
    Genetics
    The role of genetic factors in the development of OA is
    well known. Many studies have confirmed the inherited
    element for this disease, particularly for OA of the hip
    and hand joints.12,15 In one study, 50% of cases of hand
    and hip OA were attributed to inherited factors.16 In
    addition, recent studies have identified genetic mutations that place patients at high risk for OA.12,15 Specifically, a mutation in the FRZB gene is believed to put
    women at high risk for hip OA. This gene encodes a
    frizzle protein, whose role is to antagonize an extracellular Wnt ligand. Because the Wnt signaling pathway
    plays a critical role in matrix synthesis and joint development, it makes sense that a mutated frizzle protein
    would be associated with an increased incidence of
    OA.17 The ASPN gene also is described as a susceptibility gene for OA.18 Anatomic abnormalities of joints in
    patients with skeletal dysplasia are a known cause of
    early OA. There are known genetic bases for many of
    these dysplasias.19 A recent study identified a 4-Mb re-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 18: Arthritis

    gion on chromosome 17q21 that was linked to developmental hip dysplasia.20


    In addition to identifying specific genetic markers,
    some studies have examined the incidence of OA in different ethnic groups.21,22 Hip OA is rare in Chinese and
    Chinese-American populations; however, knee OA is at
    least as common in the Chinese population as it is in
    the Caucasian population.21 African populations (although not African Americans) appear to have much
    lower rates of hip OA than do Caucasians.

    of OA in the repeatedly used joints. For example, a


    high incidence of hip OA has been reported in farmers
    and a high incidence of knee and spine OA has been reported in miners. Certain types of exercises also may
    increase the risk of OA. Studies suggest that professional running increases the risk of hip and knee
    OA.27,28 Patients with impaired proprioception across
    the joint are prone to OA and to significant progression
    of the disease. This trend can be observed in patients
    with Charcot joint.

    Local Risk Factors


    Anatomy
    An abnormal joint anatomy that results in an uneven distribution of load across the joint and an increase in focal
    stresses can be a risk factor for OA. In the hip, developmental dysplasia, Legg-Calv-Perthes disease, and
    slipped capital femoral epiphysis are the most common
    reasons for early distortions in hip anatomy that can lead
    to OA later in life. The severity of the anatomic deformity determines whether OA will occur in young adulthood (seen most commonly in patients with severe abnormalities) or later in life (more common in patients
    with mild abnormalities). It was recently shown that subtle developmental abnormalities in the hip joint can lead
    to femoroacetabular impingement and secondary OA.23
    Anatomic distortion following intra-articular fractures
    also increases the susceptibility of a joint to early OA.
    Osteonecrosis secondary to a variety of etiologies, particularly if it leads to the collapse of subchondral bone,
    can produce joint irregularities that lead to OA. Additionally, malalignment across the joint can lead to uneven wear on the articular surfaces, also leading to OA.24

    Bone Density
    The role of bone as a shock absorber for the load of
    impact is not well understood; however, it has been
    shown that people with higher bone density are at an
    increased risk of OA, whereas osteoporosis has a negative association with OA.29

    Body Mass Index


    The relative risk of OA increases with obesity.26 Also,
    obese people have more severe symptoms of OA and
    are more likely to have the progressive form of the disease. Obesity has been shown to be a strong risk factor
    for the development of knee OA and, less so, for hip
    OA. Interestingly, obesity has been shown to be a
    stronger risk factor for the disease in women than in
    men. In women, the relationship of weight to the risk
    of OA is linear; weight loss in women lowers the risk of
    symptomatic disease.
    Repetitive Use Injury
    Workers who perform repetitive occupational tasks for
    many years have an increased risk of the development

    2011 American Academy of Orthopaedic Surgeons

    The initial stage of the OA disease process is silent,


    which explains the high prevalence of radiographic and
    pathologic signs of OA in clinically asymptomatic patients. Interestingly, even in the later stages of OA,
    there is a poor correlation between clinical symptoms
    and the degree of change in bone or cartilage detected
    directly by arthroscopy or indirectly by radiography or
    MRI.
    The most likely sources of pain in OA are synovial
    inflammation, joint effusion, and bone marrow edema.
    The degree to which each of these three factors is present varies from patient to patient. The pain generated
    by OA is usually exacerbated by activity and relieved
    by rest. Early in the disease, the pain is episodic, triggered often by 1 or 2 days of overuse of the involved
    joint (for example, a person with knee OA may notice a
    few days of pain after a long run). More advanced OA
    can cause pain at rest and night pain severe enough to
    awaken the patient. Pain from OA is usually described
    as deep, aching, and poorly localized; it may radiate or
    be referred to surrounding structures. In diagnosing
    OA, it is helpful to know the location of the pain and
    to perform a careful physical examination to identify
    particular motions that aggravate the pain. Groin pain,
    for example, usually indicates a hip joint disorder.
    Some patients with hip OA, however, may report knee
    pain rather than hip pain. For these patients, the key to
    the correct diagnosis of hip OA is the finding (through
    physical examination) that hip rotation increases pain.
    A wide range of additional symptoms tend to be
    present along with pain from OA. Many patients report a short-lived stiffness after inactivity (gelling). OA
    may be associated with joint instability or giving way.
    Patients may report a reduced range of motion, deformity, swelling, and crepitus. The clinician should be
    aware that certain clinical symptoms are not generally
    associated with OA. For example, even in patients with
    severe OA, systemic features such as fever, weight loss,
    anemia, and an elevated erythrocyte sedimentation rate
    are not normally present. In the process of taking a patient history, it is also important to ask how the pain

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    Trauma
    Injuries such as anterior cruciate ligament tears, meniscal tears in the knee, and labral tears in the hip can increase the susceptibility of a joint to OA and can lead
    to premature OA. Injury to joint structures, even those
    that do not require surgical repair, may increase the
    risk of OA. This finding was shown in the Framingham
    study, which demonstrated that men with a history of
    major knee injury and no surgery had a 3.5-fold increased risk of subsequent knee OA.25

    Clinical Features

    215

    Section 2: Systemic Disorders

    has affected the patients function at home, work, and


    in recreational activities and how the patient is coping
    with the pain. The physician should look for signs of
    psychological distress (for example, signs of anxiety,
    excessive pain-avoidance posturing, or the onset of insomnia) or depression (for example, early morning
    wakening, weight loss, irritability, or a marked increase
    in memory and concentration problems).
    The joints most commonly involved in primary OA
    are the metatarsophalangeal joint of the great toe, the
    proximal and distal interphalangeal joints of the fingers, the carpometacarpal joint of the thumb, and the
    joints of the hips, knees, and cervical and lumbar spine.
    Unless they are involved in a secondary form of OA,
    other joints are typically spared. OA is believed to be a
    uniformly progressive disease that invariably leads to
    joint arthroplasty; however, the disease appears to stabilize in many patients, with no worsening of symptoms or signs. In specific subgroups, the prognosis may
    be either worse or better, depending on both risk and
    protective factors.

    Diagnosis

    2: Systemic Disorders

    Classic findings of OA on plain radiographs are osteophytes, joint-space narrowing, subchondral sclerosis,
    and in more advanced disease, bone cysts. Because radiographs are not sensitive to the earliest pathologic
    features of OA, the absence of positive radiographic
    findings in a patient with symptoms of OA should not
    be interpreted as the complete absence of the disease. In
    clinical practice, the diagnosis of OA should be made
    on the basis of the patient history and physical examination. The role of radiography is to confirm clinical
    suspicions and rule out other conditions rather than to
    make an independent diagnosis.30 This role is more distinct in patients with chronic hip and hand pain because the diagnosis can often be unclear without confirming radiographs. It has been shown in crosssectional and longitudinal studies that there is no
    association, or only a weak association, between radiographic changes and functioning in patients with OA.31
    MRI can be used to diagnose other causes of joint pain
    (such as osteochondritis dissecans or osteonecrosis),
    which may otherwise be confused with OA in patients
    with joint pain. It should be noted that meniscal tears
    are nearly universally seen in patients with knee OA
    and are not necessarily a cause of increased symptoms.
    No blood tests are routinely indicated in the workup
    of patients with OA unless symptoms and signs suggest
    inflammatory arthritis. The synovial fluid analysis in
    patients with noninflammatory arthritis should usually
    demonstrate no evidence of inflammatory reaction with
    few leukocytes (<1,000 per L) and good viscosity. The
    presence of more than 1,000 leukocytes per L usually
    is indicative of inflammatory arthritis.

    Treatment
    Nonsurgical
    The goals in treating patients with OA are pain relief
    and improvement of physical function. Currently, there
    216

    Orthopaedic Knowledge Update 10

    are no disease-modifying drugs for OA, and all available pharmacologic agents aim to provide symptomatic
    relief. The treatment of patients with OA should be
    comprehensive and should follow the stepwise formula
    recommended by the American College of Rheumatology.32 Nonpharmacologic measures may include physical therapy and exercise. These treatments should be
    considered the base line for managing all patients with
    OA. Muscle weakness often accompanies OA, and increased muscle strength helps reduce the load on cartilage. Isometric (as opposed to isotonic) exercises are
    preferred because they put less stress on the involved
    joint. Perhaps some of the most important elements in
    therapy include activity modification, implementation
    of periodic rest of the affected joint, and the use of assistive walking devices to offload affected joints of the
    lower extremity.
    For patients with intermittent and mild symptoms,
    reassurance and nonpharmacologic therapies usually
    suffice; however, patients with ongoing, disabling pain
    may need pharmacotherapy. The first-line medication
    for symptomatic pain relief is a simple analgesic such as
    acetaminophen. For patients with inflammatory disease
    (as seen in erosive OA) and for those whose symptoms
    cannot be well controlled with simple analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs) are more
    effective.
    The
    new
    class
    of
    NSAIDSthe
    cyclooxygenase-2 inhibitorsare more selective and
    have decreased gastrointestinal toxicity; however, they
    also have been associated with increased cardiovascular
    events. Patients should be informed about risks before
    cyclooxygenase-2 inhibitors are prescribed.
    Nutraceuticals, such as oral glucosamine and chondroitin, have been shown to reduce pain in patients
    with knee OA, but further research is needed to confirm the effectiveness of such treatments.
    Although systemic steroids are not used in treating
    OA, intra-articular cortisone injections to reduce synovial inflammation are effective in relieving pain from
    OA. Injections should not be repeated more than a few
    times because they have been associated with an increased risk of cartilage breakdown. Intra-articular injection of hyaluronic acid can improve joint symptoms
    in a subgroup of patients with knee OA; however, the
    overall efficacy of this treatment over a placebo in patients with hip or knee OA remains controversial.33
    Surgical
    Joint arthroplasty is the single most effective treatment
    of arthritis of most joints, including the knee, hip,
    shoulder, elbow, ankle, and (perhaps) small joints of the
    hand. Joint arthroplasty is an effective treatment option
    for patients with advanced arthritis that compromises
    function and is nonresponsive to nonsurgical treatment.
    Currently, the failure rate for total knee and total hip
    arthroplasty is less than 1% per year. Better patient
    outcomes after joint arthroplasty have been reported in
    high-volume centers with surgery performed by surgeons performing more than 50 joint arthroplasties per
    year.34,35 The timing of knee or hip replacement surgery

    2011 American Academy of Orthopaedic Surgeons

    Chapter 18: Arthritis

    appears to be very important. Studies have shown that


    patients with more advanced disease have less improvement than those receiving the procedure earlier in the
    course of their disease.36,37
    Currently, there is no efficacious treatment for cartilage regeneration in patients with OA.38 Either chondrocyte transplantation or chondroplasty (abrasion arthroplasty), which may be useful in patients with
    localized cartilage damage, have no proven efficacy in
    OA.

    Inflammatory Arthritis

    2011 American Academy of Orthopaedic Surgeons

    RA is a chronic multisystem disease of unknown cause.


    The characteristic feature of established RA is persistent inflammatory synovitis, usually involving peripheral joints in a symmetric distribution. In RA, synovial
    inflammation leads to cartilage damage, bony erosion,
    and changes in joint integrity. Despite the destructive
    potential of the disease, its course is quite variable. In
    some patients, the disease remains confined to two or
    three joints and may cause only minimal destruction. In
    most patients, however, the involvement is polyarticular, with relentless progression and marked functional
    impairment. RA affects 1% to 1.5% of the population
    worldwide.39 Its incidence increases during adulthood
    and peaks at approximately age 40 to 60 years. Females are affected three times more frequently than
    males. The hallmarks of the disease are the symmetric
    involvement of multiple joints in the hands and the feet
    and a positive test for rheumatoid factor (immunoglobulin M antibody directed against the Fc portion of immunoglobulin G). Additional constitutional symptoms,
    such as weight loss, fever, and malaise, may be present.
    The presence of rheumatic factor does not establish the
    diagnosis of RA because its positive predictive value is
    poor; however, the presence of rheumatoid factor can
    have prognostic significance because patients with high
    titers tend to have more severe and progressive disease
    with extra-articular manifestation.40
    RA usually presents initially with episodes of morning stiffness that last for more than 1 hour, joint pain
    and swelling, and difficulty performing the activities of
    daily living. RA commonly involves the wrist, elbow,
    knee, foot metatarsophalangeal and proximal interphalangeal joints, and the cervical spine. The distal interphalangeal joints, and the lumbosacral spine are usually spared. Cervical spine subluxation (C1-C2)
    secondary to RA can lead to spinal instability and cord
    impingement. Patients with cervical spine instability are
    at risk for spinal injury during intubation for general
    anesthesia and should be treated with fiberoptic intubation. The diagnosis of RA is made if a patient has, for
    more than a 6-week duration, four of the seven criteria
    for RA defined by the American College of Rheumatology41 (Table 1). Extra-articular manifestations of RA
    are rheumatoid nodules and ocular, cardiac, or neurologic involvement. Rheumatoid nodules are pathognomonic and are seen in 30% of patients with RA, mostly
    on the extensor surface of the forearm. Because these
    nodules may be confused with gouty tophi, nodule aspiration is the best method to distinguish between the
    two conditions. Tophi contain monosodium urate crystals, whereas rheumatoid nodules contain cholesterol
    crystals.
    The goal of treatment is to suppress inflammation
    and preserve joint structure and function. Early, aggressive use of disease-modifying antirheumatic drugs and
    biologic response modifiers either alone or in combination has been shown to be effective in achieving treatment goals.42 Disease-modifying antirheumatic drugs
    include methotrexate, sulfasalazine, leflunomide, hy-

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    Inflammatory arthritis consists of a large group of different conditions that cause inflammation in the joint.
    The diagnosis can be made by evaluating the patients
    profile, the chronology of symptoms, the extent of joint
    involvement, and the precipitating factors. Systemic lupus erythematosus (SLE) and reactive arthritis occur
    more frequently in young patients, whereas RA is more
    prevalent in middle-age patients. Gout and spondyloarthropathies (such as ankylosing spondylitis) are more
    common in men, whereas SLE is more common in
    women.
    The nature of the onset of the disease also can be
    helpful in making the diagnosis. Septic arthritis and
    gout tend to present abruptly, whereas RA may have an
    indolent presentation. Additionally, the evolution of a
    patients symptoms may be intermittent (more common
    in crystal-induced or Lyme diseases), migratory (in
    rheumatic fever, gonococcal, or viral arthritis), or additive (in RA and psoriatic arthritis). Arthritides are typically classified as acute or chronic if symptoms persist
    for fewer than or more than 6 weeks, respectively. Reactive, infectious, or crystal-induced diseases tend to
    present acutely, whereas immunologic disease (such as
    RA) has a propensity for chronic presentation. It is also
    helpful in diagnosing inflammatory arthritis to note the
    extent and degree of articular involvement. Crystalinduced and infectious arthritis are often monoarticular, spondyloarthropathies are often oligoarticular, and
    RA is often polyarticular. Symmetric joint involvement
    is seen in RA, but spondyloarthropathies often show an
    asymmetric involvement. Additionally, RA often involves the joints of the upper extremities, whereas reactive arthritis and arthritis from gout tend to involve the
    joints of the lower extremities. Involvement of the axial
    skeleton (with the exception of the cervical spine) is a
    characteristic of spondyloarthropathies and is rare in
    RA.
    Systemic features of inflammatory arthritis such as
    fever (in SLE and septic arthritis), rash (in SLE and psoriatic arthritis), and nail abnormalities (in psoriatic or
    reactive arthritis) should be noted. Involvement of
    other organ systems, including the eyes (seen in Behet
    disease and spondyloarthritis), the gastrointestinal tract
    (seen in inflammatory bowel disease), the genitourinary
    tract (seen in reactive arthritis or gonococcemia), or the
    nervous system (seen in Lyme disease), also should be
    considered in diagnosing inflammatory arthritis.

    Rheumatoid Arthritis

    217

    Section 2: Systemic Disorders

    Table 1

    The 1987 Revised Criteria for the Classification


    of Rheumatoid Arthritis
    Guidelines for Classification
    Four of seven criteria are required to classify a patient as
    having rheumatoid arthritis
    Patients with two or more clinical diagnoses are not
    excluded
    Criteria
    Morning stiffness for at least 1 hour and present for at least
    6 weeksa
    Swelling of three or more jointsab
    Arthritis of the hand joints: arthritis of wrist,
    metacarpophalangeal, or proximal interphalangeal joints
    for 6 weeks or moreab
    Symmetric arthritisab
    Rheumatoid nodulesb
    Serum rheumatoid factor measured by a method that is
    positive in less than 5% of normal individuals
    Radiographic changes in the hand typical of rheumatoid
    arthritis must include erosions or unequivocal bony
    decalcification
    a
    b

    Criterion must be present for at least 6 weeks


    Criterion must be observed by physician

    2: Systemic Disorders

    droxychloroquine, and minocycline. Biologic response


    modifiers include etanercept, adalimumab, infliximab,
    and more recently, rituximab and abatacept. These
    medications require screening for latent tuberculosis infection before starting therapy because of the risk of reactivating the infection.43
    For those patients with severely damaged joints, total joint arthroplasty is a viable option with better outcomes in the hip, the knee, and the shoulder joints. Several reconstructive hand surgeries can lead to
    functional and cosmetic improvement. Arthroscopic or
    open synovectomy, especially in the knee, may offer
    short-term relief but does not appear to retard bone destruction or alter the natural history of the disease.

    Seronegative Spondyloarthropathies
    The spondyloarthropathies are a group of chronic inflammatory diseases with the clinical spectrum that includes ankylosing spondylitis as a prototype, reactive
    arthritis (known previously as Reiter syndrome), psoriatic arthritis, enteropathic arthritis, and juvenile-onset
    spondyloarthropathies.44,45 Undifferentiated spondyloarthropathy includes diseases with elements of the
    spondyloarthropathies that do not fulfill the accepted
    criteria for the diseases. The spondyloarthropathies
    have overlapping features and are generally characterized by peripheral arthritis and enthesitis, axial inflammation (sacroiliitis and spondylitis), and new bone formation leading to ankylosis. They often display extra218

    Orthopaedic Knowledge Update 10

    articular manifestations such as intestinal, ocular, and


    skin inflammation.
    These disorders are not associated with positive
    rheumatic factor, but show striking familial aggregation
    and typically are associated with HLA genes of the major histocompatibility complex. This association varies
    among the different forms of spondyloarthropathies
    and among different ethnic groups. Both men and
    women are affected, with an overall male predominance. Spondyloarthropathies usually begin in the late
    teens and early 20s, but they may also present in childhood (juvenile) or at an older age. The prevalence of
    spondyloarthropathies may be approximately twice as
    high as previously believed. Based on the validated criteria of the European Spondyloarthropathy Study
    Group that includes a wider disease spectrum, the overall prevalence of ankylosing spondylitis may be similar
    to RA.
    The pathogenesis of spondyloarthropathies involves
    genetic susceptibility and environmental factors.46 Genetic factors, particularly the presence of the HLA-B27
    allele, heavily influence the pathogenesis of the spondyloarthropathies. Other genes probably work in concert
    with HLA to further augment the susceptibility and
    modulate the severity of the disease. Environmental
    factors, including infectious triggers, appear to play important roles. Reactive arthritis usually develops following infection with Chlamydia trachomatis or after
    dysentery caused by different enteric organisms. The
    microorganisms implicated in reactive arthritis share
    common biologic features: they can invade mucosal
    surfaces, replicate intracellularly, and contain lipopolysaccharide in the outer membrane. The close relationship between gut inflammation and spondyloarthropathies has been established for decades. More than 50%
    of patients with spondyloarthropathies have microscopic evidence of bowel inflammation; inflammatory
    bowel disease, particularly Crohn disease, develops in
    6% to 13% of those patients.47 These observations
    have raised the theory that the inciting and perpetuating event in the spondyloarthropathies may be a breakdown in the gut-blood barrier, allowing penetration of
    intestinal bacteria.
    Ankylosing spondylitis is the most common and typical form of spondyloarthropathy. It usually presents as
    inflammatory back pain and stiffness in adolescence
    and early adulthood. It is rare for ankylosing spondylitis to present after age 45 years. The diagnosis is clinical and the presenting features are very nonspecific; for
    this reason, the diagnosis is often delayed for 5 to 6
    years, particularly in patients with an incomplete clinical picture48,49 (Table 2). The presence of anterior
    uveitis, a positive family history of spondyloarthropathy, impaired spinal mobility or chest expansion, and
    enthesitis further support the diagnosis. Radiologic involvement of the sacroiliac joints is still considered the
    hallmark of ankylosing spondylitis (Figure 1). MRI
    with gadolinium enhancement is a valuable imaging
    modality to identify sacroiliitis and enthesitis. There is
    no laboratory test to diagnose ankylosing spondylitis,
    but the HLA-B27 allele has been found in approxi-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 18: Arthritis

    Table 2

    Diagnostic Criteria for Ankylosing Spondylitisa


    (Modified, New York, 1984)
    Criteria
    1. Low back pain of at least 3 months duration improved by
    exercise but not relieved by rest
    2. Limitation of lumbar spine in sagittal and frontal plane
    3. Chest expansion decreases relative to normal values for
    age and sex
    4A. Unilateral sacroiliitis grade 3 to 4
    4B. Bilateral sacroiliitis grade 2 to 4
    a

    Definite ankylosing spondylitis if 4A or 4B and any clinical criterion (1-3)

    2011 American Academy of Orthopaedic Surgeons

    Radiograph of sacroiliitis in a patient with


    ankylosing spondylitis showing sclerosis along
    the iliac sides of the sacroiliac joints and loss of
    portions of the iliac subchondral bone, indicating erosion. (Reproduced with permission from
    Firestein GS: Image modalities in rheumatic
    disease, in Firestein G, Budd R, Harris E, eds:
    Kelleys Textbook of Rheumatology, ed 8. Philadelphia, PA, Elsevier, 2008, vol 1, pp 53-54.)

    diagnosis of reactive arthritis.51 Reactive arthritis is believed to be a self-limiting condition with a course of 3
    to 12 months; symptomatic treatment with NSAIDs as
    first-line therapy and sulfasalazine as second-line therapy are warranted.
    Psoriatic arthritis has been reported in as many as
    20% of patients with psoriasis. It occurs with the same
    frequency in men and women. The skin manifestations
    precede joint involvement in 80% to 85% of patients.
    The severity of the arthritis usually does not correlate
    with the extent of the skin disease. The patterns of disease include oligoarticular arthritis, polyarticular arthritis with distal interphalangeal joint involvement, or
    psoriatic spondylitis. Skin lesions; nail lesions, including pitting and onycholysis; and chronic uveitis are
    other manifestations that are helpful in diagnosing psoriatic arthritis. The initial therapy for joint manifestations in psoriasis includes NSAIDs; other medications
    such as methotrexate, sulfasalazine, cyclosporine, and
    TNF- blockers are used as second-line therapy.
    Enteropathic arthritis occurs in up to 20% of patients with inflammatory bowel disease, particularly in
    patients with Crohn disease. It usually presents as peripheral arthritis involving the lower extremity; however, in one fifth of patients it manifests as spondylitis
    indistinguishable from ankylosing spondylitis.52 The activity of peripheral disease correlates with the activity
    of intestinal disease, whereas the course of axial disease
    is independent of inflammatory bowel disease activity.
    The most common extraskeletal manifestations include
    uveitis and chronic skin lesions such as erythema nodosum and pyoderma gangrenosum. Treatment is different from other spondyloarthropathies in that NSAIDs
    should be used cautiously because of the potential exacerbation of the bowel disease. Sulfasalazine is a good
    medication for both inflammatory bowel disease and
    arthritis. Azathioprine and methotrexate have shown
    promising results as second-line medications.

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    mately 90% to 95% of affected white patients. However, HLA-B27 can be found in 8% to 10% of the
    white population and 2% of the black population.
    Moreover, ankylosing spondylitis develops in only 1%
    to 2% of people who are HLA-B27 positive. The erythrocyte sedimentation rate and C-reactive protein level
    are elevated in 50% to 70% of patients, but the elevations are not generally associated with disease activity.
    Ankylosing spondylitis is treated with both pharmacologic and nonpharmacologic modalities.50 Pharmacologic treatment begins with NSAIDs as the first-line
    therapy, with sulfasalazine as the second-line therapy.
    Recently, data have emerged showing the efficacy of
    TNF- blockers in controlling articular inflammation;
    however, these blockers are ineffective in preventing
    new bone formation and joint ankylosis, which are major features of the disease. Additionally, the expense
    and the adverse side-effects profile of TNF- blockers,
    particularly infection, are concerns with this medication. Nonpharmacologic therapy includes patient education, outpatient physical therapy, a home exercise
    program (including a spinal extension program), and
    proper posture. In patients with end-stage joint involvement, surgical intervention, including joint arthroplasty, can be helpful. Total hip arthroplasty is the most
    common surgical procedure in patients with ankylosing
    spondylitis. Heterotopic new bone formation can be a
    potential complication. In patients with fixed kyphotic
    deformity that results in functional impairment, surgical correction of spinal deformity through osteotomy
    may be helpful.
    Reactive arthritis is an aseptic arthritis triggered by a
    genitourinary or gastrointestinal tract infection. The arthritis usually begins 1 to 4 weeks after the infection as
    an acute and oligoarticular arthritis in the lower extremity. Enthesitis (especially in the heel), dactylitis,
    and inflammatory back pain are common. Constitutional symptoms, including low-grade fever and weight
    loss, may occur in the acute phase. Extra-articular
    manifestations such as conjunctivitis, urethritis, oral ulcers, and skin lesions in the palm and sole (keratoderma blennorrhagicum) are essential in supporting the

    Figure 1

    219

    Section 2: Systemic Disorders

    Figure 2

    Compensated polarized light microscopy of synovial fluid is used to identify calcium pyrophosphate dihydrate (A) and monosodium urate (B)
    crystals. (Reproduced with permission from
    Goldman L: Crystal deposition disease, in Goldman L, Ausiello D, eds: Cecil Medicine, ed 23.
    Philadelphia, PA, WB Saunders, 2008, vol 1, pp
    294-303.)

    Undifferentiated spondyloarthropathies are those


    that do not meet criteria for well-defined categories of
    spondyloarthropathy. This is not a new category or a
    distinct entity but it is a provisional diagnosis for differentiating patients with spondyloarthropathies from
    other forms of rheumatic diseases. The patients often
    present with nonspecific manifestations such as inflammatory back pain. Patients with undifferentiated spondyloarthropathies usually have a good prognosis and
    often respond well to NSAID therapy.

    Crystal-Associated Arthritis

    2: Systemic Disorders

    Deposition of microcrystals such as monosodium urate,


    calcium pyrophosphate dihydrate, calcium apatite, and
    calcium oxalate in the joint can result in acute or
    chronic arthritis. Because clinical presentations are often similar, synovial fluid analysis is needed to determine the type of arthritis. The other characteristics of
    synovial fluid in crystal-associated arthritis are usually
    nonspecific. Polarized light microscopy alone can identify most typical crystals with the exception of calcium
    apatite (Figure 2).
    Acute arthritis is the most common early clinical
    manifestation of gout. The first metatarsophalangeal
    joint is the typical involved joint, but tarsal, ankle, and
    knee joints are also commonly affected. Trauma, surgery, excessive alcohol ingestion, and serious medical
    illnesses may precipitate acute gouty arthritis.53 After
    several acute attacks, a proportion of patients with
    gouty arthritis may present with a chronic nonsymmetric synovitis, which causes potential diagnostic confusion with RA. Some patients present only with chronic
    gouty arthritis. Most patients (80% to 95%) are men;
    most women with gouty arthritis are postmenopausal
    and elderly. The diagnosis is usually confirmed by the
    presence of strongly birefringent needle-shaped monosodium urate crystals in aspirates of the involved joint.
    Because monosodium urate crystals often can be found
    in the first metatarsophalangeal joint and in knees not
    acutely involved with gout, arthrocentesis of these
    joints between attacks is a useful diagnostic tool. The
    serum level of uric acid has a limited role in the diagnosis of gout because it can be normal or low at the
    220

    Orthopaedic Knowledge Update 10

    Figure 3

    Radiograph showing chondrocalcinosis of the


    knee, which is seen particularly well in the lateral compartment (arrows). (Reproduced with
    permission from Mettler FA: Skeletal system, in
    Mettler FA, ed: Essentials of Radiology, ed 2.
    Philadelphia, PA, WB Saunders, 2005, vol 1, pp
    253-376.)

    time of an acute attack. The mainstay of treatment during an acute gouty attack is the administration of antiinflammatory medications such as colchicine or
    NSAIDs. For prevention of further attacks, hyperuricemic regimens and medications should be considered.
    The deposition of calcium pyrophosphate dihydrate
    crystals in articular tissues occurs in 10% to 15% of
    adults 65 to 75 years of age and in 30% to 50% of
    those older than 85 years; therefore, this is a disease of
    elderly people because more than 80% of patients are
    older than 60 years.54 The disease is often asymptomatic; however, when symptoms manifest, there are several
    patterns. Acute arthritis is very similar to acute gout
    and was originally termed pseudogout. Exacerbation of
    preexisting arthritis is another manifestation of the deposition of calcium pyrophosphate dihydrate crystals.
    The condition can appear with a severe destructive pattern like neuropathic arthropathy, or with symmetric
    proliferative synovitis, like RA. Involvement of intervertebral disk and ligaments can lead to spinal stenosis and can mimic ankylosing spondylitis. The knee
    joint is most frequently involved. A definitive diagnosis
    is verified by calcium pyrophosphate dihydrate crystals
    in the synovial fluid. Chondrocalcinosis involving cartilage or menisci seen on plain radiographs can be indicative of calcium pyrophosphate dihydrate crystals (Figure 3). The crystals are weakly birefringent and
    rhomboid in shape. The treatment of acute involvement
    includes NSAIDs or intra-articular glucocorticoids.55

    Infectious Arthritis
    Infectious arthritis can present as acute monoarticular,
    chronic monoarticular, or polyarticular arthritis. Acute

    2011 American Academy of Orthopaedic Surgeons

    Chapter 18: Arthritis

    with OA. Inflammatory arthritis consists of a large


    group of diseases that lead to joint inflammation. The
    profile of the patient, chronology of the symptoms, pattern of joint involvement, and precipitating factors are
    helpful in the diagnosis of these conditions. The main
    objective of treatment for rheumatologic conditions is
    to suppress inflammation and preserve the joint. Therefore, aggressive use of disease-modifying antirheumatic
    drugs and biologic response modifiers early in the
    course of disease is promisisng. However, for those patients with severely damaged joints, total joint arthroplasty is a viable option. Crystal-associated arthritis
    usually manifests as acute arthritis; however, it could be
    present as chronic arthropathy. Infectious arthritis
    should always be considered in adults with acute or
    chronic monoarticular arthritis, especially in immunocompromised patients.

    Annotated References
    1.

    Bolen J, Schieb L, Hootman JM, et al: Differences in the


    prevalence and impact of arthritis among racial/ethnic
    groups in the United States, National Health Interview
    Survey, 2002, 2003, and 2006. Prev Chronic Dis 2010;
    7(3):A64.
    The authors describe the prevalence of doctor-diagnosed
    OA and its impact on activities, work, and joint pain
    from six racial/ethnic groups. They concluded that arthritis affects 21% of the US population, but it disproportionately affects certain racial/ethnic groups.

    2.

    Centers for Disease Control and Prevention (CDC):


    Prevalence of disabilities and associated health conditions among adults: United States, 1999. MMWR Morb
    Mortal Wkly Rep 2001;50(7):120-125.

    3.

    Hootman J, Bolen J, Helmick C, Langmaid G: Prevalence of doctor-diagnosed arthritis and arthritisattributable activity limitationUnited States, 2003
    2005. MMWR Morb Mortal Wkly Rep 2006;55(40):
    10891092.

    4.

    Hootman JM, Helmick CG: Projections of US prevalence of arthritis and associated activity limitations. Arthritis Rheum 2006;54(1):226-229.

    5.

    Kurtz S, Ong K, Lau E, Mowat F, Halpern M: Projections of primary and revision hip and knee arthroplasty
    in the United States from 2005 to 2030. J Bone Joint
    Surg Am 2007;89(4):780-785.
    The authors attempt to formulate projections for the
    number of primary and revision total hip and knee arthroplasties that will be performed in the United States
    through 2030. They expect that the demand for both
    primary and revision joint arthroplasties will greatly increase by 2030.

    6.

    Peat G, McCarney R, Croft P: Knee pain and osteoarthritis in older adults: A review of community burden
    and current use of primary health care. Ann Rheum Dis
    2001;60(2):91-97.

    Summary
    Arthritis is a common medical problem that affects
    about one fifith of the US population. OA is the most
    common joint disease and leading cause of disability
    and impaired quality of life. It involves pathologic
    changes in all structures of the joint, including cartilage, synovium, ligaments, and subchondral bone. The
    exact etiology of primary OA is unknown; however,
    several risk factors have been recognized for the disease. The diagnosis of OA is based on the classic clinical and radiologic findings; sometimes there is a need
    for more workup to prove the diagnosis. The main objectives in treating patients with OA are pain relief and
    improvement of function. The treatment should be
    comprehensive and includes both nonpharmacologic
    and pharmacologic modalities. For patients with advanced arthritis, joint arthroplasty is the most effective
    treatment, when timed correctly. Currently there is no
    effective method for cartilage regeneration in patients

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    bacterial infection typically precedes monoarticular or


    oligoarticular arthritis. Subacute or chronic monoarticular arthritis suggests mycobacterial or fungal infection, and episodic inflammation is seen in syphilis and
    Lyme disease.56 Acute polyarticular inflammation occurs as an immunologic reaction during the course of
    endocarditis, rheumatic fever, disseminated Neisseria
    infection, and acute hepatitis B. Because acute bacterial
    infection can rapidly destroy the articular cartilage, it is
    important that all inflamed joints be promptly evaluated for the possibility of infection. The aspiration and
    analysis of synovial fluid is essential in the evaluation
    of a potentially infected joint. The definitive diagnosis
    of an infectious process relies on identification of the
    pathogen on stained smears of synovial fluid, isolation
    of the pathogen in the culture of the synovial fluid, or
    detection of the microorganism via polymerase chain
    reaction assays.
    Staphylococcus aureus and Neisseria gonorrhoeae
    are the most common cause of infectious arthritis in
    adults. Although hematogenous infection can occur in
    healthy individuals, there is an underlying host predisposition for septic arthritis in most cases. Patients with
    RA, diabetes mellitus, and malignancy and those being
    treated with steroid therapy or hemodialysis have an
    increased risk of infection with S aureus and gramnegative bacilli. Patients with RA who are treated with
    TNF inhibitors are predisposed to mycobacterial and
    other pyogenic infections.
    The treatment of nongonococcal arthritis involves
    prompt administration of antibiotics and drainage of
    the involved joint. For gonococcal arthritis, antibiotic
    therapy usually suffices.
    There are three patterns of joint involvement in
    Lyme disease: intermittent episodes of monoarthritis or
    oligoarthritis involving knee or large joints in 50%,
    waxing and waning arthralgia in 20%, and chronic inflammatory arthritis with joint destruction in 10%.
    Lyme arthritis responds well to antibiotic therapy.

    221

    Section 2: Systemic Disorders

    7.

    8.

    2: Systemic Disorders

    9.

    limiting cartilage repair. J Bone Joint Surg Am 2003;


    85(suppl 2):106-110.
    15.

    Krasnokutsky S, Samuels J, Samuels J, Abramson SB:


    Osteoarthritis in 2007. Bull NYU Hosp Jt Dis 2007;
    65(3):222-228.
    In this review article, the authors summarize the current
    pathophysiologic mechanism for OA and discuss relevant treatment modalities that are currently available or
    on the horizon.
    Barksby HE, Milner JM, Patterson AM, et al: Matrix
    metalloproteinase 10 promotion of collagenolysis via
    procollagenase activation: Implications for cartilage
    degradation in arthritis. Arthritis Rheum 2006;54(10):
    3244-3253.

    10.

    Pelletier JP, Martel-Pelletier J, Abramson SB: Osteoarthritis, an inflammatory disease: Potential implication
    for the selection of new therapeutic targets. Arthritis
    Rheum 2001;44(6):1237-1247.

    11.

    Steinbeck MJ, Nesti LJ, Sharkey PF, Parvizi J: Myeloperoxidase and chlorinated peptides in osteoarthritis: Potential biomarkers of the disease. J Orthop Res 2007;
    25(9):1128-1135.
    The authors investigated the presence of the products of
    neutrophils and macrophages, specifically myeloperoxidase, in the synovial fluid of patients with OA. They
    found that patients with early OA showed significantly
    elevated levels of myeloperoxidase, whereas levels were
    low in control patients and patients with advanced OA.

    12.

    222

    Lawerence RC, Helmick CG, Arnett FC, et al: Estimates


    of the prevalence of arthritis and selected musculoskeletal disorders in the United States. Arthritis Rheum
    1998;41(5):778-799.

    Bos SD, Slagboom PE, Meulenbelt I: New insights into


    osteoarthritis: Early developmental features of an
    ageing-related disease. Curr Opin Rheumatol 2008;
    20(5):553-559.
    The authors reviewed the possible common mechanisms
    by which recently identified consistent OA susceptibility
    genes influence the onset of OA and its progression.
    They proposed that these OA susceptibility genes may
    play a dual negative role. In early developmental processes, they may involve aberrant skeletal morphogenesis leading to malformation of joints, aberrant bone
    composition, or both, thereby increasing the biomechanical burden on the articular cartilage surface. Later
    in life, these genes may affect the propensity of articular
    chondrocytes in articular cartilage to become hypertrophic. As hypertrophic chondrocytes are unable to maintain cartilage homeostasis, these genes may, in part, be
    responsible for both the onset of OA and the progression toward clinical outcomes.

    13.

    Loeser RF, Shanker G, Carlson CS, Gardin JF, Shelton


    BJ, Sonntag WE: Reduction in the chondrocyte response
    to insulin-like growth factor 1 in aging and osteoarthritis: Studies in a non-human primate model of naturally
    occurring disease. Arthritis Rheum 2000;43(9):21102120.

    14.

    Martin JA, Buckwalter JA: The role of chondrocyte senescence in the pathogenesis of osteoarthritis and in

    Orthopaedic Knowledge Update 10

    Valdes AM, Spector TD: The contribution of genes to


    osteoarthritis. Rheum Dis Clin North Am 2008;34(3):
    581-603.
    Several linkage analysis and candidate gene studies have
    recently revealed some of the specific genes involved in
    disease risks, such as FRZB and GDF5. Based on such
    studies, the authors discuss the impact that future
    genome-wide association scans can have on the understanding of the pathogenesis of OA and on identifying
    individuals at high risk for the development of severe
    OA.

    16.

    Spector TD, MacGregor AJ: Risk factors for osteoarthritis: Genetics. Osteoarthritis Cartilage 2004;12(suppl
    A):S39-S44.

    17.

    Velasco J, Zarrabeitia MT, Prieto JR, et al: Wnt pathway genes in osteoporosis and osteoarthritis: Differential expression and genetic association study. Osteoporos Int 2010;21(1):109-118.
    The authors investigated the role of Wnt activity in patients with OA. They found that genes in the Wnt pathway are upregulated in the osteoarthritic bone, suggesting their involvement not only in cartilage distortion but
    also in subchondral bone changes.

    18.

    Kaliakatsos M, Tzetis M, Tzetis M, Kanavakis E, et al:


    Asporin and knee osteoarthritis in patients of Greek origin. Osteoarthritis Cartilage 2006;14(6):609-611.

    19.

    Nakashima E, Kitoh H, Maeda K, et al: Novel COL9A3


    mutation in a family with multiple epiphyseal dysplasia.
    Am J Med Genet A 2005;132A(2):181-184.

    20.

    Feldman G, Dalsey C, Fertala K, et al: Identification of


    a 4 Mb region on Chromosome 17q21 linked to developmental dysplasia of the hip in one 18-member, multigeneration family. Clin Orthop Relat Res 2009;468(2):
    327-344.
    The authors attempted to map and characterize the gene
    or genes responsible for developmental dysplasia of the
    hip by using family linkage analysis. They recruited one
    18-member multigenerational affected family and observed only one chromosome region with a logarithm of
    the odds (LOD) score greater than 1.5 (a 4-Mb region
    on chromosome 17q21.32, yielding a LOD score of
    1.82). Discovering the genetic basis of the disease would
    be an important step in understanding the etiology of
    this disabling condition.

    21.

    Nevitt MC, Xu L, Zhang Y, et al: Very low prevalence


    of hip osteoarthritis among Chinese elderly in Beijing,
    China, compared with whites in the United States: The
    Beijing osteoarthritis study. Arthritis Rheum 2002;
    46(7):1773-1779.

    22.

    Dominik KL, Baker TA: Racial and ethnic differences in


    osteoarthritis: Prevalence, outcome, and medical care.
    Ethn Dis 2004;14(4):558-566.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 18: Arthritis

    23.

    In this article, the authors review the hypothesis that socalled primary OA is also secondary to subtle developmental abnormalities in the hip; the mechanism in these
    cases is femoroacetabular impingement rather than excessive contact stress. The most frequent location for
    femoroacetabular impingement is the anterosuperior
    rim area and the most critical motion is internal rotation of the hip in 90 flexion. The two major types of
    femoroacetabular impingement are described; however,
    the authors explain that most hips show a mixed pattern. Surgical attempts to restore normal anatomy to
    avoid femoroacetabular impingement should be performed in the early stage of the disorder before major
    cartilage damage is present.
    24.

    25.

    26.

    Hunter DJ, Wilson DR: Role of alignment and biomechanics in osteoarthritis and implications for imaging.
    Radiol Clin North Am 2009;47(4):553-566.
    This article details the current understanding of the etiopathogenesis of OA and examines the critical role of
    biomechanics in disease pathogenesis. The different
    ways of measuring mechanical forces across the joint
    are described, including those that rely on imaging
    methods.
    Felson DT: The epidemiology of knee osteoarthritis: Results from the Framingham Osteoarthritis Study. Semin
    Arthritis Rheum 1990;20(3, Suppl 1):42-50.
    Gabay O, Hall DJ, Berenbaum F, Henrotin Y, Sanchez
    C: Osteoarthritis and obesity: Experimental models.
    Joint Bone Spine 2008;75(6):675-679.
    This study investigated the correlation between obesity
    and OA. The authors concluded that the link between
    obesity and OA may not simply result from the increased mechanical stresses on joint tissues that result
    from increased weight gain in individuals. Additional
    soluble factors such as adipokines may also play an important role in the onset of OA in obese patients.
    Spector TD, Harris PA, Hart DJ, et al: Risk of osteoarthritis associated with long-term weight-bearing sports:
    A radiologic survey of the hips and knees in female exathletes and population controls. Arthritis Rheum 1996;
    39:988-995.

    28.

    Cheng Y, Macera CA, Davis DR, Ainsworth BE, Troped


    PJ, Blair SN: Physical activity and self-reported,
    physician-diagnosed osteoarthritis: Is physical activity a
    risk factor. J Clin Epidemiol 2000;53:315-322.

    29.

    Hochberg MC, Lethbridge-Cejku M, Tobin JD: Bone


    mineral density and osteoarthritis: Data from the Baltimore Longitudinal Study of Aging. Osteoarthritis Cartilage 2004;12(suppl A):S45-S48.

    30.

    Hunter DJ, McDougall JJ, Keefe FJ: The symptoms of


    osteoarthritis and the genesis of pain. Rheum Dis Clin
    North Am 2008;34(3):623-643.

    2011 American Academy of Orthopaedic Surgeons

    31.

    Cicuttini FM, Baker J, Hart DJ, Spector TD: Association of pain with radiological changes in different compartments and views of the knee joint. Osteoarthritis
    Cartilage 1996;4(2):143-147.

    32.

    Hochberg MC, Altman RD, Brandt KD, et al: Guidelines for the medical management of osteoarthritis. Arthritis Rheum 1995;38(11):1535-1540.

    33.

    Lo GH, LaValley M, McAlindon T, Felson DT: Intraarticular hyaluronic acid in treatment of knee osteoarthritis: A meta-analysis. JAMA 2003;290(23):31153121.

    34.

    Katz JN, Barrett J, Mahomed NN, Baron JA, Wright


    RJ, Losina E: Association between hospital and surgeon
    procedure volume and the outcomes of total knee replacement. J Bone Joint Surg Am 2004;86:1909-1916.

    35.

    Katz JN, Losina E, Losina E, Barrett J, et al: Association


    between hospital and surgeon procedure volume and
    outcomes of total hip replacement in the United States
    medicare population . J Bone Joint Surg Am 2001;83:
    1622-1629.

    36.

    Lingard EA, Katz JN, Wright EA, Sledge CB; Kinemax


    Outcomes Group: Predicting the outcome of total knee
    arthroplasty. J Bone Joint Surg Am 2004;86(10):21792186.

    37.

    Nilsdotter AK, Petersson IF, Roos EM, Lohmander LS:


    Predictors of patient relevant outcome after total hip replacement for osteoarthritis: A prospective study. Ann
    Rheum Dis 2003;62(10):923-930.

    38.

    Steinert AF, Nth U, Tuan RS: Concepts in gene therapy


    for cartilage repair. Injury 2008;39(suppl 1):S97-S113.
    This article reviews the current status of gene therapy as
    a method for regeneration of damaged cartilage. The
    authors describe the classes of gene products that aid
    cartilage repair and highlight the remaining challenges
    in the field.

    39.

    Rasch EK, Hirsch R, Paulose-Ram R, Hochberg MC:


    Prevalence of rheumatoid arthritis in persons 60 years
    of age and older in the United States: Effect of different
    methods of case classification. Arthritis Rheum 2003;
    48(4):917-926.

    40.

    Bukhari M, Lunt M, Harrison BJ, Scott DG, Symmons


    DP, Silman AJ: Rheumatoid factor is the major predictor of increasing severity of radiographic erosions in
    rheumatoid arthritis: Results from the Norfolk Arthritis
    Register Study, a large inception cohort. Arthritis
    Rheum 2002;46(4):906-912.

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    27.

    The authors describe the characteristic symptoms and


    signs associated with OA and how they can be used to
    make the clinical diagnosis. The predominant symptom
    in most patients is pain. The causes of pain in OA and
    factors that contribute to its severity are discussed.

    Ganz R, Leunig M, Leunig-Ganz K, Harris WH: The


    etiology of osteoarthritis of the hip: An integrated mechanical concept. Clin Orthop Relat Res 2008;466(2):
    264-272.

    223

    Section 2: Systemic Disorders

    41.

    Arnett FC, Edworthy SM, Bloch DA, et al: The American Rheumatism Association 1987 revised criteria for
    the classification of rheumatoid arthritis. Arthritis
    Rheum 1988;31(3):315-324.

    49.

    van der Linden S, Valkenburg HA, Cats A: Evaluation


    of diagnostic criteria for ankylosing spondylitis: A proposal for modification of the New York criteria. Arthritis Rheum 1984;27(4):361-368.

    42.

    Finckh A, Simard JF, Duryea J, et al: The effectiveness


    of anti-tumor necrosis factor therapy in preventing progressive radiographic joint damage in rheumatoid arthritis: A population-based study. Arthritis Rheum
    2006;54(1):54-59.

    50.

    43.

    Bongartz T, Sutton AJ, Sweeting MJ, Buchan I, Matteson EL, Montori V: Anti-TNF antibody therapy in
    rheumatoid arthritis and the risk of serious infections
    and malignancies: Systematic review and meta-analysis
    of rare harmful effects in randomized controlled trials.
    JAMA 2006;295(19):2275-2285.

    Jacques P, Mielants H, De Vos M, Elewaut D: Spondyloarthropathies: Progress and challenges. Best Pract Res
    Clin Rheumatol 2008;22(2):325-337.
    Unresolved issues concerning the pathogenesis of spondyloarthropathies are described. The precise sites where
    inflammation originates within the joints have been controversial because enthesitis, synovitis, and bone marrow inflammation can occur during the course of spondyloarthropathies. The genetic predisposition involved
    in the origin of the close linkage between gut and joint
    inflammation is described. The effects of the different
    TNF-blocking agents to modulate extra-articular disease
    manifestations are also discussed.

    44.

    Khan MA: Update on spondyloarthropathies. Ann Intern Med 2002;136(12):896-907.

    51.

    Amor B: Reiters syndrome: Diagnosis and clinical features. Rheum Dis Clin North Am 1998;24(4):677-695.

    45.

    Olivieri I, van Tubergen A, Salvarani C, van der Linden


    S: Seronegative spondyloarthritides. Best Pract Res Clin
    Rheumatol 2002;16(5):723-739.

    52.

    Kataria RK, Brent LH: Spondyloarthropathies. Am Fam


    Physician 2004;69(12):2853-2860.

    53.
    46.

    Reveille JD, Arnett FC: Spondyloarthritis: Update on


    pathogenesis and management. Am J Med 2005;118(6):
    592-603.

    Choi HK, Curhan G: Gout: Epidemiology and lifestyle


    choices. Curr Opin Rheumatol 2005;17(3):341-345.

    54.

    Leirisalo-Repo M, Turunen U, Stenman S, Helenius P,


    Seppl K. High frequency of silent inflammatory bowel
    disease in spondylarthropathy. Arthritis Rheum 1994;
    37(1):23-31.

    Molloy ES, McCarthy GM: Hydroxyapatite deposition


    disease of the joint. Curr Rheumatol Rep 2003;5(3):
    215-221.

    55.

    Schumacher HR Jr, Chen LX: Newer therapeutic approaches: Gout. Rheum Dis Clin North Am 2006;32(1):
    235-244, xii.

    Rudwaleit M, van der Heijde D, Khan MA, Braun J,


    Sieper J: How to diagnose axial spondyloarthritis early.
    Ann Rheum Dis 2004;63(5):535-543.

    56.

    Tarkowski A: Infection and musculoskeletal conditions:


    Infectious arthritis. Best Pract Res Clin Rheumatol
    2006;20(6):1029-1044.

    2: Systemic Disorders

    47.

    48.

    224

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 19

    Disorders of the Nervous System


    Tahseen Mozaffar, MD

    Ranjan Gupta, MD

    Introduction

    Dr. Mozaffar or an immediate family member is a member of a speakers bureau or has made paid presentations on behalf of Genzyme Talecris; serves as a paid
    consultant to or is an employee of Genzyme, Baxter, and
    Talcris; has received research or institutional support
    from Talecris Biotherapeutics; and has received nonincome support (such as equipment or services), commercially derived honoraria, or other non-researchrelated
    funding (such as paid travel) from the medical director
    for Crescent Healthcare. Dr. Gupta or an immediate family member has received funding from the NIH-NINDS
    and has received research or institutional support from
    Arthrex, Smith & Nephew, and Synthes.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    The nervous system is a complex and intricate system


    that enables the individual to recognize and react to the
    environment and to interact with the environment in a
    meaningful manner. Underlying this complex system is
    its simplicity of composition, with relatively few distinct
    cell types including neurons and glial cells. The nervous
    system is organized into the central nervous system
    (CNS) and the peripheral nervous system (PNS). The
    CNS receives, processes, and initiates signals, whereas
    the PNS relays signals to and from the environment and
    the CNS. In both systems, the neuron is the principal
    cell type. Neurons communicate with their targets via
    long cytoplasmic processes called axons. In the PNS, the
    peripheral nerves are primarily composed of bundles of
    axons and their associated Schwann cells. Schwann cells
    provide protection and trophic support and are found
    in two phenotypesmyelinating and nonmyelinating.
    Myelinating Schwann cells ensheathe large-caliber axons in myelin and maintain a one-to-one relationship
    with axons. Myelination increases the speed of action
    potential propagation and allows signals to reach their
    targets in a timely manner. In contrast, nonmyelinating
    Schwann cells associate with numerous axons in structures known as Remak bundles, which enclose small
    caliber C fibers and transmit pain and temperature sensation. The loss of myelination and changes in Remak
    bundles are common signs of peripheral nerve neuropathy. This chapter will describe the structure and function of the human nervous system and discuss the
    pathophysiology of specific neuropathies that are important in orthopaedic clinical practice.

    Peripheral nerves are heterogeneous composite structures composed of neurons, Schwann cells, fibroblasts,
    and macrophages. The neuron is a polarized cell that
    forms the foundation of the nerve and consists of dendrites, the cell body, and a single axon. The cell body
    contains the nucleus, cytoplasmic organelles, and a cytoskeleton composed of neurofilaments and microtubules. The axon originates from a unique region of the
    cell body called the axon hillock, which is the site
    where the action potential of the neuron is produced.
    Axons project toward sites of innervation, where they
    form synapses. Synaptic transmissions from the axon to
    the end organ are mediated by electrochemical changes.
    In the PNS, the axons are surrounded by glial cells
    called Schwann cells, which produce myelin. If the axonal diameter is greater than or equal to 1 m, each
    Schwann cell will wrap its plasma membrane around a
    single region of an axon and develop myelin. This myelin, composed of 70% lipid and 30% protein, functions to provide fast and efficient conduction of the action potential propagating down an axon.
    Discontinuities along the length of the axon in the myelin sheath are called the nodes of Ranvier. When the
    action potential reaches a node, it depolarizes sodium
    channels. This rapid action potential propagation down
    the axon from node to node occurs by a process called
    saltatory conduction. Peripheral nerves have connective
    tissue layers to provide strength and protection to the
    nerve with its three layers: the endoneurium, perineurium, and epineurium (Figure 1). The endoneurium surrounds individual axons and their associated Schwann
    cells. It is composed of thin collagen strands that provide nourishment and protection. Multiple nerve fibers
    form a collection of axons called a fascicle. Fascicles
    are grouped and surrounded by the perineurium, which
    is composed of collagen and fibroblasts. This sheath
    provides the nerve with tensile strength, and the fibroblasts contribute to the formation of the blood-nerve
    barrier. Multiple fascicles are grouped together and surrounded by a connective tissue layer called the internal
    or interfascicular epineurium. This layer cushions the
    fascicles within the nerve and allows them to move
    freely against one another. The periphery of the entire
    nerve is covered by the external or extrafascicular
    epineurium, which protects the entire nerve from the
    surrounding environment.
    The CNS consists of functions served both in the
    brain and in the spinal cord. The brain is structurally
    organized into lobes (the gray matter) named the fron225

    Section 2: Systemic Disorders

    2: Systemic Disorders

    Figure 1

    Schematic of the peripheral nerve demonstrating the axonSchwann cell interface as well as the different layers of
    connective tissue.

    tal, temporal, parietal, and occipital lobes, each with


    distinct functions. The frontal lobes are predominantly
    tasked with execution of executive and affective functions while the parietal lobes control motor and sensory functions. The temporal lobes focus on memory
    and cognition while the occipital lobes are concerned
    with vision. Language is also controlled by these structures. The various lobes connect with each other and
    the contralateral side through nerve fiber connections
    (the white matter bundle). There are also specialized
    nuclei deep within the brain, which are concerned with
    motor control, sleep, and consciousness and awareness.
    The caudal portion of the brain is known as the brainstem and is a densely packed region of brain with many
    vital structures that control autonomic functions, respiration, eye movements, swallowing, and motor and
    sensory functions.
    The spinal cord is a vital portion of the CNS that relays sensory input from the environment to higher levels of the neuraxis, directs motor activity through somatic and visceral motor neurons, possesses intrinsic
    reflex properties, and influences the activity of spinal
    neurons through descending tracts. The spinal cord
    spans the distance from the foramen magnum to the
    second lumbar vertebrae. Axons enter and exit the spinal cord via the spinal nerves, each of which consists of
    a ventral or efferent root and a dorsal or afferent root.
    226

    Orthopaedic Knowledge Update 10

    The ventral roots carry output to the striated muscles


    from the myelinated nerve fibers of motor neurons in
    the gray matter of the ventral horn. The dorsal roots
    carry sensory input from myelinated and unmyelinated
    nerve fibers that originate from somatic sensory receptors. The cell bodies of the afferent fibers are located in
    the dorsal root ganglia. The spinal cord is further subdivided into white and gray matter. The descending
    tracts from the cortex and subcortical parts of the brain
    and the ascending fiber tracts are organized into welldemarcated and somatotopically arranged columns
    (Figure 2). These contain both myelinated and unmyelinated nerve axons. The gray matter is contained in the
    central portion of the spinal cord, which is an
    X-shaped structure containing longitudinally arranged
    neuronal cell bodies along with supporting structures
    such as glial cells, dendrites, and myelinated and unmyelinated axons. The gray matter is divided into the dorsal horn (predominantly sensory), the intermediate
    zone, and the ventral horn (purely motor). The ventral
    horn is populated by motor efferent neurons that project their axons out of the CNS via the ventral roots.
    These axons end up in various muscles in the limb and
    trunk and represent the pure efferent or motor fibers.
    The dorsal horns contain the first-order neurons that
    receive afferent input from the sensory dorsal root ganglion neurons (which in turn receive input from the

    2011 American Academy of Orthopaedic Surgeons

    Chapter 19: Disorders of the Nervous System

    Figure 2

    Schematic of the spinal cord with the somatotopically arranged columns.

    2011 American Academy of Orthopaedic Surgeons

    spinal cord and end on another neuron. These interneurons play an important role in generating the spinal reflexes.
    2: Systemic Disorders

    skin-based and other sensory receptors). The dorsal


    horn is organized into columns of nerve fibers that
    travel in a rostral fashion, otherwise known as the
    dorsal column. The dorsal columns are also organized in a lamellar structure, with sensory neurons organized in a topographical fashion. The nerve projection from the dorsal root ganglia enters the dorsal horn
    of the spinal cord through the dorsal column and synapse with these neurons in the dorsal column. Some of
    these projections either descend or ascend the dorsal
    column; some projections bypass the nuclei in the dorsal horns and synapse in the mid portions of the spinal
    cord and then ascend up in a tract of fibers, known as
    the spinothalamic tract. Projections within the dorsal
    columns as well as the spinothalamic tract eventually
    pass through the brainstem and end in the sensory relay
    nucleus, the thalamus. Descending nerve fibers from
    the motor cortex in the brain are organized in the lateral portions of the spinal cord and are known as the
    lateral corticospinal tract. These fibers, in turn, synapse
    on the interneurons (see below), which in turn synapse
    with the motor neurons in the anterior horn cells. This
    way the descending corticospinal tracts influence motor
    movements and determine the muscle tone in the extremities as well as deep tendon reflexes. Autonomic
    tracts and primary autonomic neurons are present in
    the intermediolateral column of the spinal cord in the
    thoracic regions; these are the primary autonomic neurons that control a number of autonomic functions, including sphincter control. The intermediate zone contains neurons whose projections remain within the

    Compression Neuropathies
    Compression of the neural structures, either intraspinal
    or extraspinal, leads to neurologic dysfunction. Compression of the spinal cord within the spinal canal, either through an extrinsic lesion, such as bony outgrowth, herniated disks, bleeding (hematoma), lipoma,
    or metastatic lesions, or through an intrinsic lesion,
    such as a nerve or meningeal tumor, may create a neurologic emergency with the restoration of neurologic
    functions dependent on the timing of response to correct such abnormalities. Nerve compression can occur
    outside the spinal canal, either in the exit zone, as the
    nerve roots exit the spinal canal, or along the length of
    the nerve, often at predictable sites of entrapment.
    Common causes of entrapment are ligamentous or fibrous outgrowths that pinch a nerve. Bony outgrowth (osteophytes) in the joints or bones may also
    impinge a nerve. Rarely tumors (neurofibroma or lymphoma), inflammatory conditions, such as meningeal
    adhesions, as in arachnoiditis or amyloid deposits, or
    trauma may cause such entrapments.
    Compression neuropathies of the upper extremity
    frequently occur and may require surgical treatment.
    Pathologic changes in peripheral nerves result from external mechanical forces of compression, with the

    Orthopaedic Knowledge Update 10

    227

    Section 2: Systemic Disorders

    2: Systemic Disorders

    symptoms described by patients commonly referred to


    as entrapment syndromes. The defining objective feature of compression neuropathies is the progressive decline in nerve conduction velocity. Chronic nerve compression injuries of the median, ulnar, and radial nerves
    occur in predictable locations in the wrist, forearm, and
    arm. Overuse and cumulative trauma in areas of restricted anatomic space can lead to compression of the
    nerve. The pathophysiologic changes include slowing of
    nerve conduction velocity, ischemia, edema, and eventually, neuropathy, which includes Schwann cell phenotypic changes, demyelination, and axonal dysfunction.
    Nerve changes have classically been defined on the
    basis of the ensuing morphologic changes. Even with
    the most severe injuries to a nerve, the segment of nerve
    distal to the site of injury is able to maintain its integrity up to 3 to 7 days after injury. This is true even after
    complete injuries, where all connections to the proximal segment of the nerve, and thus the neuronal structures in the spinal cord (either the motor neurons or
    dorsal root ganglia), are severed. After nerve injury, the
    distal segment of the nerve starts to disintegrate to prepare for neural regeneration through a series of coordinated events known as wallerian degeneration. This
    process is initiated by granular disintegration of the axonal cytoskeleton with the ensuing recruitment of hematogenously derived macrophages. With the myelin
    and axonal debris cleared, the remaining Schwann cells
    proliferate and the distal segment is known as the
    bands of Bugner. Neural injuries however, are variable
    and may be incomplete with damage only to either the
    myelin sheath, with resulting segmental demyelination,
    or only the axon, with resulting axonal degeneration
    without damage to the myelin. The Seddon classification helped prognosticate these injuries. The mildest injury is when only the myelin sheath is damaged without
    damage to the axon. This form, known as neurapraxia,
    has the best prognosis. Damage to axons is termed axonotmesis, and usually is reversible, especially if only a
    short segment of the axon is damaged. The prognosis is
    fair, and recovery is possible albeit never complete and
    not as good as in the case of neurapraxia. However, if
    there is a large segment of axonal damage or if there is
    severe injury which not only damages the axon but the
    surrounding neural structures, the most severe form of
    nerve injury. This form was termed neurotmesis, and
    implies a dying back phenomenon where the proximal segment of the nerve (in addition to the degeneration of the distal segment wallerian degeneration) disintegrates and the primary neurons resultantly undergo
    chromatolysis and eventual death.
    Recent studies have shown the pathophysiology of
    neuropathy resulting from compression at the cellular
    and molecular levels.1-5 Chronic nerve compression injuries of peripheral nerves are distinctly different from
    acute injuries such as those caused by crushing and
    transection. Initially, it was believed that axonal damage during chronic nerve compression injury triggers
    Schwann cells dedifferentiation and proliferation.
    However, research has indicated that axonal integrity is
    maintained and is free of pathology in chronic nerve
    228

    Orthopaedic Knowledge Update 10

    compression injuries.1 Compression neuropathies do


    not show morphometric evidence of wallerian degeneration, the hallmark of acute peripheral nerve injuries.2
    Furthermore, chronic nerve compression injuries occur
    in the absence of the early, dramatic inflammation and
    immune-mediated responses that occurs with acute injuries.2 Chronic nerve compression injuries also lead to
    subsequent demyelination and remyelination of injured
    axons.1 Thinner myelin is formed on remyelination,
    with this decrease in myelination contributing to the
    clinical presentation of slowing nerve conduction velocity in electrodiagnostic studies.1 Chronic nerve compression injury also has been shown to induce a phenotypic switch in the Schwann cell phenotype.3 An
    increase in the number of nonmyelinating Schwann
    cells and Remak bundles is observed in chronic nerve
    compression injuries.1 These Remak bundles contain an
    increased number of C fibers, which correlate with the
    pain at compression sites in compressive neuropathies.
    Schwann cells are mechanically sensitive to shear forces
    and the expression of specific surface adhesion proteins
    are altered in response to hydrostatic pressure.4,5 Thus,
    current research supports the belief that compression
    neuropathies are primarily a Schwann cellmediated
    disease. By further understanding the mechanism of injury response by Schwann cells to mechanical stimulation, molecular therapies can be developed to prevent
    injury and promote regeneration.

    Electrodiagnostic Studies
    Nerve conduction studies and needle electromyography
    (EMG) are important tools in localizing areas of compression and neuropathy within the peripheral nervous
    system. Electrodiagnostic studies are useful in distinguishing a root lesion from compression at the spinal
    level from trunk, division, or cord compression at the
    brachial or lumbar plexus, and branch compression peripherally.6 These studies also help determine the severity of the lesion and can be used to determine the prognosis of the lesion (neurapraxia with good prognosis
    versus axonotmesis/neurotmesis with a poor prognosis.
    Nerve conduction studies can further distinguish an axonal pathology from a demyelinating pathology and
    can distinguish a neurogenic lesion from a myopathic
    lesion. These studies complement the information obtained through imaging modalities.7
    Nerve conduction velocity studies are routinely performed on peripheral nerves to determine their responsiveness to electrical stimuli.8 A constant voltage electrical stimulator is used to evoke a response that is
    recorded either from a muscle in a motor nerve study
    or along the nerve in a sensory nerve study. The latency
    of the response (the time from the onset of the stimulus
    to the onset of the recorded response) is calculated and
    displayed in milliseconds. The distance that the stimulus had to travel (from the cathode of the stimulating
    electrode to the active recording electrode) is then measured with this distance then divided by the latency to
    obtain the nerve conduction velocity.9 Because motor

    2011 American Academy of Orthopaedic Surgeons

    Chapter 19: Disorders of the Nervous System

    Table 1

    Findings on Nerve Conduction Velocity Studies in Various Neuromuscular Conditions


    Condition

    Latency

    Conduction Velocity

    Amplitudes

    F-Wave Latency

    Nerveaxonal

    Normal

    Normal

    Reduced

    Normal

    Nervedemyelinating

    Prolonged

    Slow

    Normal or reduced

    Absent or prolonged

    Myopathy

    Normal

    Normal

    Reduced

    Normal

    Neuromuscular junction

    Normal

    Normal

    Reduced

    Normal

    2011 American Academy of Orthopaedic Surgeons

    syndrome. Another electrophysiologic study that is


    equally useful is the Hoffman reflex or H-reflex. The
    H-reflex is a true reflex with both an afferent and an efferent limb to the reflex. It is obtained by electrical
    stimulation of I- afferent fibers at the knee with recording from the soleus. The resulting electrical stimulation is carried back to the spinal cord by the I- afferents to the S1 level and then transmitted by synapses
    on to the anterior horn cells at that level. This results in
    a motor nerve discharge that can be recorded from the
    soleus muscle. The H-reflex is affected by sensory neuropathies, motor disorders affecting the sciatic or tibial
    nerves, and is asymmetrically affected by S1 root lesions.8
    Needle EMG studies provide complementary information to nerve conduction velocity studies regarding
    the state of health of the skeletal muscles. These muscles can be affected by primary disease of the nerve
    roots, the peripheral nerves, or the skeletal muscles
    themselves. EMG studies help differentiate and discriminate between the various conditions. EMG studies also
    can determine if the nerve lesions are acute or chronic
    and if reinnervation has occurred. In patients with a
    nerve injury, this information, along with nerve conduction velocity studies, helps determine whether the
    nerve continuity is maintained.
    To perform intramuscular EMG, a needle electrode
    is inserted through the skin into the muscle tissue.9 A
    trained physician such as a neurologist or a physiatrist
    observes the electrical activity while inserting the electrode. The insertional activity provides valuable information about the state of the muscle and its innervating
    nerve. Normal muscles at rest produce certain normal
    electrical sounds when the needle is inserted into them.
    This baseline electrical activity is evaluated when the
    muscle is at rest. Abnormal spontaneous activity often
    indicates some nerve and/or muscle damage. Subsequently, the patient is asked to contract the muscle
    smoothly. The shape, size, and frequency of the resulting motor unit potentials are judged. The electrode is
    then retracted a few millimeters, and the activity is analyzed again until at least 10 to 20 units have been collected. Each electrode track gives only a very local picture of the activity of the whole muscle. Because the
    inner structures of the skeletal muscles differ, the electrode must be placed at various locations to obtain an
    accurate study. Table 2 describes the changes seen on
    EMG studies in various pathologic conditions.

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    nerve studies include a transit through the neuromuscular junction, where an inherent delay occurs, an additional stimulus is given along a proximal segment of
    the nerve, and the conduction velocity is calculated
    along the nerve, between the two points of stimuli (to
    compensate for the delay at the neuromuscular junction). The amplitude of the response also is calculated.
    All of the responses are compared to normative data to
    determine if they are normal or abnormal. A conduction block is a delay in the conduction velocity with a
    decrease in the amplitude of the compounded action
    potential from the nerve across a site of injury. A conduction block occurs because of impaired conduction
    across the injured segment of the nerve, with either a
    partial or a complete disruption of conduction. This results in a normal distal response (distal to the site of injury) but an abnormal response as the stimulator is
    moved proximal to the site of the injury.
    An axonal injury to the nerve primarily creates a decreased amplitude on electrophysiologic examination.
    The latency and conduction velocity are not expected
    to change unless the degree of axonal injury is such that
    the myelin sheaths are also secondarily affected with
    the ensuing demyelination.10 In that situation, a slight
    prolongation in latency and slowing in conduction velocity would also occur. Demyelinating lesions primarily affect the latency of the response and thus the conduction velocity. Amplitudes would only be affected
    with demyelinating lesions if there is a severe block in
    conduction or severe desynchrony of conduction created by segmental demyelination which results in a
    temporal dispersion of the response. Myopathic lesions
    tend to affect the amplitude of the motor nerve response because the motor responses are recorded from
    muscles; sensory nerve studies are not affected by myopathies. Table 1 details the changes seen with nerve
    conduction velocity studies in various nerve and muscle
    lesions.
    Additional electrophysiologic studies can be performed to determine late responses in the motor nerve.
    These responses are known as F-waves (because the
    waves were initially recorded in the foot muscles) and
    are particularly useful for evaluating conduction problems in the proximal region of nerves such as in portions of nerves near the spinal cord. These studies are
    also very useful in evaluating disorders that affect the
    proximal region of nerves such as with a radiculopathy
    or with a demyelinating disease such as Guillain-Barr

    229

    Section 2: Systemic Disorders

    Table 2

    Findings on Needle Electromyography Studies in Various Neuromuscular Conditions


    Condition

    Insertional
    Activity

    Spontaneous Activity

    Motor Unit
    Morphology

    Recruitment

    Firing Rate

    Neurogenic: < 7 days

    Normal

    Normal

    Normal

    Reduced

    Increased

    Neurogenic: 7 days to
    3 months

    Increased

    Fibrillations and
    fasciculations; complex
    repetitive discharges

    Normal

    Reduced

    Increased

    Neurogenic: > 3
    months

    Increased

    Fibrillations and
    fasciculations; complex
    repetitive discharges

    Increased amplitude
    and duration;
    variable polyphasia

    Reduced

    Increased

    Myopathy: with
    inflammatory or
    necrotic elements

    Increased

    Fibrillations; myotonia;
    complex repetitive
    discharges

    Decreased amplitude
    and duration;
    variable polyphasia

    Early

    Normal

    Myopathy: with no
    inflammatory or
    necrotic elements

    Normal

    Normal

    Decreased amplitude
    and duration;
    variable polyphasia

    Early

    Normal

    Neuromuscular
    junction disorder

    Normal

    Normal

    Normal; decreased
    amplitude and
    duration

    Normal or early

    Normal

    Electrophysiologic Response
    to Acute Nerve Injury

    2: Systemic Disorders

    Because myelin can be repaired, unless there is secondary involvement of the axonal structures, neurapraxia
    has a good prognosis with complete recovery over several weeks. Surgery for repair of the nerve is often not
    needed and patients should be carefully followed with
    serial electrodiagnostic studies. A more severe injury may
    produce axonotmesis. In addition to the disruption of
    myelin, the axonal tube is also damaged; however, the
    surrounding neural structures (the neural tube) are intact. Thus, the architectural framework for the nerve remains intact and the recovery potential is fair. With severe or large lesions, recovery may not be as robust.
    Surgery to perform neurolysis or bridge the defect may
    be required to allow maximal neural regeneration. Because axonal structures are damaged in situations with
    severe or large lesions, the amplitude of evoked responses
    on nerve conduction velocity studies decreases progressively and often may be absent. As the injury may affect
    both sensory and motor nerves, needle EMG examination shows evidence of denervation, such as fibrillation
    potentials and the reduced recruitment of motor units.
    In acute stages, motor units may be absent in patients
    with severe injuries. Follow-up studies are even more
    crucial in this situation, especially in patients with severe
    injuries, because nerve conduction changes may reverse
    (improve) and needle EMG examination may begin
    showing signs of reinnervation.
    In neurotmesis, the most severe form of neural injury, all the neural structures are damaged, which results in complete disruption of the neural architecture.
    Nerves have inherent elastic properties, causing retraction of the cut ends and preventing any chance of spontaneous regeneration. Because of the severity of injury,
    230

    Orthopaedic Knowledge Update 10

    and the lack of trophic support from the neural body,


    rapid deterioration of nerve axons occurs. Additionally,
    a dying-back of axons extends all the way back to the
    cell body (neurons) resulting in cell death. The prognosis is poor and very early surgical intervention is required in some instances to improve recovery potential.
    Electrophysiology shows complete absence of nerve
    conduction in the affected nerves. Three days after injury, EMG will show profuse denervation.8

    Neuropathies Associated With Systemic Illnesses


    A number of systemic conditions have pathologic involvement of peripheral nerves, including diabetes mellitus, uremia, thyroid disorders and nutritional deficiencies. The degree of involvement is variable as not every
    patient with such systemic illnesses has nerve involvement. In patients with systemic disorders, diabetes mellitus, hypothyroidism, and vitamin B12 deficiency routinely appear to be the most common conditions
    associated with neuropathies.

    Diabetes
    Diabetic neuropathy is a relatively common condition
    that is associated with multiple phenotypes and is estimated to be the cause of neuropathy in 15% to 30% of
    North American patients.11 Diabetes mellitus is associated with several types of polyneuropathies: distal symmetric sensory or sensorimotor polyneuropathy, autonomic neuropathy, diabetic neuropathic cachexia,
    polyradiculoneuropathies, cranial neuropathies, and
    other mononeuropathies (Table 3). The exact prevalence of each subtype of neuropathy in diabetic patients
    is not accurately known; however, it has been estimated

    2011 American Academy of Orthopaedic Surgeons

    Chapter 19: Disorders of the Nervous System

    2011 American Academy of Orthopaedic Surgeons

    Table 3

    Various Neuropathic Syndromes Associated


    With Diabetes Mellitus and Hypoglycemia
    Diabetes Mellitus
    Distal symmetric sensory and sensorimotor polyneuropathy
    Autonomic neuropathy
    Diabetic neuropathic cachexia
    Radiculoplexus neuropathy
    Mononeuropathy/multiple mononeuropathies
    Hypoglycemia and Hyperinsulinemia
    Generalized sensory or sensorimotor polyneuropathy

    Diabetes Association in conjunction with one or more


    of the characteristic clinical diabetic neuropathy phenotypes.14 The American Diabetes Association criteria include either an elevated fasting blood glucose level (
    124 mg/dL) or an abnormal 2-hour glucose tolerance
    test ( 200 mg/dL). Tests of glycosylated hemoglobin
    are usually used to assess diabetic control rather than
    for the initial detection of diabetes. Traditionally, neuropathy was not readily attributed to diabetes unless
    the diagnosis of diabetes had been established for years.
    More recently, a statistical association was demonstrated between impaired glucose tolerance (fasting
    blood sugars between 110 to 125 mg/dL; or a 2-hour
    serum glucose, after a 75-g glucose challenge following
    a 12-hour fast, 140 to 199 mg/dL) and a small-fiber
    neuropathy phenotype (see below).
    Up to 50% of asymptomatic patients with diabetes
    mellitus have reduced sensory nerve action potential
    amplitudes along with slowed conduction velocities of
    the sural or plantar nerves, whereas up to 80% of
    symptomatic patients have abnormal sensory nerve conduction velocity studies. Quantitative sensory testing
    may show reduced vibratory and thermal perception.
    Autonomic testing may also be abnormal, particularly,
    quantitative sweat testing. Biopsies of nerves of patients
    with diabetes can show axonal degeneration, clusters of
    small regenerated axons, and segmental demyelination
    that is more pronounced distally, as expected in a
    length-dependent process. Although not clearly defined,
    the major theories about the pathogenesis of diabetic
    neuropathy involve a metabolic process, microangiopathic ischemia, or an immunologic disorder.15
    The mainstay of treatment is strict control of glucose, which can reduce the risk of developing a neuropathy or can improve an existing neuropathy.16,17 Pancreatic transplantation may stabilize or slightly improve
    sensory, motor, and autonomic function.18 More than
    20 trials of aldose reductase inhibitors have been performed and most have had negative results. Trials of
    neurotrophic growth factors also have been disappointing. A double-blind study of -lipoic acid, an antioxidant, reported significant improvement in neuropathic
    sensory symptoms such as pain and several other neuropathic end points.19

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    that neuropathy will develop in 5% to 66% of patients


    with diabetes.12 Alarmingly, diabetic neuropathy can
    also occur in children. Long-standing, poorly controlled diabetes mellitus and the presence of retinopathy and nephropathy are risk factors for the development of peripheral neuropathy in diabetic patients. In a
    large community-based study, 1.3% of the population
    had diabetes mellitus (type 1, 27%; type 2, 73%). Of
    these, approximately 66% of individuals with type 1
    diabetes mellitus had some form of neuropathy: generalized polyneuropathy, 54%; asymptomatic carpal tunnel syndrome, 22%; symptomatic carpal tunnel syndrome, 11%; autonomic neuropathy, 7%; and various
    other mononeuropathies and/or multiple mononeuropathies, 3%, which included ulnar neuropathy, peroneal
    neuropathy, lateral femoral cutaneous neuropathy, and
    diabetic amyotrophy.13 In the group with type 2 diabetes mellitus, 45% had generalized polyneuropathy,
    29% had asymptomatic carpal tunnel syndrome, 6%
    had symptomatic carpal tunnel syndrome, 5% had autonomic neuropathy, and 3% had other mononeuropathies and/or multiple mononeuropathies. Considering
    all forms of diabetes mellitus, 66% of patients had
    some type of objective sign of a diabetic neuropathy,
    but only 20% of patients with diabetes mellitus were
    symptomatic.
    Distal symmetric sensory polyneuropathy is the most
    common form of diabetic neuropathy. It is a lengthdependent neuropathy in which sensory loss begins in
    the toes and gradually progresses over time up the legs
    and into the fingers and arms. When severe, sensory
    loss may also develop in the midline of the trunk (chest
    and abdomen) and spread laterally toward the spine.
    The sensory loss is often accompanied by paresthesias,
    lancinating pains, burning sensations, and/or a deep
    aching discomfort. A severe loss of sensation can lead
    to increased risk from trauma to the extremities, with
    secondary infection, ulceration, and Charcot joints.
    Signs of an autonomic dysfunction may develop in patients with small fiber neuropathy because the autonomic nervous system is mediated by small myelinated
    and unmyelinated nerve fibers. Poor control of diabetes
    mellitus and the presence of nephropathy correlate with
    an increased risk of developing distal symmetric sensory polyneuropathy.
    A neurologic examination will show loss of small fiber function, that is, pain and temperature sensation,
    and may also show a panmodality sensory loss. Those
    with large-fiber sensory loss have reduced muscle
    stretch reflexes, particularly at the ankles; however, reflexes can be normal in patients with only small-fiber
    involvement. Muscle strength and function are typically
    normal, although mild atrophy and weakness of intrinsic foot muscles and ankle dorsiflexors may be detected. Because patients without motor symptoms or
    signs on clinical examination will often have electrophysiologic evidence of subclinical motor involvement,
    the term distal symmetric sensorimotor peripheral neuropathy is also appropriate.
    The diagnosis of diabetic neuropathy is dependent
    on the fulfillment of criteria outlined by the American

    231

    Section 2: Systemic Disorders

    Hypothyroidism
    Although hypothyroidism is more commonly associated with a proximal myopathy, neuropathy develops
    in some patients, most typically carpal tunnel syndrome. Although rare, some patients may develop a
    generalized sensory polyneuropathy characterized by
    painful paresthesias and numbness in the hands and the
    legs. Pharmacologic correction of hypothyroidism usually halts disease progression and may improve polyneuropathy.

    Inflammatory Neuropathies

    2: Systemic Disorders

    Some patients develop an autoimmune response toward


    peripheral nerves with the immune attack directed
    against peripheral nerve antigens such as myelin protein zero or myelin-associated glycoprotein. In certain
    disorders, autoimmunity develops as an aberrant response to the normal immune response to bacterial infections. A good example of this is the autoimmunity to
    nerve gangliosides in patients with Campylobacter jejuni diarrheal infections. Two immune neuropathies
    chronic inflammatory demyelinating polyradiculopathy
    (CIDP) and multifocal motor neuropathy (MMN) will
    be discussed.
    CIDP is a dynamic immune-mediated neuropathy
    characterized by either a progressive or relapsing
    course. The diagnostic approach requires a detailed
    clinical examination, the findings of electrodiagnostic
    abnormalities, and occasionally, a nerve biopsy. CIDP
    may account for 10% to 33% of initially undiagnosed
    peripheral neuropathies in large tertiary referral centers. By definition, the symptoms and signs of the neuropathy must be progressive for at least 2 months,
    which distinguishes CIDP from Guillain-Barr syndrome or the most common form of this disorder, acute
    acquired inflammatory demyelinating neuropathy. Differentiating an acute acquired inflammatory demyelinating neuropathy from CIDP can be difficult in the
    first few weeks of disease onset because it is not always
    possible to determine if the disease will continue to
    progress for at least 2 months or will reach a plateau.
    Four courses of progression in patients with CIDP have
    been described: (1) chronic monophasic, in 15% of patients; (2) chronic relapsing with fluctuations of weakness or improvement over weeks or months, in 34%;
    (3) stepwise progressive, in 34%; and (4) steady progressive, in 15%.20 In this respect, CIDP is similar to
    multiple sclerosis, an immune-mediated demyelinating
    disorder affecting the CNS.
    CIDP usually presents in adults (peak incidence at
    approximately 40 to 60 years of age) with a slightly increased prevalence in men.7 Most patients manifest
    with progressive, symmetric proximal, and distal weakness of the arms and legs. Early in the course of the illness, only distal extremity numbness and weakness
    may be apparent. If the weakness remains distal, other
    diagnoses should be considered. Although most patients (at least 80%) have both motor and sensory in232

    Orthopaedic Knowledge Update 10

    volvement, a few patients may have pure motor (10%)


    or pure sensory (5% to 10%) symptoms and signs.
    Subjective numbness in the extremities is present in
    68% to 80% of patients, whereas painful paresthesia
    occurs in 15% to 50%. The sensory examination is abnormal in most patients, particularly in large-fiber modalities (vibration and touch). Most patients with CIDP
    are areflexic or at least hyporeflexic. Most patients
    (80% to 95%) have an elevated cerebrospinal fluid
    protein level (> 45 mg/dL) with a mean of 135 mg/dL;
    some levels than may be greater than 1,200 mg/dL.
    Similar to Guillain-Barr syndrome, the cerebrospinal
    fluid cell count is usually normal. Elevated cerebrospinal fluid cell counts should lead to the consideration of
    HIV infection, sarcoidosis, Lyme disease, or lymphomatous or leukemic infiltration of nerve roots. Motor conduction studies evaluating compound muscle action potential amplitudes, distal latencies, conduction
    velocities, and F-wave latencies, as well as studies that
    look for evidence of temporal dispersion or a conduction block, are the most useful electrodiagnostic tools
    for CIDP. Most patients with CIDP have low-amplitude
    or unobtainable sensory nerve action potentials in both
    the upper and the lower extremities. Nerve biopsies are
    helpful in making the diagnosis because evidence of
    segmental demyelination and remyelination is often
    present. Although not specific for CIDP, this chronic
    demyelination and remyelination results in proliferation of surrounding Schwann cell processes, forming
    the so-called onion bulbs. Nerve biopsies are particularly useful when lymphomatous infiltration, amyloidosis, and sarcoidosis are considered in the differential diagnoses because these disorders can mimic CIDP.21
    Although CIDP is an autoimmune disorder, the antigen(s) to which the immune attack is targeted and the
    specific roles of the humoral and cellular system in the
    pathogenesis of CIDP are not known. Corticosteroids,
    plasmapheresis, and infusion of intravenous immunoglobulins have been shown to be beneficial in treating
    patients with CIDP. Intravenous immunoglobulins have
    become the treatment of choice because it has fewer
    long-term adverse side effects than corticosteroids. Of
    importance, patients treated early are more likely to respond, underscoring the need for early diagnosis and
    treatment.22
    In contrast, multifocal motor neuropathy (MMN) is
    an immune-mediated demyelinating neuropathy characterized clinically by asymmetric weakness and atrophy, typically in the distribution of individual peripheral nerves.23 MMN is often misdiagnosed as
    amyotrophic lateral sclerosis (ALS).24 Weakness in patients with MMN occurs in the distribution of individual peripheral nerves, whereas in ALS the weakness is
    in distribution of myotomes. MMN has a much lower
    incidence than ALS. MMN has a male predominance
    (male-to-female ratio of approximately 3:1) and an age
    of symptom onset usually ranging from the second to
    the eighth decades of life, with most occurring in the
    fifth decade of life. Onset in childhood is rare. Focal
    muscle weakness accompanied by cramps and fasciculations is usually first noted in the distal arms; however,

    2011 American Academy of Orthopaedic Surgeons

    Chapter 19: Disorders of the Nervous System

    Neuropathies Associated With Infections


    Nerves are commonly involved in human infectious disorders. In certain conditions, nerve involvement may
    occur secondary to direct invasion. For instance, both
    the herpes simplex virus and the HIV virus are neurotrophic and preferentially attack peripheral nerves. In
    other infectious conditions, nerve involvement may occur secondary to infection of the surrounding tissues or
    due to complications of treatment such as with leprosy.

    Leprosy
    Leprosy is caused by infection with the acid-fast bacteria Mycobacterium leprae. Leprosy is the most common cause of peripheral neuropathy in Southeast Asia,
    Africa, and South America. This infection has a spectrum of clinical manifestations ranging from tuberculoid leprosy to borderline leprosy to lepromatous leprosy. The clinical manifestations of the disease are
    determined by the immunologic response of the host to
    the infection. In tuberculoid leprosy, the cell-mediated
    immune response is intact, with focal, circumscribed inflammatory responses to the bacteria within the affected areas of the skin and nerves. The resulting skin
    lesions appear as well-defined, scattered, hypopig-

    2011 American Academy of Orthopaedic Surgeons

    mented patches and plaques with raised, erythematous


    borders. Cutaneous nerves are often affected, resulting
    in a loss of sensation in the center of the skin lesions.
    Cooler regions of the body such as the face and limbs
    are more susceptible than warmer regions such as the
    groin or axilla.28 The most common sites of involvement are the ulnar nerve at the medial epicondyle, the
    median nerve at the distal forearm, the peroneal nerve
    at the fibular head, the sural nerve, the greater auricular nerve, and the superficial radial nerve at the wrist.
    The nerves become thickened and encased with granulomas, leading to mononeuropathy or mononeuropathy
    multiplex.
    In lepromatous leprosy, cell-mediated immunity is
    severely impaired, leading to extensive infiltration of
    the bacilli and hematogenous dissemination, which
    produces confluent and symmetric areas of rash, anesthesia, and anhidrosis. The clinical manifestations tend
    to be more severe in the lepromatous subtype.29 As in
    the tuberculoid form, there is a predilection for involvement of cooler regions of the body. Infiltration of the
    organism in the face leads to the loss of eyebrows and
    eyelashes and exaggeration of the natural skin folds,
    leading to the so-called leonine facies. Superficial cutaneous nerves of the ears and distal limbs are also commonly affected. A slowly progressive symmetric sensorimotor polyneuropathy gradually develops because of
    widespread invasion of the bacilli into the epineurium,
    perineurium, and endoneurium. Distal extremity weakness may be seen, but large sensory fiber modalities and
    muscle stretch reflexes are relatively spared. Involvement of nerve trunks leads to superimposed mononeuropathies, including facial neuropathy.
    Leprosy is usually diagnosed with a skin lesion biopsy and the Fite acid-fast staining method. Nerve biopsies also can be diagnostic, particularly when there
    are no apparent skin lesions. The immune response of
    the host to the bacilli determines the histopathology.
    The tuberculoid form is characterized by granulomas
    formed by macrophages and T helper 1 lymphocytes
    caseation may be present, with typical lesions extending throughout the dermis. Importantly, bacilli are not
    seen. In contrast, in lepromatous leprosy, a large number of infiltrating bacilli, T helper 2 lymphocytes, and
    organism-laden foamy macrophages with minimal
    granulomatous infiltration are evident. Borderline leprosy can have histologic features of both tuberculoid
    and lepromatous leprosy. Polymerase chain reaction
    also may be used in making the diagnosis.
    Patients are generally treated for 2 years with multiple pharmacologic agents, including dapsone, rifampin,
    and clofazimine. Other medications include thalidomide, perfloxacin, ofloxacin, sparfloxacin, minocycline, and clarithromycin. Treatment is sometimes complicated by the so-called reversal reaction, particularly
    in patients with borderline leprosy. This reversal reaction can occur at any time during treatment and develops because of a shift in the disease phenotype to the
    tuberculoid end of the spectrum with an increase in cellular immunity during treatment. The cellular response
    is upregulated, as evidenced by an increased release of

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    weakness can initially develop in the legs. Most patients present with intrinsic hand weakness, wrist drop,
    or foot drop. The onset is usually insidious, and the
    weakness typically progresses over the course of several
    years to involve other limbs. As with CIDP, treatment
    of MMN can be complicated with relapses, and often
    patients become unresponsive to previously effective
    treatment.
    As the name implies, MMN involves two or more
    motor nerves. However, MMN usually starts as a
    mononeuropathy. Cases of monofocal motor neuropathy may represent the early presentation of MMN and
    should be treated as such. The electrophysiologic hallmark of MMN is a persistent conduction block in motor nerves in segments not usually associated with compression or entrapment.25 Sensory nerve biopsies in
    MMN are usually normal, although a slight reduction
    in myelinated fibers or axonal degeneration has been
    seen. Because sensory nerves are spared, the autoimmune attack is likely directed against an antigen that is
    relatively specific for the motor nerve. Although ganglioside antibodies are common, the pathogenic role for
    these antibodies is not known.
    Unlike in patients with CIDP, patients with MMN
    generally do not respond to corticosteroids or plasmapheresis. MMN is typically responsive to intravenous
    immunoglobulins.26 Rituximab also has recently been
    used to treat immune-mediated neuropathies, including
    MMN. Rituximab is a monoclonal antibody that binds
    to the CD20 antigen on normal and malignant B lymphocytes, destroying these cells. It is approved to treat
    B cell lymphoma and reduces peripheral B lymphocyte
    counts by 90% within 3 days.27

    233

    Section 2: Systemic Disorders

    tumor necrosis factor-, gamma-interferon, and


    interleukin-2 with new granuloma formation. This can
    result in an exacerbation of the rash and the neuropathy as well as the appearance of new lesions. High-dose
    corticosteroids blunt this adverse reaction and may
    even be used prophylactically in high-risk patients at
    the onset of treatment. Preventing leprosy is of primary
    importance. It is recommended that children exposed
    to leprosy in the household be prophylactically treated
    with rifampin daily for 6 months.

    Lyme Disease

    2: Systemic Disorders

    Lyme disease is caused by infection with Borrelia burgdorferi, a spirochete, transmitted by ticks. The deer
    tick, Ixodes dammini, is usually responsible for the disease. The ticks acquire the spirochetes by feeding on an
    infected host (such as deer) and then transmit the spirochetes to the next hosts (such as humans) at a later
    feed. It takes approximately 12 to 24 hours of tick attachment to transfer the spirochetes to the next host.
    There are three recognized stages of Lyme disease: (1)
    early infection with localized erythema migrans, (2) disseminated infection, and (3) late-stage infection.
    Neurologic complications may develop during the
    second and third stages of infection. Facial neuropathy
    is most common and is bilateral in approximately 50%
    of patients, which is rare in the differential diagnosis of
    Bell palsy. Involvement of nerves is frequently asymmetric. The presentation with a polyradiculoneuropathy may resemble Guillain-Barr syndrome.30 Approximately 50% of patients have numbness, paresthesia,
    weakness, and cramps in the distal extremities; proprioception and vibration are reduced along with muscle
    stretch reflexes.
    Immunofluorescent or enzyme-linked immunoabsorbent assay may detect antibodies directed against the
    spirochete. Because false-positive reactions are common, Western blot analysis should be performed to
    confirm a positive enzyme-linked immunoabsorbent assay. Examination of the cerebrospinal fluid should
    show lymphocytic pleocytosis and increased protein in
    patients with polyradiculitis, cranial neuropathies, and
    CNS involvement.31
    The recommended treatment of facial nerve palsies
    in adults is the combination of amoxicillin plus
    probenecid for 2 to 4 weeks. Patients who are allergic
    to penicillin can be treated with doxycycline for 2 to 4
    weeks. Adult patients with other types of peripheral
    neuropathy are treated with intravenous penicillin or
    ceftriaxone for 2 to 4 weeks. Those allergic to penicillin
    should be treated with doxycycline for 30 days.

    Neuromuscular Disorders With Orthopaedic


    Symptomatology
    Orthopaedic involvement is common in other neuromuscular conditions, including muscular dystrophy,
    Charcot-Marie-Tooth (CMT) disease, ALS, and Friedreich ataxia. See chapter 63 for additional information
    234

    Orthopaedic Knowledge Update 10

    on neuromuscular disorders. Although a detailed description of muscular dystrophies is beyond the scope
    of this chapter, the most common form is Duchenne
    muscular dystrophy, which is an X-linked muscular
    dystrophy, and is invariably fatal. The disease occurs
    secondary to a mutation in the dystrophin gene and is
    characterized by progressive proximal muscle weakness. Achilles tendon contractures are common early in
    the disease with a progressive loss of ambulation occurring by 10 years of age. Once the children are
    wheelchair-bound, scoliosis ensues and contributes to
    progressive respiratory insufficiency. If conservative
    management including physical therapy and orthosis
    fail to correct the contracture, surgical correction may
    be required to prevent loss of ambulation. Surgical correction of thoracic spine scoliosis is also recommended
    if the degree of scoliosis exceeds 40 and if there is evidence for progressive respiratory insufficiency.
    Another neuromuscular disorder with prominent
    scoliosis is Friedreich ataxia, an autosomal recessive
    disorder of the spinal cord, which predominantly affects the dorsal columns, resulting in progressive sensory ataxia. Scoliosis occurs early and often is disproportionate to the amount of neurologic dysfunction. As
    in Duchenne muscular dystrophy, scoliosis results in
    progressive respiratory dysfunction, and thus eventually needs surgical correction.

    Charcot-Marie-Tooth Disease
    Hereditary neuropathies may account for as many as
    50% of previously undiagnosed peripheral neuropathies referred for treatment to large neuromuscular centers. CMT disease is the most common type of hereditary neuropathy with the pathology focused on the
    Schwann cell. Rather than just one disease, CMT is a
    syndrome of several genetically distinct disorders.32 The
    various subtypes of CMT are classified according to the
    nerve conduction velocities and presumed pathology
    (demyelinating or axonal), mode of inheritance (autosomal dominant or X-linked), age of onset (infancy,
    childhood, or adulthood), and the specific mutated
    genes. Type 1 CMT is the most common form, with individuals usually presenting with distal leg weakness in
    the first to third decades of life. There is an early predilection for the anterior compartment (peroneal muscle group), which results in progressive foot drop. This
    leads to poor clearance of the toes when walking, particularly on uneven surfaces. Patients with type 1 CMT
    often report frequent tripping, falling, and recurrent
    ankle sprains. Affected patients generally do not report
    numbness or tingling, which can be helpful in distinguishing CMT from acquired forms of neuropathy.
    Although patients with type 1 CMT usually do not
    report sensory loss, reduced sensation in all modalities
    is apparent on examination. Muscle stretch reflexes are
    unobtainable or reduced throughout the body. There is
    often atrophy of the muscles below the knee (particularly in the anterior compartment), leading to the socalled inverted champagne bottle legs. However, in rare
    instances, patients have asymmetric pseudohypertrophy

    2011 American Academy of Orthopaedic Surgeons

    Chapter 19: Disorders of the Nervous System

    Amyotrophic Lateral Sclerosis


    Motor neuron diseases are categorized by its pathologic
    affinity for the voluntary motor system including primarily the anterior horn cells of the spinal cord, certain

    2011 American Academy of Orthopaedic Surgeons

    Figure 3

    Photograph of the foot of a patient with CMT


    disease, showing typical features of pes cavus,
    hammer toes, and peroneal muscular atrophy.

    motor cranial nerve nuclei, and corticospinal/bulbar


    tracts. ALS, also known as Lou Gehrigs disease, is the
    most notorious of these disorders.36 As in other neurodegenerative conditions, the clinical course of ALS is
    one of inexorable progression.37 The cause is unknown
    except in the small proportion of patients who have familial forms of the disease.
    The initial clinical features of ALS may be quite diverse. Typically, patients seek medical care reporting
    painless muscle weakness and atrophy.7 These signs are
    frequently asymmetric and sometimes monomelic at the
    onset. The initial deficits may be restricted in distribution but involve more than a single nerve or nerve root.
    In instances in which patients do not seek early medical
    attention or if physicians do not recognize the significance of the symptoms, patients may not be seen until
    their disorder is fairly advanced (Figure 4). Less commonly, the initial symptoms may include impaired
    speech or swallowing, reduced head control, or disordered breathing.38 Fasciculations are usually first recognized by the examining physician rather than by the patient, but may occasionally be the initial manifestation
    of the disease, particularly in those who have a preexisting awareness of their significance.37 Fasciculations,
    in the presence of weakness, particularly if multifocal
    and continuous, strongly support the diagnosis of a
    motor neuron disorder.
    Fasciculations in the absence of muscle weakness
    and EMG abnormalities, particularly if restricted in
    their distribution, are typically benign. Conversely, the
    absence of fasciculations in patients with painless
    weakness does not preclude the diagnosis of ALS, par-

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    of the calves. Most will have pes cavus, equinovarus, or


    hammer toe deformities (Figure 3), which lead to aching in the feet. Rather than having a heel strike during
    ambulation, affected people land flatfooted or on their
    toes, and thus use a steppage gait to help prevent the
    toes from catching on the ground. Approximately two
    thirds of patients with type 1 CMT also have distal
    weakness and atrophy of the arms. The most severely
    affected patients may have clawhand deformities.
    Even if there is no family history of CMT, family
    members of patients with possible CMT should be examined to determine if other members have features of
    the neuropathy. This information can be important in
    clarifying a diagnosis and in referral for appropriate genetic counseling. In addition to genetic testing, nerve
    conduction studies are the most important laboratory
    tests for evaluating patients with suspected CMT disease. The nerve conduction studies are invaluable in determining if the patient has an axonal or demyelinating
    neuropathy and in determining if a demyelinating neuropathy is uniform or multifocal, which is useful in distinguishing CMT from chronic inflammatory demyelinating polyneuropathy.33 Although nerve biopsies on
    patients with suspected type 1 CMT are not routinely
    performed, a nerve biopsy will be strikingly abnormal.
    The enlarged gross appearance of the peripheral nerves
    led to the early designation of type 1 CMT as a hypertrophic neuropathy.
    Type 1 CMT is a genetically heterogeneic disorder.
    Approximately 85% of patients with CMT type 1A
    have a 1.5-megabase duplication within chromosome
    17p11.2-12 in the gene for peripheral myelin protein
    22.34 These patients carry three copies of the PMP22
    gene rather than two. In contrast, inheritance of the
    chromosome with the deleted segment results in affected individuals having only one copy of the PMP-22
    gene and leads to hereditary neuropathy with liability
    to pressure palsies .35 Although these mutations are inherited in an autosomal dominant fashion, de novo
    mutations can occur. CMT type 1A is likely related to a
    toxic gain of function. The exact function of peripheral
    myelin protein 22 in the peripheral nerves is not
    known, but it may be important in maintaining the
    structural integrity of myelin, acting as an adhesion
    molecule, or regulating the cell cycle.
    There is currently no cure for CMT disease. Orthotics play an important role in the rehabilitation of patients; however, proper attention is required to monitor
    patients for pressure sores. Tendon transfer and muscle
    transfers are often done to improve function, but there
    are no systemic studies showing their efficacy. Ankle fusion surgery to treat severe foot drop is not currently
    favored. A trial of supplementation with ascorbic acid
    is currently under way to determine if this vitamin will
    improve neural function in patients with CMT.

    235

    Section 2: Systemic Disorders

    Figure 4

    Photographs of the hand and tongue of a patient with ALS. A, Atrophy of the intrinsic muscles of the hand along
    with fasciculations and cramps are often the most common manifestation of ALS; these symptoms may be confused with cervical radiculopathy. B, Tongue atrophy and fasciculations are common in ALS and often help in making the diagnosis. (Reproduced with permission from Amato AA, Russell JA: Neuromuscular Disorders. New York,
    NY, McGraw-Hill, 2008.)

    2: Systemic Disorders

    ticularly in patients with considerable subcutaneous tissue. An increased frequency of muscle cramping is
    common, which is often elicited during manual muscle
    testing.
    The clinical diagnosis of ALS is dependent on the
    demonstration of lower motor neuron (LMN) and upper motor neuron (UMN) signs, which progress both
    within and between different body regions.39 The most
    common ALS presentation is a patient with a combination of UMN and LMN features, limited initially in distribution, with the LMN findings typically dominating.37 The initial involvement is typically distally
    located in a hand or a foot. Initial weakness may occur
    in proximal muscles as well. A definite diagnosis cannot be made until these combined UMN and LMN
    signs spread over a period of months, both within and
    outside the initially affected body part. A definite diagnosis of ALS is uncommon at the time of the initial examination. However, a combination of UMN and
    LMN signs in the same segment or a single extremity,
    in the absence of pain or sensory symptoms, is highly
    indicative of ALS. Despite the absence of a viable differential diagnosis, many patients have unnecessary surgical procedures for presumed cervical myelopathy or
    radiculopathy. Patients are referred for further evaluation by a neurologist only after clear progression and
    worsening of their symptoms. Similarly, weakness of
    the neck extensors and the resultant neck ptosis (neck
    drop) is quite common and is often mistakenly believed
    to be related to cervical stenosis.
    With the exception of DNA mutational analysis in a
    patient with a mutation of the SOD1 gene, there are no
    laboratory tests that currently confirm the diagnosis of
    sporadic ALS or most of the familial ALS genotypes.40
    There are laboratory tests, such as those that measure
    ventilatory function, forced vital capacity, and maximal
    expiratory and inspiratory pressure, that are used to
    236

    Orthopaedic Knowledge Update 10

    monitor the course of the disease and to aid in management decisions. Although these tests may aid in the initial diagnosis, their primary purpose is to monitor
    progress, predict a prognosis, and aid in medical decision making. There are two primary pathologic features of ALS: (1) degeneration with the loss of myelinated fibers occurs in the corticospinal and
    corticobulbar pathways and (2) a loss of motor neurons within the anterior horns of the spinal cord and
    many motor cranial nerve nuclei.
    Currently, there are no effective treatments that can
    reverse or arrest disease progression in patients with
    ALS.41 As a result, the major goals in managing motor
    neuron diseases are to slow disease progression to the
    extent possible and maintain independent patient function, safety, and comfort. The care of patients with ALS
    and their families involves education, counseling, and
    symptom management. Two interventions that are often met with resistance by patients are percutaneous
    gastrostomy and noninvasive positive pressure support.
    In view of this, it may be prudent to introduce these
    concepts before the point in the patients illness when
    these interventions are really needed. Both should be
    introduced with the idea that they will improve the
    quality of life rather than the duration of life, even
    though the latter may be achieved to a certain extent as
    well. Optimal management of patients with ALS and
    their families requires extensive effort and resources
    that undoubtedly surpass the capabilities of any single
    health care worker.41

    Summary
    It is important to have a working knowledge of neurologic conditions that are routinely encountered in orthopaedic practice. Misdiagnosis may delay treatment

    2011 American Academy of Orthopaedic Surgeons

    Chapter 19: Disorders of the Nervous System

    and result in unnecessary testing and suffering. With


    the assistance and early input from neurologists, treatment may begin early. Furthermore, orthopaedic interventions such as contracture and scoliosis correction
    may be required to improve the quality of life for these
    challenging patients.

    Amato A, Russell J: Neuromuscular Disorders. New


    York, NY, McGraw-Hill, 2008.
    This book discusses the evaluation and management of
    neuromuscular disease.

    8.

    Strandberg EJ, Mozaffar T, Gupta R: The role of neurodiagnostic studies in nerve injuries and other orthopedic disorders. J Hand Surg Am 2007;32(8):1280-1290.
    This review article provides a more comprehensive discussion of electrophysiology for the orthopaedic surgeon.

    9.

    Gupta R, Mozaffar T: Neuromuscular diseases, in


    Buckwalter J, Einhorn T, OKeefe R, eds: Orthopaedic
    Basic Science: Biology and Biomechanics of the Musculoskeletal System, ed 3. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2007, pp 427-443.
    The authors discuss common neuromuscular conditions,
    the pathophysioogy of nerve injury, and factors influencing nerve regeneration.

    10.

    Chaudhry V, Cornblath DR: Wallerian degeneration in


    human nerves: Serial electrophysiological studies. Muscle Nerve 1992;15(6):687-693.

    11.

    Podwall D, Gooch C: Diabetic neuropathy: Clinical features, etiology, and therapy. Curr Neurol Neurosci Rep
    2004;4(1):55-61.

    12.

    Partanen J, Niskanen L, Lehtinen J, Mervaala E, Siitonen O, Uusitupa M: Natural history of peripheral


    neuropathy in patients with non-insulin-dependent diabetes mellitus. N Engl J Med 1995;333(2):89-94.

    13.

    Dyck PJ, Kratz KM, Karnes JL, et al: The prevalence by


    staged severity of various types of diabetic neuropathy,
    retinopathy, and nephropathy in a population-based cohort: The Rochester Diabetic Neuropathy Study. Neurology 1993;43(4):817-824.

    14.

    Dyck PJ, Karnes JL, OBrien PC, Litchy WJ, Low PA,
    Melton LJ III: The Rochester Diabetic Neuropathy
    Study: Reassessment of tests and criteria for diagnosis
    and staged severity. Neurology 1992;42(6):1164-1170.

    15.

    Polydefkis M, Griffin JW, McArthur J: New insights


    into diabetic polyneuropathy. JAMA 2003;290(10):
    1371-1376.

    16.

    The Diabetes Control and Complications Trial Research


    Group: The effect of intensive treatment of diabetes on
    the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J
    Med 1993;329(14):977-986.

    17.

    Sima AA: New insights into the metabolic and molecular basis for diabetic neuropathy. Cell Mol Life Sci
    2003;60(11):2445-2464.

    18.

    Kennedy WR, Navarro X, Goetz FC, Sutherland DE,


    Najarian JS: Effects of pancreatic transplantation on
    diabetic neuropathy. N Engl J Med 1990;322(15):
    1031-1037.

    Annotated References
    1.

    Mozaffar T, Strandberg E, Abe K, Hilgenberg LG,


    Smith MA, Gupta R: Neuromuscular junction integrity
    after chronic nerve compression injury. J Orthop Res
    2009;27(1):114-119.
    Unlike acute injuries, the neuromuscular junction is preserved with chronic nerve compression injuries even
    later after disease progression.

    2.

    Gray M, Palispis W, Popovich PG, van Rooijen N,


    Gupta R: Macrophage depletion alters the blood-nerve
    barrier without affecting Schwann cell function after
    neural injury. J Neurosci Res 2007;85(4):766-777.
    Macrophage recruitment occurs with all peripheral
    nerve injuries. As macrophages produce Schwann cell
    mitogens, they are responsible in part for the increase in
    number of Schwann cells after acute nerve injuries. This
    is not true for chronic nerve injuries where hematogenously derived macrophages are responsible for the altered blood-nerve barrier but not the ensuing Schwann
    cell proliferation.

    3.

    4.

    Frieboes LR, Gupta R: An in vitro traumatic model to


    evaluate the response of myelinated cultures to sustained hydrostatic compression injury. J Neurotrauma
    2009;26(12):2245-2256.
    Schwann cells are mechanosensitive and have the ability
    to respond to mechanical stimuli such as hydrostatic
    compression.
    Chao T, Pham K, Steward O, Gupta R: Chronic nerve
    compression injury induces a phenotypic switch of neurons within the dorsal root ganglia. J Comp Neurol
    2008;506(2):180-193.
    Chronic nerve compression injury preferentially affects
    small to medium size neurons. This preferential neuronal response to injury may explain why there is not a
    decrease in nerve conduction velocity early in the disease process.

    5.

    Pham K, Nassiri N, Gupta R: c-Jun, krox-20, and integrin beta4 expression following chronic nerve compression injury. Neurosci Lett 2009;465(2):194-198.
    Chronic nerve injury induces a demyelination and remyelination process. C-jun and Krox-20 are critical transcriptional factors in these processes. This study was
    one of the first to demonstrate an integrin response to
    compression injuries.

    6.

    Gilchrist JM, Sachs GM: Electrodiagnostic studies in the


    management and prognosis of neuromuscular disorders.
    Muscle Nerve 2004;29(2):165-190.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    7.

    237

    Section 2: Systemic Disorders

    19.

    Ametov AS, Barinov A, Dyck PJ, et al; SYDNEY Trial


    Study Group: The sensory symptoms of diabetic polyneuropathy are improved with alpha-lipoic acid: the
    SYDNEY trial. Diabetes Care 2003;26(3):770-776.

    20.

    Thomas PK, Lascelles RG, Hallpike JF, Hewer RL: Recurrent and chronic relapsing Guillain-Barr polyneuritis. Brain 1969;92(3):589-606.

    21.

    Kller H, Kieseier BC, Jander S, Hartung H-P: Chronic


    inflammatory demyelinating polyneuropathy. N Engl J
    Med 2005;352(13):1343-1356.

    22.

    Hughes RA, Bouche P, Cornblath DR, et al: European


    Federation of Neurological Societies/Peripheral Nerve
    Society guideline on management of chronic inflammatory demyelinating polyradiculoneuropathy: Report of a
    joint task force of the European Federation of Neurological Societies and the Peripheral Nerve Society. Eur J
    Neurol 2006;13(4):326-332.

    2: Systemic Disorders

    23.

    238

    Pestronk A, Cornblath DR, Ilyas AA, et al: A treatable


    multifocal motor neuropathy with antibodies to GM1
    ganglioside. Ann Neurol 1988;24(1):73-78.

    24.

    Parry GJ, Clarke S: Multifocal acquired demyelinating


    neuropathy masquerading as motor neuron disease.
    Muscle Nerve 1988;11(2):103-107.

    25.

    Olney RK, Lewis RA, Putnam TD, Campellone JV Jr;


    American Association of Electrodiagnostic Medicine:
    Consensus criteria for the diagnosis of multifocal motor
    neuropathy. Muscle Nerve 2003;27(1):117-121.

    26.

    Nobile-Orazio E, Cappellari A, Meucci N, et al: Multifocal motor neuropathy: Clinical and immunological
    features and response to IVIg in relation to the presence
    and degree of motor conduction block. J Neurol Neurosurg Psychiatry 2002;72(6):761-766.

    27.

    Regg SJ, Fuhr P, Steck AJ: Rituximab stabilizes multifocal motor neuropathy increasingly less responsive to
    IVIg. Neurology 2004;63(11):2178-2179.

    28.

    Ooi WW, Srinivasan J: Leprosy and the peripheral nervous system: basic and clinical aspects. Muscle Nerve
    2004;30(4):393-409.

    29.

    Jardim MR, Chimelli L, Faria SC, et al: Clinical, electroneuromyographic and morphological studies of pure
    neural leprosy in a Brazilian referral centre. Lepr Rev
    2004;75(3):242-253.

    30.

    Halperin J, Luft BJ, Volkman DJ, Dattwyler RJ: Lyme


    neuroborreliosis. Peripheral nervous system manifestations. Brain 1990;113(Pt 4):1207-1221.

    31.

    Logigian EL, Steere AC: Clinical and electrophysiologic


    findings in chronic neuropathy of Lyme disease. Neurology 1992;42(2):303-311.

    Orthopaedic Knowledge Update 10

    32.

    Harding AE, Thomas PK: The clinical features of hereditary motor and sensory neuropathy types I and II.
    Brain 1980;103(2):259-280.

    33.

    Lewis RA, Sumner AJ, Shy ME: Electrophysiological


    features of inherited demyelinating neuropathies: A reappraisal in the era of molecular diagnosis. Muscle
    Nerve 2000;23(10):1472-1487.

    34.

    Roa B, Garcia C, Suter U, et al: Charcot-Marie-Tooth


    disease type 1A: Association with point mutation in the
    PMP22 gene . N Engl J Med 1993;329(2):96-101.

    35.

    Amato AA, Gronseth GS, Callerame KJ, Kagan-Hallet


    KS, Bryan WW, Barohn RJ: Tomaculous neuropathy: A
    clinical and electrophysiological study in patients with
    and without 1.5-Mb deletions in chromosome 17p11.2.
    Muscle Nerve 1996;19(1):16-22.

    36.

    Swash M, Desai J: Motor neuron disease: Classification


    and nomenclature. Amyotroph Lateral Scler Other Motor Neuron Disord 2000;1(2):105-112.

    37.

    Traynor BJ, Codd MB, Corr B, Forde C, Frost E, Hardiman OM: Clinical features of amyotrophic lateral sclerosis according to the El Escorial and Airlie House diagnostic criteria: A population-based study. Arch Neurol
    2000;57(8):1171-1176.

    38.

    Chen R, GrandMaison F, Strong MJ, Ramsay DA, Bolton CF: Motor neuron disease presenting as acute respiratory failure: a clinical and pathological study. J Neurol Neurosurg Psychiatry 1996;60(4):455-458.

    39.

    Tartaglia MC, Rowe A, Findlater K, Orange JB, Grace


    G, Strong MJ: Differentiation between primary lateral
    sclerosis and amyotrophic lateral sclerosis: Examination
    of symptoms and signs at disease onset and during
    follow-up. Arch Neurol 2007;64(2):232-236.
    This article provides a guide for the clinician as to how
    to discriminate between different motor neuron disorders.

    40. Siddique T, Figlewicz DA, Pericak-Vance MA, et al:


    Linkage of a gene causing familial amyotrophic lateral
    sclerosis to chromosome 21 and evidence of geneticlocus heterogeneity. N Engl J Med 1991;324(20):13811384.
    41.

    Miller RG, Jackson CE, Kasarskis EJ, et al; Quality


    Standards Subcommittee of the American Academy of
    Neurology: Practice parameter update: The care of the
    patient with amyotrophic lateral sclerosis: drug, nutritional, and respiratory therapies (an evidence-based review). Report of the Quality Standards Subcommittee of
    the American Academy of Neurology. Neurology 2009;
    73(15):1218-1226.
    Evidence on the management of patients with ALS was
    systematically reviewed. Topics studied included slowing disease progression, nutrition, and respiratory management. Several recommendations were made.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 20

    Musculoskeletal Infection
    Edward J. McPherson, MD, FACS

    Christopher L. Peters, MD

    Introduction
    Infections involving the musculoskeletal system can
    ravage soft tissue and bone, resulting in significant destruction of an extremity. The lingering effects of an orthopaedic infection can cause significant residual pain
    and deformity. Despite the expanding growth of antibiotics and antibiotic classes, musculoskeletal infections
    remain problematic. Treatment of musculoskeletal infections imposes a significant economic strain to the
    health care system. In addition, the fear factor highlighted by multidrug-resistant bacterial infections has
    increased the anxiety level of the general population.
    This fear has created a perception that hospitalization
    increases the risk of serious health consequences, including death.

    Infection Pathomechanics in the Hospital Setting

    Dr. McPherson or an immediate family member has received royalties from Biomet and serves as an unpaid
    consultant to Biomet. Dr. Peters or an immediate family
    member has received royalties from Biomet; serves as an
    unpaid consultant to Biomet; and has received research
    or institutional support from Biomet.

    2011 American Academy of Orthopaedic Surgeons

    2: Systemic Disorders

    Most postoperative musculoskeletal infections occur


    via bacterial inoculation at the time of surgery. Some
    postoperative infections can occur as a result of bacterial contamination of the wound via open pathways to
    the deep tissue layers. Understanding the pathomechanics of bacterial contamination of a surgical wound is
    paramount in training operating room staff in appropriate best care standards to minimize bacterial inoculation risk. The Venn diagram (Figure 1) depicts the
    general parameters involved in eliciting a musculoskeletal infection. In the Venn diagram, a surgical infection
    occurs when bacteria of sufficient quantity are able to
    enter the human host, sustain their presence, replicate,
    and liberate toxin to cause damage to the host. The exposure risk is the open surgical wound itself. Bacteria
    are delivered to the open wound, and the open wound
    provides the surface area for bacterial adherence. The
    host can thwart the bacterial inoculation via its innate
    immune system. The human skin serves as the outer
    barrier to bacterial penetration. An intact and healthy

    skin layer prevents further bacterial introduction into


    the deep host tissue layers. For bacteria, virulence in
    the orthopaedic realm relates to a bacterias ability to
    attach, reproduce, and subsequently damage the host
    (for example, human host) tissue. The factors of bacterial adherence, reproduction rates, and toxin production are genetically determined.
    The operating room personnel are the primary culprits in providing the bacterial load in the operating
    room. Traditionally, wound contamination has been
    thought to be the result of direct seeding from nasopharyngeal fallout. The ecologic niche for Staphylococcus aureus in humans is the anterior nares, where S aureus can be indentified most consistently in humans.
    However, the mechanism of operating room wound
    contamination is more complex than just nasopharyngeal fallout. Current theory of operating room wound
    contamination will be discussed in subsequent paragraphs. The function of the host immunity plays a sig-

    Figure 1

    Venn diagram depicting the three major factors


    that interact to cause a musculoskeletal infection. The bacterial quantity is dependent upon
    delivery of bacteria to the host. Virulence is genetically predetermined. The environmental exposure includes the size of the surgical wound
    and the time the wound is exposed. The role of
    human host defense against microorganisms is
    the final key factor in infection pathogenesis.
    Local defense (that is, skin integrity) combined
    with human systemic immune response both
    determine whether contamination proceeds to
    colonization and overt infection. The relative
    contribution from each circle can grow or shrink
    according to each individual clinical scenario.

    Orthopaedic Knowledge Update 10

    239

    Section 2: Systemic Disorders

    Figure 2

    Diagrammatic scheme of vertical laminar flow in


    the operating room. Filtered laminar airflow
    exits the ceiling over the patient. Air return is
    located at the periphery of the room. Plexiglas
    shields can be lowered into position after the
    surgical team is in position. This will further reduce any potential vortex flow into the wound
    area.

    nificant role by determining whether wound contamination proceeds to colonization and subsequent
    infection. By recognizing weak immune hosts, the surgeon can use measures to help mitigate the risk of
    wound infection.

    Operating Room

    2: Systemic Disorders

    People inside the hospital are the source of the bacterial


    load delivered to a wound in the operating room and
    hospital setting. Bacteria are shed from the external
    body skin of each person at various rates.1 The rate of
    shedding is genetically predetermined. Shedding from
    the human body typically is in the range of 102 to 104
    bacteria per minute. High-rate shedders can release
    greater than 104 bacteria per minute. Bacteria that are
    shed from human skin attach to fomites, any inanimate
    object or substance capable of carrying infectious organisms. In the hospital setting, typical fomites include
    stethoscopes, ties, shirt sleeves, bed handrails, and
    doorknobs.2 However, the more significant fomites are
    microscopic. Small pieces of skin detritus also serve as
    fomites. These microscopic particles have a large surface area and can float within the air. When bacteria
    are shed from the human body, they are attached to microscopic skin-derived fomites.
    In the operating room, the sum total bacterial load
    available for delivery is conceptually represented by the
    following formula:

    TE = P(SRP) + A(SRA) + B(SRB) + C(SRC)... + X(SRX)


    TE = total bacterial load exposure to patient in operating
    room (OR);

    240

    SR= shedding rate

    P = patient

    A = OR person A

    B = OR person B

    C = OR person C

    X = OR person X

    Orthopaedic Knowledge Update 10

    The number of personnel in the operating room suite


    has a significant effect on bacterial delivery into a surgical wound. The more health care personnel in the
    room, the greater number of bacteria available to potentially inoculate the wound area.
    Operating room dynamics also play an important
    role in bacterial delivery into the surgical wound and
    onto operating room equipment. Movement of a person through a room generates turbulent airflow. Pressure waves of air and vortices (whirlwind circulation)
    are generated in front of and behind the moving person, respectively. In addition, the mere opening and
    closing of doors and movement of equipment creates
    wind vortices.3 All of these movements create currents
    whereby bacteria (attached to microscopic fomites) are
    circulated throughout the room. With continued movement, bacteria can eventually be deposited within the
    wound and onto operating room equipment. Minimization of movement of operating room personnel will
    curtail vortex airflow. It is important that health care
    personnel understand the importance of making all
    movements within the operating room succinct and efficient. The surgeon and all health care personnel
    should envision themselves as working in a bacterial
    nebula. The denser the human interaction, the higher
    the bacterial concentration within the nebula. This increases the chance of bacterial delivery to an open portal on the human body. By limiting the bacterial cloud
    concentration, rates of bacterial colonization can be
    significantly decreased.
    Elimination of bacteria is a key factor in thwarting
    bacterial wound contamination in the operating room.
    Two techniques to neutralize bacteria are mechanical
    filtration and ultraviolet light deactivation. Modern operating room suites have positive pressure flow filtration systems. The next level of filtration is laminar airflow systems, whereby concentrated positive pressure
    flow is directed across the room (horizontal laminar
    flow) or from a ceiling surface (vertical laminar flow).
    The return air within these systems is filtered with
    high-efficiency particulate air (HEPA) filters. HEPA filters significantly reduce the airborne particulate quantity within the room. Because health care personnel can
    stand in front of a horizontal laminar flow system, turbulent airflow around that person can create significant
    wind vortices that can deposit microscopic fomites into
    a surgical wound. It is preferable for vertical laminar
    airflow systems to be directly situated over the wound
    site. The minimization of wind vortices is enhanced in
    vertical laminar flow systems when Plexiglas shields are
    lowered into position around the table (Figure 2).
    The use of personal isolator suits (also called operating room space suits) to reduce the risk of musculoskeletal infection is controversial, although their use has resulted in a significant reduction in total hip infection
    rates. However, current personal isolator suits are different from what was used in the past. The early suits
    had an inflow and outflow tube that was connected to
    the surgeon. The exhaust side had a negative flow pressure, which removed a significant load of bacterial
    shedding from the person wearing the suit. The more

    2011 American Academy of Orthopaedic Surgeons

    Chapter 20: Musculoskeletal Infection

    Figure 3

    Schematic diagram illustrating strategic goals to reduce infection risk in the operating room (OR) when using medically implanted devices. A, When bacterial quantity is high, surgical time is long, and incision exposure is large, this
    risk for bacteria deposition into the wound area is increased. B, When bacterial quantity is low, surgical time is
    short, and incision exposure is small, the risk for bacteria deposition into the wound area is decreased.

    Hospital Floor
    Postoperative bacterial wound contamination can occur via direct contamination of an incision that has not
    yet been completely sealed off from the outer environment, or by hematogenous seeding of bacteria. Although wound inoculation on the hospital floor involves many variables, the same basic tenets similar to
    the operating room setting apply. First, patients are exposed to a bacterial load introduced by health care personnel and visitors inside the hospital; patients located
    nearby, either in the same room or adjacent rooms, also
    can contribute to the bacterial shedding load. Hospitalized patients often are immunologically challenged, and

    2011 American Academy of Orthopaedic Surgeons

    their intrinsic skin bacterial reservoir becomes populated with resistant bacteria. These patients can shed
    resistant bacteria. On the hospital floor, the sum total
    bacterial load available for delivery to a patient is conceptually represented by the following formula:

    TE = Pi(SRi) + PA(SRA) + PB(SRB)... + Px(SRx) + HA(SRA) +


    HB(SRB)... + HX(SRX) + V1(SR1) + V2(SR2)... + VX(SRX)
    TE = total bacterial load exposure to patient in hospital bed
    Pi = index patient

    SR = shedding rate

    PA = adjacent patient A
    (same room)

    HA = health care person A

    PB = adjacent patient B

    HB = health care person B

    PX = adjacent patient X

    HX = health care person X

    VA = patient visitor 1

    VB = patient visitor 2

    2: Systemic Disorders

    personnel who used the personal isolator suits, the


    greater the reduction in bacterial load. The personal
    isolator suits in current use are not closed systems. Fans
    attached to the isolator system circulate operating
    room air into the isolator suit. Exhaled air is exhausted
    through a paper filter (not HEPA) around the head, or
    flows under the surgical gown to the floor. Therefore,
    turbulent flow around the bottom of the surgical gown
    or head is created. Furthermore, the total bacterial burden is unchanged. The lack of bacterial load reduction
    with the current personal isolator suits likely explains
    the variable reduction in infection rates when these current systems are studied as a method for infection control.
    The methods to reduce bacterial wound contamination in the operating room depend on many factors, including the physical limitations of the physical plant,
    the financial resources available for filtration equipment (and maintenance), and the skill level of operating
    room health care personnel. Figure 3 depicts strategic
    goals of the operating room team to reduce bacterial
    wound inoculation. Surgery involving implant insertion
    should be done by highly skilled health care personnel,
    and should be given priority to operating rooms that
    allow personnel to work efficiently and minimize bacterial loads. Best-care practices by operating room personnel to reduce bacterial load concentrations are listed
    in Table 1.

    VX = patient visitor X

    In general, the higher the density of the resident population (health care personnel+patients+visitors), the
    greater the overall bacterial load available within the
    physical plant. On the hospital floor, bacterial wound
    contamination occurs mainly via direct contact of the
    wound from health care personnel, the patient, or visitors who assist in patient care. The delivery of fomites
    to the wound site allows transmission of bacteria to the
    surgical area. All personnel involved with direct patient
    care should follow universal precautions (hand washing
    before patient contact and the wearing of gloves) to
    minimize wound contamination. In addition, measures
    to reduce overall bacterial load to the patient (such as
    single-patient rooms) can also help reduce the risk of
    fomite transfer to the wound. This is especially important in those patients receiving medically implanted devices.
    The dynamics of bacterial flow within the air on the
    hospital floor is far less controlled than that of the operating room environment. Turbulent vortices can al-

    Orthopaedic Knowledge Update 10

    241

    Section 2: Systemic Disorders

    Table 1

    2: Systemic Disorders

    Best-Care Practices in the Operating Room When Patients Are


    Receiving Implanted Medical Devices
    Technique

    Reason

    Least amount of OR personnel needed to efficiently complete


    surgical procedure in timely fashion
    Highly skilled OR personnel required

    Fewer personnel lowers number of bacterial shedders

    Restriction of OR personnel rotations during surgical procedure


    No mandatory breaks

    Limits turbulent airflow


    Lowers number of bacterial shedders
    Prevents disruption of surgical procedure and increases
    efficiency and reduces surgical time
    Limits opening/closing of doors

    Minimal traffic flow in OR theater

    Limits turbulent airflow

    Restriction of door openings

    Limits turbulent airflow


    Keeps nonessential OR personnel from entering room

    All necessary equipment and implant supplies are positioned in


    OR before start of procedure

    Reduces door openings


    Reduces turbulent airflow
    Increases OR efficiency and reduces surgical time

    Strict adherence to sterile technique


    Accepting environment of recognized contamination

    Reduced risk of wound contamination

    Complete change of surgical attire anytime personnel leave


    confines of OR suite

    Reduced fomite contamination from outside sources

    Restriction of unsterilized equipment applied to patient;


    for example, reusable tourniquets and Velcro safety straps

    Reduced fomite contamination from other patients who may


    have resistant bacteria

    Fresh surgical attire daily (including cloth surgical caps)

    Reduced fomite load from dirty attire


    Reduced fomite contamination from outside sources

    Unscrubbed personnel wash hands before entering OR room

    Reduced fomite contamination from outside sources and


    other patients

    Vigorous terminal cleaning of OR at end of day and after any


    potentially infected case
    Includes top side of OR lights and fixed equipment

    Reduced fomite contamination from other patients who may


    have resistant bacteria

    Culture surveillance of OR on regular basis

    Assesses quality of decontamination procedures


    Assesses for presence of resistant bacteria

    All OR personnel shower every morning before work

    Reduced fomite load brought to OR theater

    OR = operating room

    low microcurrents to flow into a patients room when


    the doors are open. The movement of equipment and
    the disruption of the local physical plant structures
    (when structural repairs are needed) create additional
    turbulent airflow. Furthermore, the increased fomite
    reservoirs on the hospital ward allow bacteria additional chances for patient inoculation.
    On the hospital floor, the bacterial elimination process is less robust than that of the operating room environment. Filtration systems are more dependent on
    the age of the physical plant and the ventilation
    schemes for each floor. The particulate quantity allowed in the air on the hospital floor is generally no
    better than any other office building. Best-care practices to reduce bacterial load concentrations and
    wound colonization on the hospital ward are listed in
    Table 2.
    242

    Orthopaedic Knowledge Update 10

    Bacteria Characteristics and Defense Mechanisms

    Biofilm
    Bacteria involved in musculoskeletal infections exist
    primarily in the human host as a biofilm, a phenotypic
    expression of a bacterial species representing a unique
    form of existence. The first evidence of a biofilm on a
    medically implanted device was presented in 1980, and
    biofilm (glycocalyx) associated with musculoskeletal infection was first described in 1984.4 It is estimated that
    500,000 people in the United States die as a result of
    biofilm-associated infections. The anticipated occurrence of biofilm infections on medically implanted devices is expected to rise in the next decade.
    All bacterial species, including many fungi, are capable of producing a biofilm. Bacteria can exist either in a
    planktonized state (similar to individual plankton that

    2011 American Academy of Orthopaedic Surgeons

    Chapter 20: Musculoskeletal Infection

    Table 2

    Postoperative Wound Care Measures to Reduce Wound Contamination


    Multilayered wound closure
    Especially avoid sutures that run from skin through to deep tissue layers; bacterial biofilm will track along sutures
    Single hospital rooms for patients receiving implanted medical devices
    Eliminates exposure to bacterial shedding from patients who may harbor resistant bacteria
    Modify anticoagulation technique when needed to minimize deep wound drainage
    Any conduit out is an open conduit for bacteria to enter
    Keep wounds dry with frequent dressing changes
    Bacteria on moist skin can exist deeper than on dry skin
    Clean surrounding incision edges at time of dressing change with bactericidal/static agent (that is, alcohol, betadine, soap and
    water)
    Positive airflow from patient room outward to floor
    Rigorous postdischarge decontamination of hospital rooms. Aggressive environmental ward cleaning when MRSA or other
    highly resistant bacteria are isolated
    Hospital screening of HCP and patients for highly resistant organisms when hospital related outbreaks are documented.
    HCP = health care personnel, MRSA = methicillin-resistant Staphylococcus aureus.

    2011 American Academy of Orthopaedic Surgeons

    Figure 4

    2: Systemic Disorders

    exist in the sea) or in a biofim state.5 A bacterial biofilm comprises bacterial cells and a hydrated extracellular matrix (ECM). The extracellular matrix is a polysaccharide coating made by bacteria that contains host
    proteins acquired by the bacterial network. The ECM
    holds the bacterial cells together, forming a collective
    colony, which in its mature form has a well-defined sophisticated architecture (Figure 4). Most of the biofilm
    is filled by the ECM. Depending on species, less than
    30% of the volume is filled by bacterial cells.6 The biofilm forms a base layer that allows adherence to the target interface. The outer layers form discrete structures
    such as columns and mushrooms. Streamers can form
    in the outer layers that may break off to infect contiguous areas or enter the bloodstream to seed distant
    sites hematogenously. Within the biofilm exists channels that provide access to environmental nutrients and
    also allow communication between each other via signaling molecules.7 In addition, bacteria communicate
    with each other in the biofilm with nanowires, which
    are small cellular connections between bacteria that allow direct cell-to-cell communication8 (Figure 5). Biofilms also form on human body tissues that are compromised. Examples of human tissue biofilm infections
    include chronic infections involving bone, inner ear,
    bladder, prostate, and lung.9
    A biofilm forms when the quantity of bacteria
    reaches a quorum, a genetically determined level.
    Lactone-derived molecules known as quorum-sensing
    molecules are produced by bacteria and are released
    into the extracellular environment. As bacteria adhere
    and complete their rate of exponential growth,
    quorum-sensing molecules are released. Once bacteria
    reach a quorum, the concentration of quorum-sensing
    molecules is high enough to trigger the phenotype expression of the biofilm state.10 The biofilm state represents a metamorphosis whereby all bacteria that exist
    within the biofilm state work as a collective.

    Diagrammatic depiction of a biofilm on a medically implanted device. The biofilm forms a base
    layer from which outer growths occurs. The
    outer layer can form streamers of biofilm that
    can break off to infect other nearby areas or
    enter the blood system to seed distant sites
    hematogenously.

    The biofilm state confers significant resistance to


    host immunologic attack using multiple defenses.5
    These immunologic defense mechanism are outlined in
    Table 3. To date, biofilms cannot be completely removed once they form. Mechanical scrubbing can remove a biofilm from an implant, but small areas always
    remain.

    Host Defense
    Host defense mechanisms consist of two major categories: systemic defense and local defense.11 The human
    host has developed a complex and adaptive immune
    system that monitors all areas of the body for microorganism invasion. Through a combination of antibodies,
    signaling molecules, and specialized cells, the human

    Orthopaedic Knowledge Update 10

    243

    Section 2: Systemic Disorders

    Figure 5

    Enhanced scanning electromicrograph of a bacterial biofilm that shows intricate connections between bacteria that allow cell-to-cell communication within the biofilm network. The other
    form of communication is via signaling molecules liberated by bacteria within the biofilm.
    (Copyright Yuri Gorby, PhD, San Diego, CA.)

    immune system is able to maintain a vigilant defense.


    Maintenance of optimum immune system surveillance
    requires multiorgan support. There are many associated medical conditions and disease states that affect
    proper function of the immune system. In addition,
    congenital defects in immune systemic development
    and function also predispose the host to infection. Furthermore, viral infections can attack specific immune
    cell lines, resulting in immune system compromise.12
    The major conditions associated with altered immune
    system function are listed in Table 4. Of the factors
    listed, some conditions can be treated to improve immune system function. For example, improving patient
    nutrition and cessation of immune suppressive drugs
    (when possible) can improve immune function. Optimizing diabetic care, smoking cessation, and alcohol
    cessation will also improve system function. Other conditions cannot be changed. In this situation, hypervigilance in surgical technique and during postoperative
    care are required to optimize infection prevention.
    Local defense consists of the skin and endothelial
    linings of the alimentary canal and respiratory tract,

    Table 3

    General Biofilm Properties That Promote Infection in Humans


    Biofilm acts as a mechanical barrier that presents inward diffusion of several antimicrobial agents. This can increase minimal
    bactericidal contractions by 100-fold
    Within the biofilm there are pH differences that allow some bacteria to become dormat while others remain active. Those
    dormant cells are able to resist antibiotic attack and subsequently develop resistance to antibiotics
    2: Systemic Disorders

    Biofilms display antiphagocytic properties allowing bacteria to evade clearance by the host immune system
    Biofilm protects the organism from direct antibody and complement-mediated bactericidal mechanisms and
    opsonophagocytosis
    There are currently no methods or chemicals to completely dissolve a biofilm. Current research is focusing on developing
    signaling molecules that signal the biofilm collective to dissolve and disperse

    Table 4

    Factors That Impair Systemic Immune Function


    Advanced age (older than 80 years)
    Allogeneic blood transfusion
    (during and shortly after transfusion)
    Alcoholism
    Asplenia

    Immune deficiency states


    Aquired immune deficiency
    (for example, HIV-1)
    Congenital immune deficiency
    (for example, chronic granulomatous disease, Di George syndrome)
    Dysplasia/neoplasia immune system
    (leukemia, lymphoma, myelodysplasia)

    Autoimmune disease states


    (for example, rheumatoid arthritis, SLE)

    Immunosuppressive drugs
    (for example, corticosteroids, methotrexate, anti TNF- agents)

    Chronic hypoxia
    (for example, COPD)

    Intravenous drug abuse

    Hemaglobinopathy
    (for example, sickle cell disease, thalasemia)

    Malignancy
    Malnutrition

    Hepatic insufficiency cirrhosis

    Renal insufficiency chronic uremia


    Tobacco abuse

    SLE = systemic lupus crythematosus, COPD = chronic obstructive pulmonary disease, HIV-1 = human immunodeficiency virus type 1, TNF- = tumor necrosis factor

    244

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 20: Musculoskeletal Infection

    2011 American Academy of Orthopaedic Surgeons

    musculoskeletal infection. A multitude of bacterial species exist on teeth as a biofilm state. Chronic tooth decay allows the biofilm to penetrate deeper within the
    mucosal layer and closely appose bone. Furthermore,
    chronic gingival inflammation allows entry of bacteria
    and biofilm plaques into the body any time the mouth
    is mechanically disturbed, such as during mastication
    and tooth brushing. Recurrent bacteremia at increased
    levels is a major risk factor for hematogenous seeding,
    especially of the hosts who are immunocompromised.
    When elective major reconstructive surgery with medically implanted devices is planned, specific questioning
    and examination should be conducted to determine the
    need for dental care and restoration before surgery.
    Chronic conditions within the respiratory tract and
    digestive system can also predispose to bacteremia.
    Conditions in the digestive tract such as Crohn disease
    and diverticulosis, if not carefully controlled, can lead
    to repetitive episodes of bacteremia. Similarly, within
    the respiratory tract chronic bronchitis or other parenchymal diseases also predispose to bacterial invasion.
    Close monitoring and treatment is needed to maintain
    the health of these systems. For example, in patients
    with diverticular disease or colonic polyps, maintenance endoscopic examinations will help to assess and
    treat the disease process.

    Musculoskeletal Infection Conditions

    Adult Osteomyelitis
    The three major routes of bacterial bone inoculation in
    adult osteomyelitis are hematogenous, direct innoculation (penetrating wounds, open fractures, surgery), and
    contiguous spread from an adjacent infection. The
    other less frequent source of infection is reactivation of
    a bone infection that has occurred in infancy or childhood. Unlike pediatric osteomyelitis where hematogenous seeding is the most common source, the more
    common mechanisms of bacterial delivery in adults are
    from direct inoculation and contiguous spread. These
    mechanisms are more common in adults for several
    reasons. First, high-energy injuries are more frequent.
    Second, there is a trend toward more frequent use of
    medically implanted devices to stabilize fractures.
    Third, the rich vascular supply present in the metadiaphyseal region of growing long bones in pediatric patients is reduced in the adult. Fourth, as medical technology increases life expectancy, more patients with
    vascular compromise of the extremities are being
    treated. These patients develop localized extremity infections that can spread to bone.
    S aureus is the most common organism involved.
    Staphylococcus species have numerous mechanisms for
    adherence to bony surfaces, making this species the
    most commonly involved in bone infection. However,
    any opportunistic organism can be involved if a patients systemic immunity and local wound protection
    are compromised. Pseudomonas aeruginosa and gramnegative organisms must be suspected in intravenous

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    and also includes the limb vasculature and neural innervations that support normal limb function. Damage to
    any of these systems raises the risk of local bacterial entry and subsequent infection to the musculoskeletal system. In the skin, small portals of entry are created by
    conditions that damage the protective skin layer. Patients having chronic venous insufficiency develop
    lower leg swelling from valvular incompetence and
    chronic hydrostatic loads to the lower legs. Areas of
    taut, shiny skin are easily traumatized on a microscopic
    level, causing the creation of entry points for bacteria.
    In addition, local hypoxia occurs in the areas of increased hydrostatic tension, which limits systemic immune response. Chronic lymphedema in an extremity
    results in infection susceptibility by a similar mechanism of persistent limb swelling and increased skin tension. Intrinsic skin conditions also provide areas for
    bacterial entry. Chronic dermatitis, psoriasis, traumatic
    burns, and rashes from medicines all can create portals
    for microorganism entry.11
    Neuropathic conditions also predispose to localized
    skin trauma. The lack of feeling in weight-bearing regions allows excess mechanical stress to be applied to
    the skin, resulting in blisters, skin cracks, and tears.
    Mechanical alterations in gait as a result of neurologic
    disorders apply abnormal mechanical loads to the skin
    in weight bearing regions. Furthermore, the disruption
    of autonomic regulatory control to the peripheral extremity alters the functions of sweating and oil production. Disruption of these functions predisposes the skin
    to localized trauma, again creating portals of entry for
    bacteria. Better patient education and surveillance are
    needed to enhance long-term preventive care. Furthermore, regular inspections and early intervention by
    health care professionals can mitigate the effects of
    crippling musculoskeletal infections.
    Vascular insufficiency at all levels of delivery plays
    an important role in the initiation and persistence of
    musculoskeletal infection. Localized hypoxia at an infection site inhibits immune system function. The inability to deliver immune-functional cells, combined
    with chronic local hypoxia, limits the immune cellular
    response to microorganism attack. Many methods are
    used to assess the vascular status of a limb. Generally,
    measurement of cutaneous oxygen tension at the local
    site, along with pulse pressure measurements to the
    limb, are accepted screening techniques. Local scarring
    as a result of multiple surgeries and trauma is a risk
    factor for infection. The local tissue area lacks an adequate vascular supply, which inhibits immune system
    function. An area of significant scarring (multiple incisions or loss of the normal soft tissue layer) lacks pliability and is more prone to superficial tearing. This
    creates small portals of entry for bacteria. In addition,
    if an incision is made through an area of nonpliable
    scar tissue, wound healing is delayed and the local area
    is at risk for bacterial inoculation. Similarly, radiation
    fibrosis significantly alters soft-tissue pliability and local host defense is compromised.
    In the mouth, dental disrepair is frequently overlooked by health care personnel when evaluating for

    245

    Section 2: Systemic Disorders

    Table 5

    Cierny-Mader Staging System for Osteomyelitis


    Anatomic type
    Stage 1 Medullary osteomyelitis
    Stage 2 Superficial osteomyelitis
    Stage 3 Localized osteomyelitis
    Stage 4 Diffuse osteomyelitis
    Physiologic class
    A Host: normal host
    B Host: systemic compromise (Bs)
    Local compromise (Bl)
    Systemic and local
    compromise (Bls)
    C Host: treatment worse than
    disease
    Systemic (Bs)-systemic

    Local (Bl)-local

    Malnutrition

    Chronic lymphedema

    Renal, hepatic failure

    Venous stasis

    Diabetes mellitus

    Major vessel compromise

    Chronic hypoxia

    Arteritis

    Immune disease

    Extensive scarring

    Malignancy

    Radiation fibrosis

    Extremes of age

    Small vessel disease

    Immunosuppression or immune
    deficiency

    Neuropathy

    2: Systemic Disorders

    Asplenic patients
    HIV/AIDS
    Alcohol and/or tobacco abuse

    drug users. Host deficiencies in immunity that lead to


    bacteremia predispose a patient to hematogenous seeding of bone.
    In acute osteomyelitis, suppurative infection can
    compromise the vascular supply to bone. When the
    medullary and periosteal blood supplies are both disrupted, bone necrosis occurs. The dead bone, a sequestra, serves as a platform for biofilm formation. Once a
    biofilm forms, the disease process becomes chronic.13
    At this point, the only method to eradicate the infection
    is removal of the dead bone (sequestrectomy) along
    with radical dbridement of nonviable soft tissue.
    Therefore, prompt diagnosis and treatment of acute osteomyelitis is needed to prevent the dreaded protracted
    course of chronic osteomyelitis. In chronic osteomyelitis, viable new bone will form around the infection region to support the weakened bone. The new periosteal
    bone that is seen encasing an area of dead infected bone
    is called an involucrum. In addition, endosteal new
    bone can form, which can obliterate the medullary canal. This appears radiographically as bony sclerosis.
    In acute osteomyelitis the clinical presentation is
    variable. This is a function of host immunity response
    246

    Orthopaedic Knowledge Update 10

    (full function versus suppression). The surgeon must be


    vigilant when the patient has a blunted response to infection (with conditions such as diabetic peripheral
    neuropathy or anergy due to advanced age). Acute
    symptoms include fever, chills, local pain, swelling, and
    erythema over the infected bone. An infection can also
    present as vague, nonspecific pain along with generalized malaise. In the situation of direct inoculation or
    contiguous spread, localized bone pain, swelling, and
    erythema are present. Wound drainage is frequently
    noted in the area of the previous trauma, surgical
    wound, or infected wound. In a chronic infection, a local draining sinus is frequently noted. Localized pain is
    noted at the infection site. If a sinus tract closes, a localized abscess can develop. The patient will usually
    note increasing redness, swelling, and pain at the infection site. Systemic bacteremia may ensue if not treated.
    In addition, a chronic draining sinus can undergo malignant transformation into squamous cell carcinoma in
    approximately 1% of patients.14
    The diagnosis of osteomyelitis requires a high index
    of suspicion. Patient groups that should be suspected of
    osteomyelitis include those with systemic immune suppression, open fractures, chronic open wounds, and
    medically implanted devices into bone. Laboratory examination should include complete blood count (CBC),
    erythrocyte sedimentation rate (ESR), and assessment
    of C-reactive protein (CRP) level. The white blood cell
    (WBC) count may be elevated in patients with acute osteomyelitis, but is often normal in those with chronic
    osteomyelitis. The ESR and CRP are most often elevated in both acute and chronic osteomyelitis. However, if the patient is immunosuppressed (because of
    medications or malnutrition) these markers can remain
    low. In this scenario, the surgeon must be diligent in the
    diagnostic evaluation. The CRP level is used to monitor
    effective treatment. With effective treatment, the CRP
    level will start to decline after several weeks. With curative treatment, it should return to normal. Imaging
    studies include radiographs, MRI, and bone scintigraphy. MRI will show changes in cortical bone, the medullary canal, and surrounding soft tissues 2 to 3 weeks
    before any changes are seen radiographically.15 Definitive diagnosis of osteomyelitis is provided by obtaining
    bone specimens for culture. All bone specimens should
    be sent for Gram stain and cultures (aerobic, anaerobic,
    fungal, and mycobacterial). Cultures of draining sinus
    tracts are not reliable for predicting which organism is
    growing in the infected bone site. If the clinical situation allows, all bone cultures should be obtained before
    antibiotics are initiated.
    Treatment of adult osteomyelitis is best assessed in
    the context of the hosts capacity to respond to an infection. A commonly used staging system for treatment
    in adult osteomyelitis that takes into account the location and type of infection11 is the Cierny-Mader classification system (Table 5). More importantly, the classification rates the quality of the host to respond to an
    infection. A weak host will require more aggressive
    treatment to eradicate the infection.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 20: Musculoskeletal Infection

    Adult Septic Arthritis


    Acute septic arthritis by pyogenic bacteria can cause
    significant long-term joint debility if not properly recognized and treated. Almost every organism has been
    reported to cause septic arthritis. The three mechanisms
    of bacterial joint inoculation are hematogenous seeding, direct inoculation (surgery, needle injection, traumatic puncture), and contiguous spread from an adjacent infection. The most frequently involved joints in
    adults, in descending order, are the knee, hip, elbow,
    and ankle.16

    2011 American Academy of Orthopaedic Surgeons

    Acute septic arthritis in adults can be separated into


    two major patient groups: young (age 15 to 40 years),
    healthy, sexually active patients with gonococcal pyogenic arthritis and elderly or immunocompromised patients with nongonococcal septic arthritis.17 In gonococal septic arthritis, the infecting organism is Neisseria
    gonorrhoeae. It is the most common cause of acute
    joint infection in persons 15 to 40 years of age in the
    United States. The clinical presentation is variable but
    typically includes migratory polyarthralgias, fever, rash,
    urethral or vaginal discharge, and tenosynovitis. A patient with disseminated gonnococcal infection may report few genital symptoms. More than 50% of these
    infections are polyarticular. The infected joint shows irritability to active and passive range, and a joint effusion is present. Blood cultures most often are negative
    (less than 10%). Joint aspiration cultures are also frequently negative (less than 25%). Because patients with
    gonococcal septic arthritis are healthy, prompt treatment results in a generally good prognosis.
    In elderly or immunocompromised patients, the infection is most often monoarticular.18 Blood and joint
    aspiration cultures are frequently positive. S aureus is
    the most common organism involved followed by
    Streptococcus species. In patients with sickle cell disease, Salmonella species is frequently isolated. In HIVinfected patients, S aureus is still the most frequently
    isolated organism. However, there is a much wider array of opportunistic organisms isolated from this group
    of patients. In patients with direct inoculation via a dog
    or cat bite, Pasteurella multocida is commonly noted.
    In human bites, Eikenella corrodens is an organism frequently associated with septic joint infection. In patients with a history of intravenous drug abuse, both P
    aeruginosa and S aureus are frequently found.
    Elderly patients and patients with immune system
    compromise are more likely to develop bacteremia and
    hematogenous seeding of a joint. Elderly patients are
    more prone to septic arthritis because the immune system response displays a reduced vigor with age. Furthermore, concomitant medial comorbidities also impair immune system response. Common medical
    conditions that impair host immunity include diabetes,
    cancer, smoking abuse, alcoholism, inflammatory autoimmune conditions, renal failure, cirrhosis, malnutrition, HIV, and intravenous drug abuse. In addition,
    medications that are used to treat life-threatening conditions, such as corticosteroids, antineoplastic agents,
    and antitumor necrosis factor- agents, also impair
    host immunity.19
    The clinical presentation of a patient with a septic
    joint may be blunted because of coexisting medical
    conditions and significant immunosuppression. Therefore, a high index of suspicion is the first requirement
    for successful diagnosis. The patient with a suspected
    joint infection typically notes a rapid onset of pain in
    the affected join. Limping and an inability to bear
    weight on the affected limb occur. Irritability and withdrawal to attempted passive range are noted. The infected joint is warm and an effusion is present. The
    overlying skin will often have a pink-colored erythema.

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    In acute osteomyelitis, surgical dbridement is almost always required. In primary hematogenous seeding, any abscess in bone and surrounding tissue requires prompt surgical dbridement and decompression
    before sequestration occurs. In cases of direct inoculation (open fracture or open surgical stabilization with
    implanted hardware) the wound is fully opened, dbrided, and vigorously lavaged. Soft-tissue deficiencies
    over bone require coverage with a muscle flap transfer
    (rotational or free flap depending on location). In cases
    of contiguous spread from chronic open wounds, definitive treatment also requires careful assessment of the
    vascular supply to the local area. Local perfusion to a
    wound area is evaluated with cutaneous oxygen tension
    measurements. If perfusion is inadequate, vascular bypass surgery is needed to reestablish local tissue perfusion. If bypass surgery is not possible, limb ablation
    may be required for definitive treatment. Bone takes 3
    to 4 weeks to revascularize after dbridement. During
    this time period, it is important to protect this at risk
    area with antibiotics until healing and revascularization
    occur. Patients should be treated with antibiotics for 4
    to 6 weeks, starting when the last dbridement procedure ended.
    The goal of treatment of chronic osteomyelitis is to
    eradicate all tissue surfaces that allow biofilm to persist. Surgical dbridement requires removal of all medically implanted devices, dead bone, and devascularized
    scar tissue (the avascular fibroinflammatory rind surrounding a chronic bone infection). Bone is removed to
    a region where visible bleeding is noted. Punctate
    bleeding from the surface of cortical bone is termed the
    paprika sign. The infected bone is stabilized either with
    splinting/casting or with application of an external fixator. Fixation pins are placed remotely away from the
    infection site. Dead spaces within bone are filled with
    polymethylmethacrylate antibiotic-loaded beads. Once
    the bone dead space is treated, the antibiotic beads are
    removed, usually after 4 to 6 weeks. Definitive stabilization is performed along with a bone grafting procedure, or bone transport (distraction osteogenesis) as indicated. Overlying soft-tissue deficiencies must be
    covered at the time of the dbridement surgery. A muscle flap transfer is used to cover deficient areas. A muscle flap provides soft-tissue coverage, but also brings to
    the local area a rich vascular supply that promotes
    healing and neogenesis. Furthermore, a muscle flap also
    allows systemic antibiotic delivery to the infected area.

    247

    Section 2: Systemic Disorders

    2: Systemic Disorders

    Radiographs are required to assess for adjacent bone


    involvement and to detect intra-articular hardware
    (plates, screws, anchors). When indicated, MRI is obtained to assess for adjacent infections in the periarticular soft tissues and bone. Any case of suspected joint
    infection requires a blood culture. Serum blood tests include CBC, CRP, and ESR. Serum leukocyte count is
    often elevated, but can be normal. The CRP level is almost always elevated. The ESR is usually elevated, but
    can be normal.
    Aspiration of the suspected joint is mandatory to establish the diagnosis and to identify an organism. Joint
    fluid is analyzed for cell count with differential, cultures (aerobic, anaerobic, fungal, and mycobacterial
    cultures), glucose level, Gram stain (including acid-fast
    stain), and crystal analysis (urate and calcium pyrophosphate). In septic arthritis, the joint fluid glucose
    level is less than 60% of the simultaneous serum glucose level. The fluid lacks a positive string sign (mucin
    clot). The joint fluid appears cloudy or purulent. Typically, joint fluid with greater than 50,000 WBC per mL
    and greater than 75% polymorphonuclear leukocytes
    (PMNs) is indicative of infection, whereas lower cell
    counts suggest noninfectious causes. However, there
    can be substantial overlap. In patients in whom immune suppression medications have been aggressively
    used, the cutoff value of 50,000 cells/mm3 may be too
    high. When the clinical presentation is equivocal but
    suggests infection (acute-onset joint pain, clinical immune suppression, and joint fluid WBC 30,000 to
    50,000 cells/mm2), the joint should be considered infected.20 Waiting for culture results can cause untoward
    joint destruction and debility. In addition, bacteria may
    fail to grow from infected joint fluid, particularly if the
    patient was pretreated with antibiotics, the organism is
    fastidious, or the fluid was not optimally processed.
    The decompression of a septic joint is controversial.
    Treatment modalities include serial needle aspiration,
    arthroscopic lavage, and arthrotomy with or without
    synovectomy. The main goal of treatment is to prevent
    the rapid destruction of articular cartilage. The suppurative process in septic arthritis releases proteolytic enzymes from PMNs, which irreversibly break down articular cartilage. Therefore, the more thorough clearing
    of PMNs from the joint, the less chance for long-term
    joint damage. The choice of treatment should take into
    consideration the following factors: lifespan of the joint
    (young patients need a healthy joint for a long period
    of time), associated medical comorbidities, and the
    ability of the patient to sustain a surgical procedure. As
    a general rule, immunocompromised patients require
    more help in infection eradication, and more often require aggressive lavage and dbridement. Open procedures have a greater chance to clear out bacteria and
    PMNs. If serial aspiration is initially chosen to treat
    septic arthritis, the joint fluid PMN count must be carefully monitored. If the PMN count remains high despite
    appropriate antibiotic treatment, open surgical dbridement is mandatory. Serial aspiration should not be performed on deep joints such as the hip and small joints.
    248

    Orthopaedic Knowledge Update 10

    Intravenous antibiotic therapy is initiated immediately after joint and blood cultures have been obtained.
    In young, healthy adults, coverage should encompass
    treatment of S aureus and N gonorrhoeae. In the immunocompromised patient, treatment should cover S aureus and P aeruginosa. Peak antibacterial serum concentrations should exceed the minimal inhibitory
    concentration of the infecting organisms by fivefold to
    tenfold, and will generally provide optimal antibiotic
    treatment. For gonococcal septic arthritis, the duration
    of antibiotic treatment is 1 week. For all other cases,
    treatment duration is 4 weeks with a minimum of 2
    weeks of parenteral antibiotics. An oral antibiotic may
    be used only if it is sensitive to the infecting organism.
    In addition, the patient must be able to tolerate the antibiotic, and must be compliant with the dosing regimen.
    In chronic septic arthritis or recurring disease, the
    goal is to eradicate the infection in preparation for later
    salvage reconstruction (arthroplasty or fusion). In
    chronic or recurrent disease, a radical synovectomy is
    required. In addition, all abscesses and bony lesions
    surrounding the joint are aggressively dbrided. Parenteral antibiotics are administered for 4 to 6 weeks. Effectiveness of treatment is determined by aspirations of
    the joint after completion of a full course of antibiotic
    therapy. In addition, treatment is monitored by following the serum CBC, CRP, and ESR levels during and after the treatment period.

    Pediatric Osteomyelitis
    Children have a propensity to develop musculoskeletal
    infection from hematogenous seeding. Other routes of
    bacteria delivery include direct seeding (from trauma,
    foreign body inoculation, or surgery). In addition, infection can result from contiguous spread from an adjacent infection site. Children have more frequent episodes of bacteremia; thus, bacterial delivery to bone
    can develop.21 Osteomyelitis generally affects children
    younger than 13 years; males are more commonly affected. Children younger than 13 years are generally
    more susceptible for infection because the immune system has yet to fully develop. Fifty percent of cases occur in patients younger than 5 years.
    In primary hematogenous osteomyelitis, the metaphysis of long bones is most frequently affected by bacterial inoculation. At this site in long bones, nonanastomosing capillary vessels make sharp loops under the
    growth plate and enter a system of large venous sinusoids. Blood flow slows and becomes turbulent, and
    bacteria can lodge in this region. In addition, the area
    adjacent to the growth plate has a lower oxygen tension and lower pH level, which gives bacteria a tactical
    advantage. Furthermore, the end capillary region and
    sinusoids lack phagocytic lining cells. These factors
    combined make the area more susceptible as a nidus
    for bone infection.22
    The most common organism causing pediatric osteomyelitis is S aureus.23 The next most common organism
    is group A -hemolytic streptococci (GABHS). GABHS
    2011 American Academy of Orthopaedic Surgeons

    Chapter 20: Musculoskeletal Infection

    2011 American Academy of Orthopaedic Surgeons

    blood is obtained, the fluid is still sent for culture and


    analysis. Fifty percent to 85% of patients have a positive bone aspiration.
    Treatment of acute pediatric osteomyelitis consists of
    prompt evaluation and subsequent administration of
    intravenous antibiotics. The antibiotics should cover S
    aureus and GABHS. In communities where methicillinresistant S aureus (MRSA) is prevalent, antibiotics for
    treatment of MRSA should be used until definitive culture results are available.29 Patients with sickle cell disease should have coverage for S aureus and Salmonella
    species.30 Intravenous antibiotics should be administered for 4 to 6 weeks. Treatment can be transitioned to
    oral antibiotics provided that the patient is compliant,
    the organism is adequately sensitive to the antibiotic,
    the antibiotic has good bioavailability to achieve adequate serum levels, and the clinical picture continues to
    improve. A minimum of 2 weeks of intravenous antibiotics is recommended before changing to an oral regimen. Serial monitoring with CBC, ESR, and CRP is required for effective treatment. Surgical intervention is
    required when an abscess is present. Abscess is detected
    by bone biopsy (pus upon aspiration) or MRI. Surgery
    is also required if sepsis of the adjacent joint is present.
    In some cases, a low-grade (subacute) osteomyelitis
    slowly develops over a period of months.31 The patient
    is initially asymptomatic and later presents with pain or
    a limp. The radiographic findings show bone loss that
    can often resemble a tumor. A Brodie abscess describes
    a localized, well-circumscribed bone abscess that is not
    associated with systemic illness. The most common site
    is the distal tibial metaphysis. In the case of subacute
    osteomyelitis, a bone biopsy will help determine the diagnosis. It is important to remember the general rule:
    always culture what you biopsy and biopsy what you
    culture. Treatment of subacute osteomyelitis is surgical dbridement followed by a course of parenteral antibiotics for 4 to 6 weeks.

    2: Systemic Disorders

    is more commonly seen in neonates. Haemophilius influenzae is a much less common pathogen due to vaccination against this species.24
    The acute infection, once developed, can spread to
    adjacent bony areas through the haversian and Volkmann canal systems. The infection can perforate
    through the cortical bone and can further spread along
    the bone under the periosteum, which is elevated by the
    inflammatory process. In the neonate, the infection can
    spread to the epiphysis and joint surfaces through capillaries that cross the growth plate. In the infant older
    than 1 year, the capillaries that extend into the epiphysis atrophy, confining the infection to the metaphysis
    and diaphysis. Adjacent joint infection can occur when
    the metaphyseal portion of the bone is intracapsular
    (proximal radius, humerus, and femur). Cortical perforation of a metaphyseal region that is intracapsular will
    deliver bacteria directly into the joint.24
    The clinical presentation of pediatric osteomyelitis
    varies according to age groups. In neonates, findings include local edema and decreased motion of the limb
    (pseudoparalysis). Joint swelling of the adjacent joint is
    common (60%). Joint swelling requires an arthrocentesis to evaluate for septic arthritis. Not infrequently, fever is absent. In children, the immune system response
    is more developed. Findings typically include acute onset of fever, irritability, and lethargy. Local findings include localized swelling, inflammation, and erythema.
    The child will either limp or may not be able to bear
    weight on the affected limb. Older children and adolescents will describe pain that is nearly constant. Pain is
    localized to the infection site.
    The evaluation for pediatric osteomyelitis includes a
    CBC, CRP, and ESR. The CRP is almost always elevated (98% of cases with acute hematogenous osteomyelitis). The ESR is less reliable in neonates and in patients with sickle cell disease.25 Measurement of plasma
    procalcitonin (PCT) is a newer serologic test. PCT levels rise rapidly with bacterial infections but remain low
    in viral infections and other inflammatory processes. In
    pediatric osteomyelitis, plasma PCT levels were elevated in 58% of cases.26 Because most cases of pediatric osteomyelitis originate from hematogenous seeding,
    blood cultures are mandatory. The imaging modality of
    choice is MRI.27 Hematogenous osteomyelitis in older
    children usually involves a single site. In neonates,
    polyostotic involvement occurs in 30% of patients and
    can be detected by bone scintigraphy.28 In addition, in
    young children who refuse to walk and are unable to
    localize the source of pain, a bone scan is useful to help
    identify a site of infection.
    Definitive diagnosis of the pathogen is obtained via
    bone aspiration. The technique involves insertion of an
    18-gauge spinal needle at the site of maximal tenderness. Aspiration should start as the needle reaches the
    cortex. If pus is obtained, which is indicative of subperiosteal abscess formation, the fluid is sent for culture and analysis. If no pus is obtained, the needle is
    advanced gently through the cortex and into the cancellous bone of the metaphysis. If pus is obtained, the diagnosis of medullary osteomyelitis is confirmed. If only

    Pediatric Septic Arthritis


    As in pediatric osteomyelitis, the source of infection in
    pediatric septic arthritis is dependent on developmental
    age. The bacterial spectrum in septic arthritis is similar
    to that seen in pediatric osteomyelitis. In addition, Kingella kingae is detected in pediatric arthritis based on
    PCR studies, but is difficult to grow in culture.32 The
    knee and hip are the most commonly affected joints. In
    neonates in whom small capillaries still cross the epiphyseal growth plate, the most common source of infection is adjacent osteomyelitis. However, neonates
    still can develop septic arthritis from hematogenous
    seeding. In infants and children, the most common
    source of infection is hematogenous seeding. Septic arthritis can occur in cases where the metaphyseal portion of a joint is intracapsular (proximal radius, humerus, or femur). Pediatric osteomyelitis primarily
    involves the metaphyseal region of the long bone. If the
    infection breaks through the relatively thin metaphyseal
    cortex in the neonate and infant, the infection will be
    contiguously delivered into the joint. Septic arthritis

    Orthopaedic Knowledge Update 10

    249

    Section 2: Systemic Disorders

    2: Systemic Disorders

    can develop from direct inoculation (traumatic puncture and surgery).33


    A septic joint presents with localized joint swelling,
    warmth, and irritability with active and passive motion. Refusal by the neonate to use the extremity (pseudoparalysis) is noted. In the older child, significant limp
    or refusal to bear weight on the extremity is noted. Fever and malaise are frequent. Laboratory tests include
    CBC with differential, CRP, and ESR. In almost all
    cases, the CRP and ESR will be elevated in septic arthritis. In contrast, the serum leukocyte count may be
    normal in up to 50% of cases. In a deep joint (such as
    the hip) in which clinical examination is difficult, ultrasonography or MRI can be used to determine joint inflammation and distention. MRI is also needed to rule
    out osteomyelitis in the adjacent bone. Aspiration of a
    swollen, irritable joint is mandatory to provide a definitive diagnosis and determine the need for surgical
    drainage and lavage. Joint fluid studies should include
    cell count with differential, cultures with sensitivities,
    Gram stain, glucose level, and protein levels. The differential diagnosis of a reactive joint effusion includes
    contiguous osteomyelitis, toxic synovitis, trauma, and
    autoimmune inflammatory arthritis (such as juvenile
    rheumatoid arthritis, acute rheumatic fever, Kawasaki
    disease, and serum sickness). Sometimes the clinical
    presentations and laboratory examination overlap,
    making early definitive diagnosis difficult. The destructive process of proteolytic enzymes upon articular cartilage can have long-term disabling consequences.
    Thus, if clinical doubt is present, surgical drainage
    should be considered and the diagnosis of infection
    made in retrospect. A joint fluid PMN count greater
    than 50,000 cells/mm3 warrants immediate surgical
    drainage. In inflammatory disease, the joint fluid leukocyte count ranges from 20,000 to 50,000 cells/mm3, the
    overlap region with septic arthritis. In this scenario,
    careful review of patient history, family history, Gram
    stain, and joint fluid differential must all be considered
    to determine the need for surgical drainage.
    Surgical decompression of an acute septic joint can
    be accomplished by open arthrotomy or arthroscopy.34
    A vigorous lavage is used to flush out proteolytic enzymes and bacteria. Prompt surgical decompression of
    the hip is required to prevent collateral damage. Specifically, protracted joint distention of the hip with pus
    can cause osteonecrosis from vessel compression. Also,
    capsular destruction can cause joint subluxation/
    dislocation.35 In any joint, prolonged joint infection can
    lead to adjacent bone infection. Serial joint aspiration
    has been used to treat septic arthritis in joints readily
    accessible to needle aspiration. However, careful monitoring is required. If the clinical picture fails to improve
    within 24 to 36 hours, surgical decompression is required. Serial joint aspiration is not recommended for
    small joints or the hip.
    Antibiotics should be started immediately after cultures have been obtained. Antibiotic therapy should
    target those pathogens based on age and medical comorbidities. In a septic joint in a patient older than 12
    years, antibiotics should include coverage for gonococ250

    Orthopaedic Knowledge Update 10

    cal septic arthritis. Intravenous antibiotics are initially


    administered. Conversion to oral antibiotics is allowed
    once the clinical situation improves and definitive sensitivities are obtained.36 Total duration of antibiotics in
    septic arthritis is 3 weeks. Monitoring of the joint by
    clinical examination and serial testing of serum CBC,
    CRP, and ESR is used to assess effectiveness of treatment. If clinical relapse occurs, the evaluation should
    focus on the presence of adjacent osteomyelitis.

    Foot Puncture Wounds


    The musculoskeletal structures of the foot are vulnerable to puncture injuries due to the significant mechanical stress placed on the sole of the foot during gait.
    Puncture wounds sometimes cause infection. The penetrating object, when it travels through a shoe, collects
    bacteria from the inner sole, which itself serves as a
    bacterial culture medium.37 As a result, Pseudomonas
    species and S aureus are the most frequently encountered organisms involved with puncture infections.
    Treatment of foot puncture wounds depends on the
    time of presentation. In an early presentation (within
    hours of injury), the focus is on preventing a deep infection. The shoe is inspected to see if any fragments are
    missing that may have been pushed into the wound.
    The offending puncture object is inspected (if brought
    in) to see if it is intact or broken. Radiographs are required to examine for a retained foreign body and to
    look for any bony violations. Any puncture near the
    metatarsal head should be carefully assessed for intraarticular puncture. If a retained foreign body is suspected, or an intra-articular puncture is strongly suspected, formal surgical irrigation and dbridement are
    required. If a foreign body is not suspected, the irrigation and dbridement can be performed with local anesthesia in the clinic. Close follow-up is mandatory to
    reassess for developing infection. Prophylactic oral antibiotic administration after acute puncture injury is
    controversial. If indicated, antibiotic selection should
    include coverage for Pseudomonas species and S aureus.38
    When a patient presents several days after a foot
    puncture and reports increasing pain and a swollen
    foot, the focus is on assessing the extent of infection.
    Radiographs are used to look for retained foreign bodies and any bony violations. A careful examination of
    foot joints is required to assess for intra-articular infection (most typically the metatarsophalangeal joint).
    Pain during passive motion of a suspected joint is a
    worrisome sign of septic arthritis that warrants arthrotomy, lavage, and dbridement. When the joint is not involved, dbridement is required when a retained foreign object is suspected, or the clinical presentation
    suggests a deep soft-tissue infection.39 Prompt intervention is required to prevent infection from spreading
    along fascial planes. Surgical dbridement includes dbridement of the puncture tract, curettement of bone,
    culturing of soft tissues and bone, copious irrigation,
    and open packing of the wound. Intravenous antibiotics should be administered for 2 weeks, and should in-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 20: Musculoskeletal Infection

    clude coverage for Pseudomonas species and S aureus.40


    For any patient who presents with a penetrating foot
    wound, tetanus immunization status must be verified; if
    status is unclear, tetanus vaccination is required.

    Periprosthetic Joint Infection

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    Infection of a joint with a medically implanted device is


    termed a periprosthetic joint infection. The term
    periprosthetic is used because the surrounding soft tissues and bone are frequently affected by the infection
    process. It also emphasizes the principle that all structures of the joint (soft tissues, bone, and implant) need
    to be addressed during surgical dbridement procedures. The most common reason for reinfection of a
    two-stage exchange arthroplasty procedure is inadequate dbridement of the periprosthetic soft tissue and
    bone. With current surgical technique, the incidence of
    periprosthetic infection in major joint replacement centers in the United States is less than 1% (0.39% to
    0.97%).39,41,42 Most periprosthetic infections manifest
    with overt clinical symptoms within the first year of the
    joint replacement.
    The mechanisms of joint inoculation in periprosthetic joint infection are direct inoculation of the joint,
    hematogenous seeding, and contiguous spread from an
    adjacent infection focus. The knee is the most commonly affected joint, followed by the hip. The most
    common organisms involved in periprosthetic joint infection are Staphylococcus epidermidis (or coagulasenegative Staphylococcus species) and S aureus. The
    high incidence of S epidermidis infections reflects the
    mechanism of fomite delivery into the surgical wound
    at the time of surgery. S epidermidis is shed by operating room personnel. With dynamic turbulent flow in
    the operating room theater, bacteria are delivered to the
    surgical site and to operating room equipment. S aureus is a frequent organism due to its multiple mechanisms of bacterial adherence, which provide a tactical
    advantage for this organism.43 Hematogenous seeding
    of a prosthetic joint more often occurs in immunocompromised patients. In this situation, a wide variety of
    organisms can infect the joint, including Enterococcus,
    gram-negative rods, anaerobic organisms, and fungi.
    Many staging systems are used to categorize
    periprosthetic joint infection.44,45 The more recent staging system introduced by the Musculoskeletal Infection
    Society incorporates three major categories to objectively describe the infection and the patient in a progressive system to reflect worsening disease severity46
    (Tables 6 and 7). The first category describes the temporal presentation and infection state of the periprosthetic joint infection. An early postoperative infection is
    defined as an infection that presents less than 3 weeks
    from the index joint arthroplasty procedure. An early
    postoperative infection is an acute infection defined as
    a nonbiofilm state. A late infection occurs in a medically implanted joint device of any age and also is defined as a nonbiofilm state. The infection is clinically
    determined to be less than 3 weeks in duration. Bacteria are delivered to the joint via hematogenous trans-

    port or from direct seeding from adjacent soft tissues


    that are infected (such as abscess, cellulitis, or traumatic wound). A chronic infection is currently defined
    as an infection in any joint arthroplasty that is judged
    to be of 3 weeks duration or longer. In a chronic
    periprosthetic infection, a biofilm coating has enveloped the prosthetic implant, ensuring perpetual survival of the infection.
    The second category of the staging system rates the
    ability of the patient or host to combat the infection
    with a systemic immune response. The objective factors
    defining this category focus on the competency of the
    host immune system and related medical conditions
    that affect proper functioning of the immune system. A
    patient is considered either uncompromised, compromised, or significantly compromised. The third category grades the extent of osseous and soft-tissue compromise surrounding the affected joint. This category
    includes local soft-tissue factors that can potentially impair local wound healing, and also allow subsequent reinfection at the index site. The staging system incorporates all three categories in the following fashion: stage
    equals infection type plus systemic host grade plus local
    extremity grade. Examples of the nomenclature include
    I-A-1, II-B-2, III-C-1.
    A chronic periprosthetic infection is defined by the
    Musculoskeletal Infection Society as an infection where
    the infecting organism has transformed into a biofilm
    state. At present, the sobering reality is that once a biofilm has formed, it cannot be completely eradicated unless prosthetic implants are surgically removed and the
    surrounding wound is radically dbrided. Thus, in this
    staging system, an acute infection of a joint implant is
    considered salvageable. In a chronic infection, the infected implant is considered nonsalvageable and should
    be removed. At present, any prosthetic arthroplasty
    where the infection is clinically judged to be of 3 weeks
    duration or longer is considered chronic. However, it
    has been shown that in an optimum environment, a
    biofilm can form on an implant in as few as 72 hours.
    Therefore, the definition of chronic infection may
    change to an even shorter time interval. It is hoped that
    a simple testing method to detect the presence of a biofilm on a medically implanted device will be developed
    soon. When this test is available, the definition of a
    chronic periprosthetic infection will no longer be arbitrary.
    Similar to adult osteomyelitis, the health of the host
    is an important aspect of periprosthetic infection care.
    The inability of a weak host to vigorously fight an infection with systemic immune support may result in
    persistent infection at a low-grade level, or even at lifethreatening levels. In a patient who is medically compromised, one of two options must be chosen. The first
    option (when possible) is to improve medical host grading with therapy designed to positively affect the patients immune system. Treatment of the host would
    hopefully improve the systemic immune response and
    positively affect infection eradiation. In the future,
    medical therapy may allow modification of treatment
    of periprosthetic joint infection. If the host immune sys251

    Section 2: Systemic Disorders

    Table 6

    Musculoskeletal Infection Society Staging for Periprosthetic Infection


    Category
    Infection type

    Grading
    I

    Description
    Early postoperative infection (< 3 weeks postoperative)
    Nonbiofilm state

    II

    Late occurring infection (< 3 weeks duration)


    Nonbiofilm state

    III

    Late chronic infection ( 3 weeks duration)


    Biofilm state

    Uncompromised (no compromising factors)

    Compromised (1 to 2 compromising factors)

    Significant compromise (Fewer than two compromising factors)

    Either from early postoperative infection or late-occurring infection


    Systemic host grade
    (medical/immune status)

    or one of the following:


    Absolute neutrophil count < 1,000
    CD4 T-cell count < 100
    Intravenous drug abuse
    Chronic active infection at other site
    Dysplasia/neoplasm of immune system (For example, myelodysplasia,
    chronic lymphocytic leukemia)

    2: Systemic Disorders

    Local extremity grade

    Uncompromised (no compromising factors)

    Compromised (one to two compromising factors)

    Significant compromise (fewer than two compromising factors) or one of the


    following:
    Soft-tissue loss requiring muscle transposition or free flap transfer
    Bone loss requiring structural allograft or substituting megaprosthesis
    Local wound irradiation 4,000 rad

    Stage = infection type + systemic host grade + local extremity grade; eg, I-A-1, III-B-2

    tem cannot assist in the eradication of the bacterial infection, then treatment must be modified to extirpate
    the infection surgically (with wide radical resection or
    amputation). This method is described as a tumoresque removal of the infection.
    The third factor is the grading of the local wound.
    An intact soft-tissue envelope with normal tissue perfusion is critical to eradicating the infection at the local
    site. An intact vasculature, at all levels of tissue support, is necessary to deliver oxygen, immune cells, and
    signaling mediators to the area of infection. If the local
    wound is damaged significantly, then undamaged fresh
    tissue can be used to help fill deficits and reestablish a
    sound local environment. Local muscle rotational flaps
    252

    Orthopaedic Knowledge Update 10

    are helpful in this regard. If there is poor extremity perfusion, then a vascular bypass procedure may be
    needed to improve blood flow to the local wound.
    Sometimes the local wound is so pervasively damaged
    by the infection that satisfactory salvage is impossible,
    and an amputation is recommended.
    The presentation of a periprosthetic joint infection is
    variable due to host factors and the inherent virulence
    of the infecting organism. Most frequently, joint pain,
    effusion, and loss of joint range of motion are noted. In
    an acute presentation, a significant limp and inability
    to bear weight are evident. Often the affected joint is
    warm and overlying erythema is present. In chronic infections, a draining sinus or boil is seen around the

    2011 American Academy of Orthopaedic Surgeons

    Chapter 20: Musculoskeletal Infection

    2011 American Academy of Orthopaedic Surgeons

    Table 7

    Musculoskeletal Infection Society Staging for


    Periprosthetic Infection - Compromising Factors
    Systemic Host Compromising Factors
    Age 80 years
    Alcoholism
    Chronic active dermatitis/cellulitis
    Chronic indwelling catheter (out through skin)
    Chronic malnutrition (albumin 3.0 g/dL)
    Current nicotine use (inhalational or oral)
    Diabetes (requiring oral agents and/or insulin)
    Hepatic insufficiency (cirrhosis)
    Immunosuppressive drugs (eg, methotrexate, prednisone,
    cyclosporine, anti-TNF agents)
    Malignancy (history of, or active)
    Renal insufficiency with uremia (dialysis)
    Systemic autoimmune inflammatory disease (for example,
    rheumatoid arthritis, systemic lupus erythematosus)
    Systemic immune compromise from infection or disease (eg,
    HIV, sickle cell disease, splenectomy)
    Local Extremity Grade (Wound) Compromising Factors
    Infection of a revision arthroplasty
    Recurrent infection after joint dbridement with prosthesis
    retention
    Recurrent infection after prosthetic exchange protocol
    Recurrent open foot sores (neuropathic or structural)

    2: Systemic Disorders

    joint. In low-grade infections, there is a paucity of systemic symptoms.


    Evaluation of periprosthetic infection first includes a
    high index of suspicion. All joint arthroplasty procedures cause pain, warmth, and swelling for up to 3 to 4
    weeks after the index procedure. However, the surgeon
    should be suspicious of infection when pain and narcotic use escalates rather than recedes; range of motion
    decreases; swelling of the joint increases; skin erythema
    is noted; and wound drainage develops. For a suspected
    periprosthetic joint infection, recommended studies include a serum CRP, ESR, and CBC with differential. An
    elevated CRP level is the most frequently elevated serum test. An elevated CRP level can also be present in
    other conditions such as autoimmune inflammatory
    disease states. Therefore, review of the cell count and
    clinical picture are also needed. The combination of
    normal CRP and ESR levels reliably predicts the absence of infection. A joint aspiration is required to confirm the presence of infection. Joint fluid studies should
    include Gram stain, culture (aerobic, anaerobic, fungal,
    and mycobacterial), cell count with differential, crystal
    analysis, and mucin clot quality. With a periprosthetic
    joint infection, joint fluid analysis will show an elevated WBC count with a preponderance of PMNs. Because host immunity can be blunted, the threshold
    WBC level in joint fluid in a periprosthetic joint infection can be low. As a general guide, when the joint fluid
    WBC is greater than 10,000 cells/mm3 and there is a
    preponderance of PMNs, joint infection should be
    strongly suspected.47 Radiographs of the affected joint
    are needed to rule out other sources of joint irritability
    (such as bone fracture, mechanical breakage, or dislocation). Bone scintigraphy is useful when evaluating for
    a chronic periprosthetic infection where the diagnosis
    of the painful joint arthroplasty is unclear. An indiumlabeled WBC scan is a useful technique to detect a
    chronic periprosthetic infection.
    The treatment of periprosthetic joint infection is outlined in Table 8. In an acute infection (nonbiofilm
    state) the goal is prompt surgical lavage and dbridement of the infected joint arthroplasty to prevent biofilm formation. If an acute periprosthetic joint infection
    is suspected and laboratory data corroborate, immediate surgical intervention is recommended. One should
    not wait for culture results because biofilm formation
    on an implant can occur quickly. Open surgical dbridement with component retention is recommended.
    During the dbridement procedure, modular parts
    should be removed. The thin, light, yellow fibrin layer
    that is seen between metal and polyethylene modular
    parts serves as a site for bacterial adherence and persistence. The dbridement procedure should include debulking of inflammatory synovium and copious lavage.
    Arthroscopic lavage of an acute periprosthetic joint infection does not accomplish all technical goals of
    periprosthetic joint infection dbridement and is not
    routinely recommended. The best prospect for arthroscopic lavage is a patient who is very ill and cannot
    tolerate the stress of an open dbridement procedure.
    Intravenous antibiotics are administered for 6 weeks af-

    Multiple incisions (creating skin bridges)


    Sinus tract
    Vascular insufficiency to extremity: absent extremity pulses,
    calcific arterial disease, venous insufficiency with skin
    plaques or intermittent sores

    ter the dbridement procedure. The prognosis for infection for recovery is good (generally 90% success). Recurrence is more likely seen in medical C hosts. In
    chronic periprosthetic infection, bacteria have formed a
    biofilm and have had time to invade the prosthetic
    bone interface. Curative treatment requires removal of
    prosthetic implants, infected bone, and devascularized
    soft tissues. The two-stage exchange protocol is considered the most prudent course and is recommended for a
    chronic periprosthetic joint infection.48 A single-stage
    exchange protocol can provide a good rate of success in
    experienced centers. A single-stage exchange is best
    suited for patients who are medically uncompromised
    (type A host) and have normal soft tissues (type 1
    wound). A single-stage exchange protocol requires meticulous, coordinated care by the entire operating room
    team. This technique is best reserved for those centers
    logistically able to handle an arduous single-stage exchange protocol.

    Orthopaedic Knowledge Update 10

    253

    Section 2: Systemic Disorders

    Table 8

    2: Systemic Disorders

    Management of Periprosthetic Joint Infection


    Infection Type

    Duration

    Treatment

    Early postoperative
    infection

    Less than 3 weeks from initial joint


    arthroplasty
    Nonbiofilm state

    1. I and D with retention of components


    Exchange of modular polyethylene parts
    Postoperative IV antibiotics (6 weeks)
    2. Arthroscopic lavage if patient is too medically ill to
    undergo an open dbridement procedure
    3. Treat as chronic infection if I and D fails

    Late-occurring
    infection

    Less than 3 weeks from joint seeding 1. I and D with retention of components
    Exchange of modular polyethylene parts
    event
    Postoperative IV antibiotics (6 weeks)
    Hematogenous seeding or
    2. Arthroscopic lavage if patient is too medically ill to
    Local spread to joint from
    undergo an open dbridement procedure
    adjacent infection
    Nonbiofilm state
    3. Treat as chronic infection if I and D fails

    Chronic Infection

    More than 3 weeks from initial joint 1. Two-stage exchange with interval period IV antibiotics
    replacement
    Interpositional high-dose antibiotic-loaded
    Seeding event
    polymethylmethacrylate spacer
    Biofilm state
    IV antibiotics 4 to 6 weeks after resection
    Reimplantation in 9 to 12 weeks if free of infection
    Indicated when anticipated joint function is good
    2. Single-stage exchange
    IV antibiotics 4 to 6 weeks after exchange
    Best reserved to centers specialized in periprosthetic joint
    infection management
    Best indication: Medial A host, type 1 wound
    3. Two-stage arthrodesis with an interval period of IV
    antibiotics
    Indicated when surrounding musculoskeletal tissues are
    severely damaged and anticipated joint function is poor
    Interpositional high-dose antibiotic-loaded
    polymethylmethacrylate spacer when needed for joint
    stabilization
    4. Permanent resection arthroplasty with IV antibiotics
    IV antibiotics 4 to 6 weeks
    Indicated when risk of reinfection is high (medial C host)
    and patient unable to tolerate major reconstructive
    procedure
    Joint provides functional mobility with bracing
    5. Amputation/disarticulation
    IV antibiotics 4 to 6 weeks
    Indications
    Painful neuropathic arthropathy
    Uncontrolled recurrent infection (usually medial C host)
    Severe soft-tissue destruction and patient unable to
    tolerate multiple reconstructive procedures to salvage
    limb
    Permanent resection will not provide functional mobility
    with bracing

    IV = intravenous, I and D = irrigation and dbridement.

    In a two-stage protocol, the resected joint is stabilized with an acrylic antibiotic-loaded polymethylmethacrylate spacer to provide sustained, high-dose antibiotic delivery to the infected joint tissue and exposed
    bone.49 If supporting ligaments and bone are intact,
    an articulating spacer construct can be used; one that
    allows limited motion helps to maintain soft- tissue
    pliability.50 Joint motion exercises are to be limited because excess motion and weight bearing can cause
    254

    Orthopaedic Knowledge Update 10

    an acrylic synovitis to develop. If supporting ligamentous and/or bony structures are deficient, then a static
    spacer must be used. Intravenous antibiotics are administered for 4 to 6 weeks. Reevaluation for infection is performed after antibiotic administration has
    been completed (usually 10 to 14 days after completion). Reconstruction of the infected joint is predicated
    on a benign clinical examination, a normal serum
    laboratory analysis (normal CBC, CRP, and ESR val-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 20: Musculoskeletal Infection

    Table 9

    Dental Prophylaxis for Prosthetic Joint Arthroplasty Patients


    Patient Status

    Recommended Antibiotic

    Regimen

    Patients not allergic to penicillin

    Cephalexin, cephradine, or
    amoxicillin

    2 g orally 1 h before dental procedure

    Patients not allergic to penicillin and unable


    to take oral medications

    Cefazolin or ampicillin

    Cefazolin 1 g or ampicillin 2 g
    Intramuscularly or intravenously 1 h
    before dental procedure

    Patients allergic to penicillin

    Clindamycin

    600 mg orally 1 h before dental procedure

    Patients allergic to penicillin and unable to


    take oral medications

    Clindamycin

    600 mg intravenously 1 h before dental


    procedure

    2011 American Academy of Orthopaedic Surgeons

    tion is treated with intravenous antibiotics. The joint is


    supported with external bracing. The patient is allowed
    ambulation with assistive devices (cane, crutch, or
    walker). Permanent resection arthroplasty is chosen
    over amputation when the resected joint can provide
    acceptable support for ambulation and pain levels are
    acceptable. An amputation is chosen when the infection
    process is life or limb threatening or anticipated pain
    and suffering will be great. Chronic neuropathic pain in
    an extremity in the face of a severe periprosthetic joint
    infection is an indication for amputation. When severe
    soft-tissue damage and bone loss has occurred, an amputation is chosen when the reconstructive process is
    too arduous for the patient to handle (such as multiple
    procedures in a compromised host). When the infection
    becomes life threatening, an urgent amputation/
    disarticulation is the recommended procedure. Limb
    ablation removes the infection mass, thus allowing the
    immune system to focus on primary wound healing.
    Dental prophylaxis is recommended for all patients
    who have undergone a joint arthroplasty. Prophylactic
    antibiotic coverage for dental procedures should be
    given for the first 2 years after surgery. Patients who
    are immunocompromised or immunosuppressed should
    receive lifetime prophylactic antibiotics. Examples of
    immunocompromised conditions include inflammatory
    arthropathies (rheumatoid arthritis, systemic lupus erythematosus) and medication-induced immunosuppression. Patients with comorbidities that alter immune system function should also receive lifetime dental
    prophylaxis. Examples include previous prosthetic joint
    infection, diabetes, and malignancy. Table 9 outlines
    the recommended prophylactic antibiotic coverage for
    dental procedures.
    In communities where MRSA is endemic, preoperative office screening for MRSA is advocated for those
    patients considered at risk for MRSA colonization.51,52
    At-risk groups include patients who have recently been
    or reside in a hospital or extended-stay care facility, patients with a history of MRSA colonization, and patients who are immune compromised. Screening can be
    performed in the office with a nares and/or axillary
    swab culture. Eradication of the MRSA carrier state is
    recommended before any elective joint arthroplasty or

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    ues), and aspiration cultures showing no growth. In the


    second stage, the type of reconstructive process depends on the patients medical status and local wound
    condition.
    For most patients, the medical status after the initial
    resection procedure is stable, and the reconstructive
    procedure can proceed. The quality of the local wound
    determines the type of reconstructive process. In most
    cases, joint arthroplasty can be performed. A requirement for total joint reconstruction includes an intact
    neuromuscular status to support the joint. Medullary
    stem support and adjacent screw fixation are needed to
    support the prosthesis. Joint constraint built into the
    prosthetic system is often required to support attenuated ligamentous structures. Endoprosthetic implants
    or bulk support allografts may be required to replace
    segmental deficiencies in bone. The disadvantage of using a bulk support allograft for reconstruction is that
    the surrounding tissues (damaged by infection) may
    have an attenuated blood supply, limiting host-graft
    healing. Furthermore, if an allograft is placed in a superficial position (such as the proximal tibia) it can become easily infected from minor wound dehiscence or
    prolonged drainage. Once the allograft is colonized
    with bacteria, eradication of the infection is nearly impossible. The allograft is a dead porous structure in
    which bacteria can easily hide. In contrast, deficits
    filled by solid metal have only an outer surface to
    which bacteria can adhere. If colonization does occur,
    successful treatment with irrigation and dbridement
    before a biofilm is allowed to form is possible. In the
    second-stage procedure, soft tissues are covered with a
    rotational muscle flap if a secure water-tight and
    tension-free closure cannot be attained. The vascular
    status of the limb requires careful assessment when
    considering a rotational muscle flap procedure. Inadequate arterial supply to the extremity can result in flap
    necrosis.
    When severe soft-tissue and bone damage has occurred, alternative techniques for joint salvage are required. In cases where the medical status is compromised and the risk of recurrent infection is high, a
    permanent resection arthroplasty is an alternative treatment. The infected implant is removed and the infec-

    255

    Section 2: Systemic Disorders

    Table 10

    2.

    Miller LG, Diep BA: Clinical practice: colonization, fomites, and virulence: rethinking the pathogenesis of
    community-associated methicillin-resistant Staphylococcus aureus infection. Clin Infect Dis 2008;46(5):752760.
    The authors discuss community-associated MRSA infection and strategies for prevention.

    3.

    Ritter MA: Surgical wound environment. Clin Orthop


    Relat Res 1984;190(190):11-13.

    4.

    Gristina AG, Costerton JW: Bacterial adherence and the


    glycocalyx and their role in musculoskeletal infection.
    Orthop Clin North Am 1984;15(3):517-535.

    5.

    Donlan RM, Costerton JW: Biofilms: survival mechanisms of clinically relevant microorganisms. Clin Microbiol Rev 2002;15(2):167-193.

    6.

    Shirtliff ME, Leid JG, Costerton JW: The basic science


    of musculoskeletal infection, in Musculoskeletal Infections. Calhoun JH, Mader JT, eds: Marcel Dekker Inc.
    New York, NY, 2003, pp 1-61.

    7.

    Balaban N, Novick RP: Autocrine regulation of toxin


    synthesis by Staphylococcus aureus. Proc Natl Acad Sci
    U S A 1995;92(5):1619-1623.

    8.

    Reguera G, McCarthy KD, Mehta T, Nicoll JS, Tuominen MT, Lovley DR: Extracellular electron transfer via
    microbial nanowires. Nature 2005;435(7045):10981101.

    9.

    Hall-Stoodley L, Costerton JW, Stoodley P: Bacterial


    biofilms: from the natural environment to infectious diseases. Nat Rev Microbiol 2004;2(2):95-108.

    10.

    Cirioni O, Giacometti A, Ghiselli R, et al: RNAIIIinhibiting peptide significantly reduces bacterial load
    and enhances the effect of antibiotics in the treatment of
    central venous catheter-associated Staphylococcus aureus infections. J Infect Dis 2006;193(2):180-186.

    11.

    Mader JT, Calhoun JH: Staging and staging application


    in osteomyelitis, in Calhoun JH, Mader JT, eds: Musculoskeletal Infections New York, NY, Marcel Dekker Inc.
    2003, pp 149-182.

    12.

    Globerson A, Effros RB: Ageing of lymphocytes and


    lymphocytes in the aged. Immunol Today 2000;21(10):
    515-521.

    13.

    Brady RA, Leid JG, Calhoun JH, Costerton JW, Shirtliff


    ME: Osteomyelitis and the role of biofilms in chronic
    infection. FEMS Immunol Med Microbiol 2008;52(1):
    13-22.
    The authors discuss current understanding of biofilms
    and molecular interactions of bacteria.

    14.

    Bauer T, David T, Rimareix F, Lortat-Jacob A: [Marjolins ulcer in chronic osteomyelitis: Seven cases and a review of the literature]. Rev Chir Orthop Reparatrice
    Appar Mot 2007;93(1):63-71.

    Treatment Protocol for MRSA-Colonized Patient


    14-day protocol
    Bactroban intranasal ointment 2%. Apply to nares twice
    daily
    Rifampin 300 mg by mouth twice daily
    Bactrim DS by mouth twice daily
    Hibiclens (chlorhexidine gluconate) bath daily for 5
    minutes. Immerse entire body (including scalp) to face.
    Wash face with wash cloth. Use 1 oz of Hibiclens
    solution (chlorhexidine gluconate 4%) in warm bath
    water.
    Repeat MRSA screen

    orthopaedic procedure. This reduces MRSA bioburden


    to patients within the health care facility. A treatment
    protocol for MRSA carriers is listed in Table 10.

    Summary

    2: Systemic Disorders

    The competition between human host defense and environmental microorganisms is a battle that will continue in perpetuity. Infection prevention remains the
    best method to thwart microorganism destruction seen
    in musculoskeletal infections. An understanding of the
    concept of bacterial shedding and microorganism inoculation allows the orthopaedic surgeon and health care
    team to maximize efforts to ameliorate the risk of orthopaedic infections. An understanding of the concept
    of bacterial biofilm is key to providing appropriate care
    once a musculoskeletal infection is established. Compromise in human host defense requires a more aggressive surgical treatment regimen to eradicate an established musculoskeletal infection. By using staging
    systems for osteomyelitis and periprosthetic joint infection, treatment regimens can be evaluated and tailored
    to address various levels of host weakness. Future research is directed toward developing methods to eradicate a biofilm that do not require surgical extirpation
    of host tissue and implanted medical devices. Research
    also is focused on biofilm dissolution with detergents
    or signaling molecules that will instruct a biofilm to
    dissipate. It is hoped that methods to boost host immunity to combat musculoskeletal infections will be developed. The goal is to rely less on antibiotic therapy and
    surgical dbridement to help maintain limb function
    and quality of life.

    Annotated References
    1.

    256

    Bethune DW, Blowers R, Parker M, Pask EA: Dispersal


    of Staphylococcus aureus by patients and surgical staff.
    Lancet 1965;1(7383):480-483.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 20: Musculoskeletal Infection

    The authors compared the current epidemiology of musculoskeletal infection with historical data and evaluated
    the degree of disease severity within the current epidemiology.

    The authors report on seven patients with squamous cell


    skin carcinoma in whom wounds related to deep bone
    infections had developed. Nonsurgical treatment was
    unsuccessful in four patients, and three required amputation.
    15.

    Pineda C, Vargas A, Rodrguez AV: Imaging of osteomyelitis: Current concepts. Infect Dis Clin North Am
    2006;20(4):789-825.

    16.

    Favero M, Schiavon F, Riato L, Carraro V, Punzi L:


    [Septic arthritis: A 12 years retrospective study in a
    rheumatological university clinic]. Reumatismo 2008;
    60(4):260-267.
    The authors reevaluated septic arthritis cases discharged
    over a 12-year period to study risk factors, clinical and
    laboratory characteristics, causative microorganisms,
    and possible increase in frequency.

    17.

    18.

    Geirsson AJ, Statkevicius S, Vkingsson A: Septic arthritis in Iceland 1990-2002: Increasing incidence due to
    iatrogenic infections. Ann Rheum Dis 2008;67(5):638643.
    The authors studied the effect of the increase in diagnostic and therapeutic joint procedures on the incidence
    and type of septic arthritis. The importance of sterile
    technique and firm indications for joint procedures is
    emphasized.
    Mathews CJ, Coakley G: Septic arthritis: Current diagnostic and therapeutic algorithm. Curr Opin Rheumatol
    2008;20(4):457-462.
    An evidence-based algorithm for diagnosis and treatment of bacterial septic arthritis is discussed.

    20.

    McGillicuddy DC, Shah KH, Friedberg RP, Nathanson


    LA, Edlow JA: How sensitive is the synovial fluid white
    blood cell count in diagnosing septic arthritis? Am J
    Emerg Med 2007;25(7):749-752.
    The authors studied the sensitivity of the current standard for synovial fluid leukocytosis analysis in the diagnosis of infectious arthritis or a septic joint.

    21.

    De Boeck H: Osteomyelitis and septic arthritis in children. Acta Orthop Belg 2005;71(5):505-515.

    22.

    Jansson A, Jansson V, von Liebe A: [Pediatric osteomyelitis]. Orthopade 2009;38(3):283-294.


    The authors discuss diagnostic and therapeutic approaches for childhood osteomyelitis.

    23.

    Gafur OA, Copley LA, Hollmig ST, Browne RH,


    Thornton LA, Crawford SE: The impact of the current
    epidemiology of pediatric musculoskeletal infection on
    evaluation and treatment guidelines. J Pediatr Orthop
    2008;28(7):777-785.

    2011 American Academy of Orthopaedic Surgeons

    McCarthy JJ, Dormans JP, Kozin SH, Pizzutillo PD:


    Musculoskeletal infections in children: Basic treatment
    principles and recent advancements. Instr Course Lect
    2005;54:515-528.

    25.

    Khachatourians AG, Patzakis MJ, Roidis N, Holtom


    PD: Laboratory monitoring in pediatric acute osteomyelitis and septic arthritis. Clin Orthop Relat Res 2003;
    409:186-194.

    26.

    Hgle T, Schuetz P, Mueller B, et al: Serum procalcitonin for discrimination between septic and non-septic
    arthritis. Clin Exp Rheumatol 2008;26(3):453-456.
    The authors studied the diagnostic value of serum procalcitonin and determined that it is highly sensitive and
    specific for septic arthritis, depending on the clinical setting.

    27.

    Blickman JG, van Die CE, de Rooy JW: Current imaging concepts in pediatric osteomyelitis. Eur Radiol
    2004;14(suppl 4):L55-L64.

    28.

    Schmit P, Glorion C: Osteomyelitis in infants and children. Eur Radiol 2004;14(suppl 4):L44-L54.

    29.

    Hawkshead JJ III, Patel NB, Steele RW, Heinrich SD:


    Comparative severity of pediatric osteomyelitis attributable to methicillin-resistant versus methicillin-sensitive
    Staphylococcus aureus. J Pediatr Orthop 2009;29(1):
    85-90.
    The authors attempted to determine whether there were
    significant differences in predetermined measures of disease severity among 97 patients with hematogenous osteomyelitis of varying etiologies.

    30.

    Al-Ola K, Mahdi N, Al-Subaie AM, Ali ME, Al-Absi IK,


    Almawi WY: Evidence for HLA class II susceptible and
    protective haplotypes for osteomyelitis in pediatric patients with sickle cell anemia. Tissue Antigens 2008;
    71(5):453-457.
    The authors determined that specific HLA haplotypes
    influence sickle cell anemia osteomyelitis risk, and specific HLA types may be markers for identifying sickle
    cell anemia patients at high risk for osteomyelitis.

    31.

    Hughes LO, Mader JT: Pediatric osteomyelitis, in Calhoun JH, Mader JT, eds: Musculoskeletal Infections.
    New York, NY, Marcel Dekker Inc. 2003, pp 473-493.

    32.

    Yagupsky P: Kingella kingae: From medical rarity to an


    emerging paediatric pathogen. Lancet Infect Dis 2004;
    4(6):358-367.

    33.

    Yuan HC, Wu KG, Chen CJ, Tang RB, Hwang BT:


    Characteristics and outcome of septic arthritis in children. J Microbiol Immunol Infect 2006;39(4):342-347.

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    19.

    Frazee BW, Fee C, Lambert L: How common is MRSA


    in adult septic arthritis? Ann Emerg Med 2009;54(5):
    695-700.
    The authors studied the proportion of MRSA in emergency department patients with adult septic arthritis.

    24.

    257

    Section 2: Systemic Disorders

    2: Systemic Disorders

    34.

    35.

    Rutz E, Brunner R: Septic arthritis of the hip: Current


    concepts. Hip Int 2009;19(suppl 6):S9-S12.
    The authors discuss etiology and therapeutic options for
    septic arthritis of the hip.

    36.

    Ballock RT, Newton PO, Evans SJ, Estabrook M, Farnsworth CL, Bradley JS: A comparison of early versus
    late conversion from intravenous to oral therapy in the
    treatment of septic arthritis. J Pediatr Orthop 2009;
    29(6):636-642.
    The authors studied records of 186 patients from two
    childrens hospitals and concluded that clinical outcome
    in patients with septic arthritis converted to oral antibiotic therapy early in treatment based on defined criteria
    was similar to those patients converted later.

    37.

    Chang HC, Verhoeven W, Chay WM: Rubber foreign


    bodies in puncture wounds of the foot in patients wearing rubber-soled shoes. Foot Ankle Int 2001;22(5):409414.

    38.

    Raz R, Miron D: Oral ciprofloxacin for treatment of infection following nail puncture wounds of the foot. Clin
    Infect Dis 1995;21(1):194-195.

    39.

    258

    El-Sayed AM: Treatment of early septic arthritis of the


    hip in children: Comparison of results of open arthrotomy versus arthroscopic drainage. J Child Orthop
    2008;2(3):229-237.
    In a prospective controlled study, the authors compared
    results of open arthrotomy compared with those of arthroscopic drainage in the treatment of septic arthritis
    of the hip in children.

    Lavery LA, Peters EJ, Armstrong DG, Wendel CS, Murdoch DP, Lipsky BA: Risk factors for developing osteomyelitis in patients with diabetic foot wounds. Diabetes
    Res Clin Pract 2009;83(3):347-352.
    The results of this prospective study suggest that independent risk factors for developing osteomyelitis are
    deep, recurrent, multiple wounds; these findings may
    help in the diagnosis of foot osteomyelitis in high-risk
    patients.

    40.

    Jacobs RF, McCarthy RE, Elser JM: Pseudomonas osteochondritis complicating puncture wounds of the foot
    in children: A 10-year evaluation. J Infect Dis 1989;
    160(4):657-661.

    41.

    Peersman G, Laskin R, Davis J, Peterson M: Infection in


    total knee replacement: A retrospective review of 6489
    total knee replacements. Clin Orthop Relat Res 2001;
    392:15-23.

    42.

    Pulido L, Ghanem E, Joshi A, Purtill JJ, Parvizi J:


    Periprosthetic joint infection: The incidence, timing, and
    predisposing factors. Clin Orthop Relat Res 2008;
    466(7):1710-1715.
    The authors identified current risk factors of periprosthetic joint infection after modern joint arthroplasty.
    The incidence and timing of periprosthetic joint infection were also determined. Level of evidence: II.

    Orthopaedic Knowledge Update 10

    43.

    Herrmann M, Vaudaux PE, Vaudaux PE, Pittet D, et al:


    Fibronectin, fibrinogen, and laminin act as mediators of
    adherence of clinical staphylococcal isolates to foreign
    material. J Infect Dis 1988;158(4):693-701.

    44.

    Jmsen E, Huhtala H, Huhtala H, Puolakka T, Moilanen T: Risk factors for infection after knee arthroplasty: A register-based analysis of 43,149 cases. J Bone
    Joint Surg Am 2009;91(1):38-47.
    The authors used a large register-based series to study
    risk factors for infection after primary and revision knee
    replacement.

    45.

    McPherson EJ, Woodson C, Holtom P, Roidis N,


    Shufelt C, Patzakis M: Periprosthetic total hip infection:
    Outcomes using a staging system. Clin Orthop Relat
    Res 2002;403(403):8-15.

    46.

    McPherson EJ: Periprosthetic total knee infection, in


    Calhoun JH, Mader JT, eds: Musculoskeletal Infections.
    New York, NY, Marcel Dekker Inc, 2003, pp 293-324.

    47.

    Ghanem E, Parvizi J, Burnett RS, et al: Cell count and


    differential of aspirated fluid in the diagnosis of infection at the site of total knee arthroplasty. J Bone Joint
    Surg Am 2008;90(8):1637-1643.
    The authors used receiver operating characteristic
    curves to determine cutoff values for fluid leukocyte
    count and neutrophil differential to help diagnose infection at the site of a prosthetic joint.

    48.

    Burnett RS, Kelly MA, Hanssen AD, Barrack RL: Technique and timing of two-stage exchange for infection in
    TKA. Clin Orthop Relat Res 2007;464:164-178.
    The authors present classification and alternatives to a
    two-stage exchange procedure for infection in total knee
    arthroplasty and discuss current diagnosis and monitoring of infection. Level of evidence: V.

    49.

    Greene N, Holtom PD, Warren CA, et al: In vitro elution of tobramycin and vancomycin polymethylmethacrylate beads and spacers from Simplex and Palacos. Am
    J Orthop (Belle Mead NJ) 1998;27(3):201-205.

    50.

    Yamamoto K, Miyagawa N, Masaoka T, Katori Y,


    Shishido T, Imakiire A: Cement spacer loaded with antibiotics for infected implants of the hip joint. J Arthroplasty 2009;24(1):83-89.
    The authors used antibiotic-impregnated cement spacers
    in 17 cases of infection after total hip arthroplasty and
    bipolar arthroplasty. Results were good, with no recurring infection after a 3-year, 2-month follow-up period.

    51.

    Mohanty SS, Kay PR: Infection in total joint replacements: Why we screen MRSA when MRSE is the problem? J Bone Joint Surg Br 2004;86(2):266-268.

    52.

    Sankar B, Hopgood P, Bell KM: The role of MRSA


    screening in joint-replacement surgery. Int Orthop
    2005;29(3):160-163.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 21

    Pain Management
    Sharon M. Weinstein, MD, FAAHPM

    Introduction

    Dr. Weinstein or an immediate family member serves as


    a paid consultant to or is an employee of Wyeth Optum.

    2011 American Academy of Orthopaedic Surgeons

    Basic Physiology of Pain


    Pain is defined as a complex psychophysiologic phenomenon. It is the perceptual product of a complex integration of multiple brain circuits. Pain is a necessary
    and physiologic function of the nervous system. Pathologic pain results from abnormal nervous system functioning (neuropathic pain). A great deal of information
    has been learned in recent decades about the peripheral
    and central neurophysiologic mechanisms of human
    pain, including how acute pain states can become
    chronic conditions. A discrete human brain locus for
    the conscious perception of pain probably does not exist.
    Within the human nervous system there are mechanisms to transmit nociceptive signals, to inhibit nociception and produce analgesia, and to release analgesic
    mechanisms (antianalgesia) that facilitate healing and
    recovery. Human pain has both sensory (discriminative) and affective dimensions. The process of nociception begins when a noxious stimulus is transduced in
    the peripheral tissues. Nociceptive signals are transmitted over peripheral nerves to the central nervous system. Ascending transmission and modulation occur at

    2: Systemic Disorders

    Orthopaedic surgeons should be familiar with the basic


    assessment, diagnosis, and treatment of pain in various
    clinical settings (Table 1). Injury and surgery can cause
    acute pain. Some orthopaedic conditions may be associated with persistent or chronic pain that can significantly limit the patients functional status if not adequately managed. Collaboration between orthopaedic
    surgeons and other caregivers is required to provide
    state-of-the-art pain management in patients requiring
    both acute and chronic care.
    Pain remains medically undertreated for several reasons, including deficient professional education, societal concerns regarding the use of opioid analgesics
    (narcotics), and professional fear of regulatory agency
    influence. The lack of availability of analgesic drugs is
    also a significant problem in many areas of the world.
    The direct costs of unrelieved pain can be measured
    in dollars, in lost productivity, and in lives lost to suicide. Pain costs $60 to $100 billion each year in the
    United States alone.1 The loss of functional status and
    poor quality of life are frequent, intangible costs of unrelieved pain.
    Pain associated with noncancerous chronic conditions is highly prevalent. An estimated 75 million
    Americans suffer from chronic pain. Headache and low
    back pain are the most common types of noncancerrelated pain in developed countries. More than 26 million Americans between the ages of 20 and 64 years experience frequent back pain, and two thirds of
    American adults will have back pain during their lifetime.2 Other common conditions include inflammatory
    and degenerative musculoskeletal conditions, headache,
    jaw and lower facial pain (temporomandibular dysfunction, temporomandibular joint syndrome), neuropathic pain syndromes, and fibromyalgia (a complex
    condition involving generalized body pain and other
    symptoms). Chronic painful conditions in underdeveloped countries are more likely to be related to malnutrition; infectious diseases; and trauma, including limb
    amputation. Millions of the worlds inhabitants are affected by these conditions.

    General Considerations

    Table 1

    Basic Assessment and Treatment of Pain


    Preoperative Assessment
    Orthopaedic surgeon
    Anesthesiologist
    Primary care provider
    Pain specialist
    Intraoperative Care
    Orthopaedic surgeon
    Anesthesiologist
    Immediate Postoperative Care
    Orthopaedic surgeon
    Anesthesiologist
    Pain specialist
    Follow-up Care
    Orthopaedic surgeon
    Primary care provider
    Pain specialist

    Orthopaedic Knowledge Update 10

    259

    Section 2: Systemic Disorders

    Table 2

    Pathophysiologic Classification of Pain


    Nociceptive
    Somatic
    Visceral
    Nonnociceptive
    Neuropathic
    Psychogenic (rare)
    Unclassified Soft-Tissue Pain Syndromes
    Myofascial pain syndrome
    Fibromyalgia pain syndrome
    (Adapted with permission from Weinstein SM: Non-malignant pain, in Walsh D:
    Palliative Medicine. Philadelphia, PA, WB Saunders, 2009, pp 931-937.)

    2: Systemic Disorders

    spinal and supraspinal levels. Neuroanatomic pathways


    of nociceptive processing involve a human thalamic nucleus specific for pain and widely distributed cerebral
    cannabinoid receptors. Another receptor also widely
    distributed in the brain is termed the orphan opioid receptor; its natural ligand (nociceptin or orphanin FQ)
    appears to facilitate pain perception in animals and
    may be involved in learning and memory. Many chemical mediators and neurotransmitters involved in pain
    transduction, transmission, modulation, and perception
    have been identified. It is known that opioid receptors
    are widely distributed in nonneural tissues throughout
    the nervous system, leading to specific targets for pain
    relief, such as opioid joint injections. The contribution
    of other neurotransmitters, such as serotonin and norepinephrine, to the inhibition of pain signaling also is
    known.

    Pathophysiology and Pain Diagnosis


    Advances in neuroscience research in learning, memory,
    and neural plasticity have helped to elucidate the
    pathophysiology of chronic pain states. It has been observed that both membrane excitability and synaptic
    transmission are enhanced in sensory neurons with
    damaged axons. Signal proteins that are synthesized in
    response to such sensitization are probably distributed
    throughout the neuronal arbor and thus affect structural remodeling. Perceptions are encoded in both anatomic structures and temporal patterns of neural activity in the brain.
    Pain is a dynamic perceptual product of higher cortical processing. It is important to note that the central
    nervous system responds to nociceptive signals acutely
    with activity at the spinal cord, the brainstem, and the
    thalamus, and with immediate alterations in cortical
    somatosensory synaptic patterns. Structural as well as
    functional changes occur with repeated noxious stimuli, persistent damaging stimuli, or as a result of direct
    injury to the nervous system itself. Chronic noncancerous pain in humans may be attributable to pathologic
    functioning of a damaged nervous system at any level.
    A working classification of pain states, based on the
    260

    Orthopaedic Knowledge Update 10

    two broad categories of pain (nociceptive and nonnociceptive), is summarized in Table 2. Simple mechanisms
    for myofascial and fibromyalgia pain have not been
    identified.

    Acute Pain
    In the setting of injury, adequate control of acute pain
    is a necessary part of stabilizing the injured patient for
    further diagnostic evaluation and treatment. When surgery is planned, pain should be anticipated and a pain
    management plan should be developed before surgery
    whenever possible. Patients may be most cooperative
    when they are advised in advance of what can be expected and how pain will be managed. Medical evidence has accumulated indicating that applying nonpharmacologic and pharmacologic interventions in
    both preoperative (preemptive or preventive) and postoperative phases produces the best outcomes.3-6 These
    outcomes include pain prevention, faster recovery,
    shorter hospitalization time, and improved patient satisfaction.
    Current standards of pain management include the
    formal assessment of pain, the diagnosis of different
    physiologic mechanisms of pain, and the development
    of individualized treatment with nonpharmacologic
    and pharmacologic strategies. The synthesis of knowledge of how to minimize acute pain and improve postoperative recovery continues to advance, permitting
    some major orthopaedic procedures to be done in the
    outpatient or day-surgery setting.7,8 Specific pain management protocols are suggested for particular clinical
    situations such as geriatric hip fracture repair9 and for
    more refined perioperative analgesic techniques.10-12
    The optimal combination of analgesic medications and
    the use of vitamin C for postoperative pain prevention
    have been reported.13,14 The orthopaedic surgeon is in a
    pivotal position to prevent chronic pain by identifying
    unrelieved pain in the acute setting and by collaborating with other clinicians providing pain management.
    Consultation with pain specialists is suggested when
    patients with acute pain are not progressing as expected and for the collaborative management of persistent pain.

    Persistent Pain in Orthopaedic Patients


    Steps in the management of persistent (chronic) pain
    are (1) evaluating the patient and establishing the pain
    diagnoses, (2) identifying any curative treatments, (3)
    maximizing nonpharmacologic analgesic interventions,
    (4) tailoring analgesic medications to the individual,
    and (5) monitoring the patient for response to treatment and modifying the treatment plan accordingly.

    Patient Evaluation
    A thorough evaluation of the patient with persistent
    pain includes a comprehensive history, a physical exam-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 21: Pain Management

    Table 3

    Table 4

    PQRST Mnemonic for Eliciting a Complete


    History of Pain

    Physical Examination of the Patient With Pain

    P = palliative, provocative factors (what factors make pain


    better or worse)

    Patients appearance and vital signs


    Evidence of abnormalities such as weight loss, muscle
    atrophy, deformities, trophic changes

    Q = quality, word descriptors (such as burning or stabbing)


    R = region, radiation, referral (where does it hurt? does pain
    move or travel? radicular or nonradicular pattern?)
    S = severity (pain intensity rating scales or word descriptors)
    T = temporal factors (such as onset, duration, daily
    fluctuations, when did it start, constant and/or
    intermittent, how long does it last, better or worse at
    certain times of the day)
    (Adapted with permission from Weinstein SM: Non-malignant pain, in Walsh D:
    Palliative Medicine. Philadelphia, PA, WB Saunders, 2009, pp 931-937.)

    2011 American Academy of Orthopaedic Surgeons

    Pain Site Assessment


    Inspect the pain site(s) for abnormal appearance or color of
    overlying skin, change of contour, visible muscle spasm
    Palpate the site(s) for tenderness and texture
    Use percussion to elicit, reproduce, or evaluate the pain and
    any tenderness on palpation
    Determine the effects of physical factors such as position,
    pressure, and motion
    Neurologic Examination
    Mental status: level of alertness, higher cognitive functions,
    affect
    Cranial nerves
    Motor system: muscle bulk and tone, abnormal movements,
    manual motor testing, reflexes
    Sensory system: light touch and pin prick test to assess for
    allodynia, evoked dysesthesia, hypoesthesia,
    hyperesthesia, hypoalgesia, hyperalgesia, hyperpathia
    Coordination, station, and gait
    Musculoskeletal Examination
    Body type, posture, and overall symmetry
    Abnormal spine curvature, limb alignment, and other
    deformities
    Range of motion (spine, extremities)
    For muscles in neck, upper extremities, trunk, and lower
    extremities: observe for any abnormalities such as atrophy,
    hypertrophy, irritability, tenderness, trigger points

    2: Systemic Disorders

    ination, and a review of diagnostic information. The


    gold standard of pain assessment remains the patients
    self-report. Clinicians can use the PQRST mnemonic to
    elicit a complete pain history (Table 3). Certain characteristics suggestive of neuropathic pain should be elicited. Typically, patients describe burning or lancinating
    pain. Some patients report unusual symptoms such as
    painful numbness, itching, or crawling sensations. Neuropathic pain may also manifest as new, bizarre sensations that may frighten the patient and confuse clinicians. The detailed history is crucial to the diagnosis of
    specific pathophysiologic mechanisms of persistent
    pain.
    Pain intensity rating scales are used in clinical practice to establish a baseline against which the efficacy of
    analgesic interventions can be assessed. Many patients
    must be encouraged to verbalize their pain, and most
    need to learn how to report pain intensity. In circumstances in which patients are unable to communicate,
    behavioral observations may substitute for the patients
    report of pain intensity. Standardized tools are available to assess preverbal children and impaired adults.
    The Behavioral Pain Scale (BPS) and the FLACC Behavioral Pain Assessment Scale (acronym FLACC: face,
    legs, activity, cry, and consolability) have been validated in adult and pediatric populations.15,16
    There are different temporal patterns of persistent
    pain: constant pain, daily pain, intermittent/recurring
    pain that is predictable or regular, and intermittent/
    recurring pain that is unpredictable or irregular. Analgesic treatment approaches vary considerably according
    to the temporal pattern of the painful condition.
    Standardized pain assessment tools capture the impact of pain on mood, sleep, appetite, physical activities and social functioning. A psychosocial assessment
    should be performed and the meaning of pain to the individual and family should be explored. The expression
    of pain is influenced by a patients prior experience and
    social and cultural milieu. Psychosocial stressors should
    be elicited. A patients usual coping strategies and social

    General

    (Adapted with permission from Weinstein SM: Non-malignant pain, in Walsh D:


    Palliative Medicine. Philadelphia, PA, WB Saunders, 2009, pp 931-937.)

    support system should be understood. When formulating a medical treatment plan that includes the prescription of controlled substances, it is especially important
    to identify prior or current psychological dependency
    on licit or illicit drugs, including alcohol. Prior pain
    treatments, including prescription and nonprescription
    medications, and their relative efficacies should be recorded.
    It is important to assess the patients general physical
    condition and to identify physical findings that help to
    elucidate the pathophysiology of the reported pain (Table 4). The physiologic signs of acute painelevated
    blood pressure, respiratory rates, and pulse ratesare
    not reliable in patients with subacute and chronic pain.
    The pain specialist will perform a complete physical
    examination including a detailed neurologic examination, especially if neuropathic pain is suspected. Pain in
    an area of reduced sensation, allodynia (pain elicited by
    normally nonpainful stimuli), and hyperpathia (summation of painful stimuli) indicate neural dysfunction.
    The diagnosis of a complex regional pain syndrome,

    Orthopaedic Knowledge Update 10

    261

    Section 2: Systemic Disorders

    Table 5

    Diagnostic Testing for Persistent Pain Associated With a Noncancerous Condition


    Types of Tests

    Uses for the Tests

    Screening laboratory test: complete blood cell count, chemistry


    profile (for example, electrolytes, liver, enzymes, blood urea
    nitrogen, creatinine), urinalysis, erythrocyte sedimentation rate

    Screen for medical illnesses, organ dysfunction

    Disease-specific laboratory tests: includes autoantibodies and sickle


    cell test

    Autoimmune disorders, sickle cell disease

    Imaging studies: radiographs, CT, MRI, ultrasound, myelography

    Detection of tumors, other structural abnormalities

    Diagnostic procedures: lumbar puncture for cerebrospinal fluid


    analysis

    Detection of various central nervous system illnesses

    Electrophysiologic tests: electromyography (direct examination of


    skeletal muscle), nerve conduction velocity (examination of
    conduction along peripheral nerves)

    Detection of myopathy, neuropathy, radiculopathy

    Diagnostic nerve block: injection of a local anesthetic to determine


    the source and/or mechanism of the pain

    Identification of structures responsible for the pain


    (such as sacroiliac or facet joint blocks),
    differentiation of pain pathophysiology

    (Adapted with permission from Weinstein SM: Non-malignant pain, in Walsh D: Palliative Medicine. Philadelphia, PA, WB Saunders, 2009, pp 931-937.)

    2: Systemic Disorders

    previously termed sympathetically maintained pain


    (causalgia or reflex sympathetic dystrophy), is suggested when there are signs of marked sympathetic nervous dysfunction and other physical abnormalities.
    A careful mechanical and soft-tissue evaluation is
    part of the comprehensive pain evaluation. Soft-tissue
    conditions may contribute to ongoing pain. Muscle
    spasms, tender musculotendinous points of fibromyalgia, or discrete muscle trigger points may be palpated;
    when stimulated, pain may be referred to another site
    in a predictable pattern (criteria for myofascial pain
    syndrome).

    Pain Diagnosis
    Correlation should be made between clinical symptoms; physical signs; and diagnostic, laboratory, and radiographic information to establish the pain diagnosis
    (Table 5). There is no definitive test to confirm pain,
    and the pain diagnosis depends not only on clinical assessment, but also on the clinicians complete understanding of normal and abnormal nervous system physiology as previously described. In patients with chronic
    orthopaedic conditions, there are likely to be multiple
    pathophysiologic mechanisms underlying the patients
    reported pain; each should be clearly identified to form
    the basis of a multimodal treatment plan.
    Low back pain, arthritides, neuropathic pain (such
    as painful diabetic neuropathy, postherpetic neuralgia,
    and pain from nerve injury),17,18 and other conditions
    require daily management on the part of the patient
    that includes lifestyle modifications. Published guidelines for the management of chronic painful conditions
    outline the proper diagnosis, nonpharmacologic approaches, and pharmacologic treatment.19
    262

    Orthopaedic Knowledge Update 10

    Pain Treatment

    Nonpharmacologic Interventions
    Anesthetic and Neurosurgical Procedures
    Many anesthetic procedures can be done in the outpatient setting.20
    Patients with pain may also be evaluated by the neurosurgeon to determine the indication for implanted intrathecal systems for opioid delivery, neuroaugmentation (nervous system stimulation), or neuroablative
    (destructive) surgical procedures. Nonpharmacologic
    strategies using neurostimulation or neuroaugmentation techniques are being refined and may produce pain
    relief that lessens the requirement for systemic medications.21
    Physical Treatment and Psychological and Behavioral
    Interventions
    Specific treatments (such as soft-tissue manipulation)
    for myofascial pain and musculoskeletal disorders may
    be performed in the clinic. Patients with pain should be
    referred to physical medicine and rehabilitation physicians to determine the need for rehabilitation and occupational and physical therapy programs.
    Pain specialists work closely with psychiatrists and
    mental health practitioners to evaluate and treat pain
    along with concurrent psychiatric or psychological conditions. Cognitive and behavioral therapy, relaxation
    training, hypnosis, individual therapy, family psychotherapy, and psychoeducational support groups are
    useful as adjunctive outpatient pain treatments.20 Spiritual support is a part of maintaining overall wellness
    especially in the setting of life-threatening illness and
    end-of-life care. Many patients with chronic noncancerous pain use a variety of complementary and alterna-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 21: Pain Management

    tive medicine techniques for pain relief.22 Clinicians


    should inquire about their patients use of these methods.

    people, and marginalized people. It is recognized that


    societal concerns related to drug abuse and diversion
    should not outweigh a patients rights to compassionate, effective pain treatment.

    Pharmacologic Treatment
    Analgesic medications are considered to have broad effects, including reducing transduction of painful peripheral stimuli, altering pain transmission within the central nervous system, or altering pain perception at the
    higher cortical level. Nonsteroidal anti-inflammatory
    drugs (NSAIDs) and acetaminophen, the opioids, and an
    assorted group of medications referred to as adjuvant analgesics or coanalgesics are the three main classes of
    drugs used to treat pain.
    Complex pharmacotherapy is the rational combination of analgesic medications that work through different mechanisms within the human nervous system to
    produce pain relief. Many patients with chronic noncancerous pain are prescribed medications from more
    than one drug class. The best results are obtained by individualized medication management in the context of
    a well-established therapeutic relationship. NSAIDs
    and acetaminophen are used for mild nociceptive pain.
    Patients requiring long-term treatment should be monitored for cumulative renal and hepatic toxicity.

    Adjuvant Analgesics
    Adjuvant analgesics are a heterogeneous class of medications, which are administered to provide additive analgesic effects, to counteract the adverse side effects of
    more traditional analgesics such as NSAIDs and opioids, and/or to treat a concurrent symptom. Adjuvant
    analgesics include antidepressants, anticonvulsants, antihistamines, psychostimulants, muscle relaxants, antispasmodics, and oral local anesthetics. Topical agents
    are useful to spare systemic drug burden.23

    Evidence-Based Guidelines
    Numerous professional societies and government agencies have developed guidelines and policies for the
    treatment of chronic noncancerous pain.19,24-27 General
    policies emphasize the obligation of clinicians to properly assess and treat pain. Clinical guidelines detail the
    management approaches and outline specific considerations for special populations, such as children, elderly

    2011 American Academy of Orthopaedic Surgeons

    The successful management of chronic noncancerous


    pain is dependent on individualized care. Clinicians
    working with patients on a long-term basis to manage
    pain follow several outcome variables to judge the efficacy of the pain management plan. These include the
    patients self-report of pain intensity, pain relief, side effects of treatment, adverse events, quality of life, and
    functional status. Patients with severe persistent pain
    related to orthopaedic conditions that are not expected
    to resolve will likely benefit from pain specialty care in
    conjunction with primary orthopaedic care. Ongoing
    communication between care providers is important,
    especially when patients are treated with complex pharmacotherapy, including controlled substances.

    Special Considerations
    The Pediatric Population
    Although much progress has been made in identifying
    pain in children, pain management in the pediatric population remains challenging.28,29 Medications for pain
    are generally tested in only adults, leaving questions regarding appropriate pediatric dosing, efficacy, and
    safety. In 2001, the American Academy of Pediatrics
    developed guidelines for managing acute pain in infants, children, and adolescents.30 More recently, organizational changes needed for improved pain management in hospitalized children have been identified.31
    Regional anesthesia and spinal techniques for postoperative pain control in children have been tested.32-34 A
    specific approach to acute postoperative pain control in
    children with chronic disabilities has been described. A
    conceptual model and practice framework for managing chronic pain in children and adolescents also has
    been proposed.35 Parental beliefs and worries regarding
    adolescent chronic pain have been explored, relating to
    the meaning of pain itself and concerns with effects of
    medications.36

    2: Systemic Disorders

    Opioid Analgesics
    Oral administration of opioid analgesics is preferred
    because of convenience and costs. Modified release or
    long-acting preparations are recommended to produce
    more uniform serum drug levels and to enhance patient
    compliance with dosing. Alternative methods of administration are considered when the oral method is unavailable, if oral dosing is impractical, or if systemic
    adverse side effects are unmanageable. Patients may remain ambulatory with external pumps for subcutaneous, intravenous, or intraspinal (epidural, intrathecal)
    drug delivery. Implantable systems for the administration of intrathecal opioid and nonopioid medications
    are available.

    Outcomes of Pain Management

    The Elderly Population


    Pain management in elderly patients also has been a focus for guideline development. In 2009, the American
    Geriatric Society updated its guideline for the pharmacologic management of chronic pain in older persons,
    specifying risks and benefits of different analgesics and
    outlining the role of opioid analgesics in the treatment
    of pain.37 A higher prevalence of chronic painful orthopaedic conditions requiring clinical management can be
    expected in the aging US population. Interdisciplinary
    programs to reduce pain and improve function in older
    adults after orthopaedic surgery have been tested.9
    Given the prevalence of hip fractures, coordinated orthogeriatric care is suggested for this subpopulation;38
    the perception of pain as an important clinical variable
    in this setting is recognized.39

    Orthopaedic Knowledge Update 10

    263

    Section 2: Systemic Disorders

    Opioid Therapy
    The management of chronic pain with long-term opioid
    therapy remains controversial, although some patients
    clearly benefit from this treatment approach.40 Federal
    standards indicate that prescribers have dual responsibilities to treat patients adequately while taking steps to
    minimize prescription drug diversion and abuse. Current guidelines emphasize the comprehensive evaluation
    and multidisciplinary treatment of patients with severe
    chronic pain. The use of written treatment agreements
    and regular monitoring, including drug screening, are
    suggested when controlled substances are prescribed.19
    Long-term opioid therapy should be prescribed only by
    clinicians with adequate knowledge, skill, and the necessary clinical infrastructure with interdisciplinary support. There are no established patient selection criteria
    for opioid therapy; clinicians are advised to follow relevant literature as it emerges.

    2: Systemic Disorders

    Methadone Therapy
    Methadone is an effective, inexpensive analgesic that is
    generally available. It is a potent, synthetic diphenylheptane-derivative opioid agonist. Its pharmacokinetics and
    pharmacodynamics vary considerably from those of
    morphine. Methadone has high oral bioavailability, three
    times that of morphine. Methadone is metabolized extensively by the cytochrome P450 system. Unlike modified or time-released opioid formulations, methadone
    has a rapid and extensive initial distribution phase,
    which occurs within 2 to 3 hours, and a prolonged elimination phase, which may last from 15 to 60 hours.
    Methadone can accumulate to high levels with repeated
    dosing. Rates of elimination from the body vary widely.
    The broad interindividual variability in methadone metabolism also confers special risks when patients are undergoing dose conversion from other opioids to
    methadone.41-43
    There is emerging concern that patients prescribed
    methadone by inexperienced practitioners may be at increased risk of death from inadvertent drug accumulation and its resultant respiratory depression.44 As a result of this evidence, in November 2006 the United
    States Food and Drug Administration issued a specific
    warning to prescribers regarding methadone.45
    There also has been increasing attention to the potential cardiac toxicity associated with methadone.
    Daily doses of more than 100 mg may be associated
    with cardiac arrhythmias, including the potentially fatal torsades de pointes. Caution in prescribing methadone is advised in the opioid-nave patient (a patient
    who has not taken opioids). Equianalgesic conversion
    ratios should be used conservatively when converting
    opioid prescriptions, especially in conversions from
    other opioids to methadone. Clinicians prescribing
    methadone for the first time are strongly encouraged to
    consult with a qualified pain specialist regarding doses
    and titration schedules.46-49
    264

    Orthopaedic Knowledge Update 10

    The Role of the Orthopaedic Surgeon in Palliative and End-of-Life Care


    The World Health Organization defines palliative care
    as an approach to care that improves quality of life of
    patients facing life-threatening illness and their families,
    through the prevention and relief of suffering by means
    of early identification and impeccable assessment and
    treatment of pain and other problems, physical, psychosocial, and spiritual.50 Although palliative care
    specialists have become more widely available for consultation, the care of patients at the end of life is central
    to the practice of medicine and surgery.
    There are three elements which define palliative
    care: (1) medical symptom management, (2) psychosocial and spiritual support of the patient and family, and
    (3) advanced care planning.51 An integrated palliative
    care model implies treatment of patients starting at the
    time of diagnosis and continuing throughout the course
    of the illnessfrom treatment to cure, in disease relapse, or through disease progression to death.
    Regardless of the prognosis, soon after receiving a
    diagnosis of a life-limiting condition, most patients will
    receive disease-modifying therapy, medical supportive
    care, and palliative care aimed at relief of symptoms
    (the integrated model). However, as the disease progresses to death, the goals of care for the terminally ill
    patient shift away from cure-oriented medical treatment to providing comfort and dignity at the end of
    life. Specifically, goals shift to relief of pain and other
    distressing symptoms, maintenance of function, support of family and personal relationships, avoidance of
    impoverishment, and attentiveness to meaningful activities and spiritual issues.
    Orthopaedic surgeons play varied clinical roles in the
    setting of life-limiting illness. They may act as the primary treating physician for patients with conditions
    that are curable by surgical intervention (for example,
    certain sarcomas). They may provide intensive care of
    critically ill surgical patients, some of whom have a
    poor prognosis. The orthopaedic surgeon may also act
    as a partner in the management of patients with various
    life-limiting illnesses such as cancer. They may be called
    on to evaluate the use of possible palliative surgical care
    in patients with advanced illness. For example, procedures such as hip joint replacement may significantly
    improve functional status and overall quality of life
    even in patients with incurable widely metastatic bone
    disease. The fundamental principles of palliative care
    should be understood by the orthopaedic surgeon and
    applied in the settings in which they practice, regardless
    of if they are acting in a primary or collaborative role.
    During the past decade, numerous policy statements
    and guidelines have been developed for palliative and
    end-of-life care in the United States. It has been noted
    that historically there is little discussion of palliative
    and end-of-life care in surgical textbooks, despite the
    important contributions surgeons can make.52
    Multispecialty, interdisciplinary care of seriously ill
    and dying patients is now standard practice. This re-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 21: Pain Management

    Table 6

    Palliative Orthopaedic Surgical Interventions


    General Goals
    Reconstruction
    Restoration of function
    Symptom control
    Disease control
    Tumor resection
    Control of hemorrhage, discharge, odor
    Wound management
    Specific Procedures
    Bone
    Fracture stabilization
    Spine
    Laminectomy
    Decompression of spinal cord or cauda equina
    Stabilization
    Vertebroplasty
    Kyphoplasty

    Ethical Considerations
    Ethical considerations may arise in relation to declining
    to intervene and withdrawing specific medical interventions. Advance care planning is essential for the prevention of unwanted interventions and, more importantly,
    for supporting families when they act as surrogate decision makers in choosing to accept, decline, or stop
    specific interventions.

    2011 American Academy of Orthopaedic Surgeons

    2: Systemic Disorders

    quires teamwork in both the inpatient and outpatient


    settings. Orthopaedic surgeons will relate to other physicians, nurses, mental health professionals, spiritual
    advisors and clinical support staff of various disciplines. Extensive discussions with patients, families,
    and other health care professionals in this setting require time and patience.53,54 Surgeons should have palliative care competencies in five areas: patient care,
    medical knowledge, communication, professionalism,
    and systems-based practice.55
    It is important for the orthopaedic surgeon to characterize planned surgeries as either curative or palliative. When terminally ill patients present with advanced
    disease that requires palliative surgery, the patient must
    be assessed with the intent of resolving symptoms; controlling pain, the morbidity of disease, and therapy regimens; and improving the patients quality of life. After
    assessing the patient, the orthopaedic surgeon will recommend the intervention that will best maximize
    symptom relief and minimize complications. When a
    procedure is selected and performed with palliative intent, treatment goals must be clearly defined and communicated to the patient and family. Because treatment
    choices can greatly affect a patients final days, effective
    palliation of terminally ill patients demands the highest
    level of surgical judgment.56 Preoperative assessment
    and discussions are important because the goals of the
    patient, family, and orthopaedic surgeon should be
    complementary57,58 (Table 6).

    Health care professionals have an obligation to provide treatments that carry a favorable balance of benefits to burdens or risks. Treatments with a favorable
    balance should be offered with the appropriate recommendation. In many circumstances the balance of benefits to burdens or risks are not clearly overwhelming
    and are regarded as optional; these decisions may be
    more difficult for patients and families. Treatments that
    have only a minimal chance of benefit but which have
    overwhelming burdens or risks for the patient should
    not be offered.
    The moral dilemmas that arise in palliative care and
    end-of-life care regarding treatments intended primarily
    to prolong or sustain life relate to the balance between
    the benefits and the burdens of treatment. Medical professions do not have a duty to extend life at all costs. In
    certain circumstances, such as when treatment is considered futile, when burdens and risks greatly outweigh
    the benefits of treatment, when treatment will not further the total good of the patient, and when treatments
    are not available because of resource constraints, it is
    ethical for providers not to offer life-prolonging treatment. This last aspect may pose the most difficult dilemma for physicians. A more extensive discussion of
    these ethical issues is beyond the scope of this chapter.
    Health care professionals practicing palliative and
    end-of-life care are encouraged to read, reflect, and discuss difficult issues as they arise. Orthopaedic surgeons
    are strongly encouraged to be familiar with principles
    of medical ethics and to participate in family conferences, interdisciplinary treatment planning meetings,
    and ethics committees.

    Summary
    With continued basic and clinical research, improvements are anticipated in diagnostic imaging, which will
    better define clinical pain states; new pharmacologic
    and nonpharmacologic treatments of pain; and in the
    development of standardized measures of clinical outcomes in pain management. To best serve their patients
    in all clinical settings, orthopaedic surgeons should
    have a basic understanding of pain physiology and familiarity with state-of-the-art pain management techniques.

    Annotated References
    1. The NIH Guide: New Directions in Pain Research I.
    Washington, DC: Government Printing Office, 1998.
    2.

    American Pain Society: Pain Facts. 2005. http://


    www.ampainsoc.org

    3.

    Hebl JR, Dilger JA, Byer DE, et al: A pre-emptive multimodal pathway featuring peripheral nerve block improves perioperative outcomes after major orthopedic
    surgery. Reg Anesth Pain Med 2008;33(6):510-517.

    Orthopaedic Knowledge Update 10

    265

    Section 2: Systemic Disorders

    The authors report that a comprehensive, preemptive,


    multimodal analgesic regimen improved perioperative
    outcomes and resulted in fewer adverse events, shorter
    hospitalization times, and a significant reduction in urinary retention and ileus formation in patients treated
    with total hip or total knee arthroplasty. Level of evidence: III.
    4.

    Grape S, Tramer MR: Do we need preemptive analgesia


    for the treatment of postoperative pain? Best Pract Res
    Clin Anaesthesiol 2007;21:51-63.
    The authors suggest that routine multimodal analgesic
    treatment is better supported than preemptive approaches at this time.

    6.

    Duellman TJ, Gaffigan C, Milbrandt JC, Allan DG:


    Multi-modal, pre-emptive analgesia decreases the length
    of hospital stay following total joint arthroplasty. Orthopedics 2009;32(3):167.

    2: Systemic Disorders

    The authors of this retrospective study reported that,


    compared to standard patient-controlled analgesia, multimodal preemptive analgesia resulted in better outcomes for patients, including a decrease in the likelihood of discharge to a skilled nursing facility. Level of
    evidence: III.
    7.

    12.

    Choi PT, Bhandari M, Scott J, Douketis J: Epidural analgesia for pain relief following hip or knee replacement. Cochrane Database Syst Rev 2003;3:CD003071.

    13.

    Montane E, Vallano A, Vallano A, Aguilera C, Vidal X,


    Laporte JR: Analgesics for pain after traumatic or orthopaedic surgery: What is the evidence. A systematic
    review. Eur J Clin Pharmacol 2006;62(11):971-988.

    14.

    Besse JL, Gadeyne S, Galand-Desm S, Lerat JL, Moyen


    B: Effect of vitamin C on prevention of complex regional pain syndrome type I in foot and ankle surgery.
    Foot Ankle Surg 2009;15(4):179-182.
    This quasi-experimental study demonstrates the effect of
    vitamin C in preventing complex regional pain syndrome type I after foot and ankle surgery. Level of evidence: II.

    15.

    Nilsson S, Finnstrm B, Kokinsky E: The FLACC behavioral scale for procedural pain assessment in children aged 5-16 years. Paediatr Anaesth 2008;18(8):767774.
    The FLACC tool is appropriate for use in pediatric settings.

    16.

    Cade CH: Clinical tools for the assessment of pain in sedated critically ill adults. Nurs Crit Care 2008;13(6):
    288-297.
    The Behavioral Pain Scale has been validated for use in
    pediatric and adult populations.

    17.

    Morley-Foster P: Prevalence of neuropathic pain and


    need for treatment. Pain Res Manag 2006;11(suppl A):
    5A-10A.

    18.

    DworkinRH, Backonja M, Rowbotham MC, et al: Advances in neuropathic pain: Diagnosis, mechanisms, and
    treatment recommendations. Arch Neurol 2003;60(11):
    1524-1534.

    Berger RA, Sanders SA, Thill ES, Sporer SM, Della Valle
    C: Newer anesthesia and rehabilitation protocols enable
    outpatient hip replacement in selected patients. Clin Orthop Relat Res 2009;467(6):1424-1430.
    The authors report that newer anesthesia and outpatient
    rehabilitation protocols may result in better outcomes at
    a higher cost. Level of evidence: IV.

    8.

    Parker RD, Streem K, Schmitz L, Martineau PA; Marguerite Group: Efficacy of continuous intra-articular
    bupivacaine infusion for postoperative analgesia after
    anterior cruciate ligament reconstruction: A doubleblinded, placebo-controlled, prospective, and randomized study. Am J Sports Med 2007;35(4):531-536.
    The authors report the results of this study to evaluate
    outcomes of continuous intra-articular bupivacaine infusion for postoperative analgesia after anterior cruciate
    ligament reconstruction. This technique produced no
    distinct advantage in terms of reported pain and analgesic consumption in the postoperative period. Level of
    evidence: I.

    Reuben SS, Buvanendran A: Preventing the development


    of chronic pain after orthopaedic surgery with preventive multimodal analgesic techniques. J Bone Joint Surg
    Am 2007;89(6):1343-1358.
    Effective multimodal analgesic techniques are reviewed
    in this article.

    5.

    11.

    Parvizi J, Porat M, Gandhi K, Viscusi ER, Rothman


    RH: Postoperative pain management techniques in hip
    and knee arthroplasty. Instr Course Lect 2009;58:769779.
    The authors present a review of current multimodal and
    preemptive analgesia techniques.

    9.

    Morrison RS, Flanagan S, Fischberg D, Cintron A, Siu


    AL: A novel interdisciplinary analgesic program reduces
    pain and improves function in older adults after orthopedic surgery. J Am Geriatr Soc 2009;57(1):1-10.
    The authors report the results of a study to evaluate the
    effect of a multicomponent intervention on pain and
    function after orthopaedic (hip and knee) surgery in a
    large metropolitan hospital. Level of evidence: I.

    10.

    266

    Hudcova J, McNicol E, Quah C, Lau J, Carr DB: Patient controlled opioid analgesia versus conventional
    opioid analgesia for postoperative pain. Cochrane Database Syst Rev 2006;4:CD003348.

    Orthopaedic Knowledge Update 10

    19. Model Policy for the Use of Controlled Substances for


    the Treatment of Pain. Dallas, TX, Federation of State
    Medical Boards of the United States, Inc., 2004.
    20. Weinstein SM: Non-malignant pain, in Walsh D, Caraceni AT, Fainsinger R, eds: Palliative Medicine. Miamisburg, OH, Elsevier, 2008.
    A review of the assessment and interdisciplinary management of chronic noncancerous pain is presented.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 21: Pain Management

    21.

    22.

    Nicolaidis S: Neurosurgical treatments of intractable


    pain. Metabolism 2010;59(suppl 1):S27-S31.
    A thorough review of state-of-the art neurosurgical pain
    interventions is presented.

    in a large pediatric cohort demonstrated feasibility and


    safety. Level IV.
    Khoury CE, Dagher C, Ghanem I, Naccache N, Jawish
    D, Yazbeck P: Combined regional and general anesthesia for ambulatory peripheral orthopedic surgery in children. J Pediatr Orthop B 2009;18(1):37-45.
    The authors report on pain control and parental satisfaction in this prospective study of combined regional
    anesthesia and general anesthesia to support ambulatory
    surgery in children. Combined techniques resulted in
    improved patient pain control and better parental satisfaction. Level of evidence: IV.

    34.

    Tobias JD: A review of intrathecal and epidural analgesia after spinal surgery in children. Anesth Analg 2004;
    98(4):956-965.

    35.

    Kozlowska K, Rose D, Khan R, Kram S, Lane L, Collins


    J: A conceptual model and practice framework for managing chronic pain in children and adolescents. Harv
    Rev Psychiatry 2008;16(2):136-150.
    The integrated, family-based assessment and treatment
    approach to pain is aimed at restoration of normal functioning and improved symptom control. Level of evidence: IV.

    36.

    Guite JW, Logan DE, McCue R, Sherry DD, Rose JB:


    Parental beliefs and worries regarding adolescent
    chronic pain. Clin J Pain 2009;25(3):223-232.
    This retrospective review indicates that parental beliefs
    about pain may have implications for treatment in adolescents. Level of evidence: III.

    37.

    American Geriatrics Society Panel on Pharmacological


    Management of Persistent Pain in Older Persons: Pharmacological management of persistent pain in older persons. J Am Geriatr Soc 2009;57(8):1331-1346.
    An updated review of guidelines for best practices in the
    medical management of persistent pain in elderly patients is presented.

    38.

    Pioli G, Giusti A, Barone A: Orthogeriatric care for the


    elderly with hip fractures: Where are we? Aging Clin
    Exp Res 2008;20(2):113-122.
    The coordinated, multidisciplinary care for elderly patients with hip fractures provided by an orthogeriatric
    center is described.

    39.

    Arinzon Z, Gepstein R, Shabat S, Berner Y: Pain perception during the rehabilitation phase following traumatic hip fracture in the elderly is an important prognostic factor and treatment tool. Disabil Rehabil 2007;
    29(8):651-658.
    Pain intensity is a prognostic factor that predicts outcomes of rehabilitation following hip fractures in elderly
    patients. Level of evidence: II.

    40.

    Trescot AM, Helm S, Hansen H, et al: Opioids in the


    management of chronic non-cancer pain: An update of
    American Society of the Interventional Pain Physicians
    (ASIPP) Guidelines. Pain Physician 2008;11(2, suppl)
    S5-S62.

    Nation Center for Complementary and Alternative


    Medicine Web site. http://Nccam.nih.gov. Accessed January 22, 2010.
    This site provides information on the safety and effectiveness of alternative therapies not considered part of
    conventional allopathic medicine.

    23. Principles of Analgesic Use in the Treatment of Acute


    Pain and Cancer Pain, ed 6. Skokie, IL, American Pain
    Society, 2008.
    This text is an updated guide to medication management of pain.
    24. Guidelines for the Management of Pain in Osteoarthritis, Rheumatoid Arthritis, and Juvenile Chronic Arthritis, ed 2. Skokie, IL, American Pain Society, 2002.
    25. Guidelines for the Management of Acute and Chronic
    Pain in Sickle Cell Disease. Skokie, IL, American Pain
    Society, 1999.
    26. Guidelines for the Management of Fibromyalgia Syndrome Pain in Adults and Children. Skokie, IL, American Pain Society, 2005.
    27. Pain Control in the Primary Care Setting. Skokie, IL,
    American Pain Society, 2006.
    28.

    Greco C, Berde C: Pain management for the hospitalized pediatric patient. Pediatr Clin North Am 2005;
    52(4):995-1027.

    29.

    Walker SM: Pain in children: Recent advances and ongoing challenges. Br J Anaesth 2008;101(1):101-110.
    The author reviews current practice challenges and research initiatives in pediatric pain management.

    30.

    American Academy of Pediatrics, Committee on Psychosocial Aspects of Child and Family Health; Task
    Force on Pain in Infants, Children, and Adolescents:
    The assessment and management of acute pain in infants, children, and adolescents. Pediatrics 2001;108(3):
    793-797.

    31.

    Dowden S, McCarthy M, Chalkiadis G: Achieving organizational change in pediatric pain management. Pain
    Res Manag 2008;13(4):321-326.
    Deficiencies in pediatric pain management and barriers
    to achieving effective pain management are discussed.
    Institutional improvement strategies are presented.

    32.

    Dadure C, Bringuier S, Raux O, et al: Continuous peripheral nerve blocks for postoperative analgesia in children: Feasibility and side effects in a cohort study of
    339 catheters. Can J Anaesth 2009;56(11):843-850.
    A study to evaluate the indications, efficacy, and adverse
    events of the use of continuous peripheral nerve blocks

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    2: Systemic Disorders

    33.

    267

    Section 2: Systemic Disorders

    The authors present a review of the current guidelines


    for opioid therapy of noncancerous pain.
    41.

    Corkery JM, Schifano F, Ghodse AH, Oyefeso A: The


    effects of methadone and its role in fatalities. Hum Psychopharmacol 2004;19(8):565-576.

    42.

    Karch SB, Stephens BG: Toxicology and pathology of


    deaths related to methadone: Retrospective review. West
    J Med 2000;172(1):11-14.

    43.

    Wolff K: Characterization of methadone overdose: Clinical considerations and the scientific evidence. Ther
    Drug Monit 2002;24(4):457-470.

    44.

    Centers for Disease Control and Prevention (CDC): Increase in poisoning deaths caused by non-illicit drugs
    Utah, 1991-2003. MMWR Morb Mortal Wkly Rep
    2005;54(2):33-36.

    2: Systemic Disorders

    45.

    268

    US Food and Drug Administration Web site. Public


    Health Advisory: Methadone Use for Pain Control May
    Result in Death and Life-Threatening Changes in
    Breathing and Heart Beat. http://www.fda.gov/Drugs/
    DrugSafety/PublicHealthAdvisories/ucm124346.htm.
    Accessed January 25, 2010.

    49.

    Fanoe S, Hvidt C, Hvidt C, Ege P, Jensen GB. Syncope


    and QT prolongation among patients treated with
    methadone for heroin dependence in the city of Copenhagen. Heart 2007;93(9):1051-1055.
    The authors present the findings of a clinical review of
    methadone-related cardiac conduction changes and adverse effects.

    50.

    WHO Expert Committee: Cancer Pain Relief and Palliative Care. Geneva, Switzerland, World Health Organization, 1998.

    51.

    Weinstein SM: Integrating palliative care in oncology.


    Cancer Control 2001;8(1):32-35.

    52.

    Easson AM, Crosby JA, Librach SL: Discussion of death


    and dying in surgical textbooks. Am J Surg 2001;
    182(1):34-39.

    53.

    Lee KF, Purcell GP, Hinshaw DB, Krouse RS, Baluss M:


    Clinical palliative care for surgeons: Part 1. J Am Coll
    Surg 2004;198(2):303-319.

    54.

    Lee KF, Johnson DL, Purcell GP, Hinshaw DB, Krouse


    RS, Baluss M: Clinical palliative care for surgeons: Part
    2. J Am Coll Surg 2004;198(3):477-491.

    55.

    Surgeons Palliative Care Workshop: Robert Wood Johnson Foundation Office of Promoting Excellence in Endof-Life Care: Executive summary of the report from the
    field. J Am Coll Surg 2003;196(5):807-815.

    56.

    Cullinane CA, Borneman T, Smith DD, Chu DZ, Ferrell


    BR, Wagman LD: The surgical treatment of cancer: A
    comparison of resource utilization following procedures
    performed with a curative and palliative intent. Cancer
    2003;98(10):2266-2273.

    46.

    Martell BA, Arnsten JH, Krantz MJ, Gourevitch MN:


    Impact of methadone treatment on cardiac repolarization and conduction in opioid users. Am J Cardiol
    2005;95(7):915-918.

    47.

    Pearson EC, Woosley RL: QT prolongation and torsades de pointes among methadone users: Reports to
    the FDA spontaneous reporting system. Pharmacoepidemiol Drug Saf 2005;14(11):747-753.

    48.

    Peles E, Bodner G, Kreek MJ, Rados V, Adelson M:


    Corrected-QT intervals as related to methadone dose
    and serum level in methadone maintenance treatment
    (MMT) patients: A cross-sectional study. Addiction
    2007;102(2):289-300.

    57.

    Miner TJ, Jaques DP, Shriver CD: A prospective evaluation of patients undergoing surgery for the palliation
    of an advanced malignancy. Ann Surg Oncol 2002;9(7):
    696-703.

    A clinical review of methadone dose-related cardiac


    conduction changes is presented, showing that in some
    patients dangerous prolongation of QT interval can be
    dose related.

    58.

    Frasscia FJ, Frasscia DA, Jacofsky DJ, Sim FH: Palliative orthopaedic surgery, in Berger AM, Portenoy RK,
    Weissman DE, eds: Principles and Practice of Palliative
    Care and Supportive Oncology, ed 2. Philadelphia, PA,
    Lippincott Williams and Wilkins, 2002, pp 722-730.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    This page intentionally left blank

    This page intentionally left blank

    Chapter 22

    Shoulder Trauma: Bone


    Joseph A. Abboud, MD

    N. Douglas Boardman III, MD

    Clavicle Fractures
    The clavicle, one of the most commonly fractured
    bones, accounts for 2.6% to 4% of all adult fractures
    and approximately 35% of injuries to the shoulder girdle.1 Clavicle fractures can involve the midshaft (69%
    to 83%), lateral end (28%), and/or medial end (2% to
    3%) and are typically caused by either a fall on an outstretched arm or a direct blow. Shaft fractures occur
    most commonly in young adults, whereas lateral and
    medial fractures are more common in elderly patients.2

    Presentation
    In displaced midshaft fractures, the sternocleidomastoid and trapezius muscles pull the medial fragment superiorly and posteriorly, respectively, whereas the
    weight of the arm and pectoralis major pull the lateral
    fragment inferomedially, producing ptosis of the involved shoulder. With severely angulated or comminuted fractures, fragments may buttonhole subcutaneously through the platysma muscle (Figure 1). Because
    the clavicle is in close proximity to the brachial plexus
    and subclavian vessels, associated neurovascular injury
    may occur (3%).2

    Radiographic Evaluation
    A clavicle fracture is typically initially visualized on AP
    radiographs of the shoulder or the chest. A true AP
    view of the clavicle and a 30 cephalic tilt view should
    be obtained to allow biplanar assessment of the bony
    deformity. CT with three-dimensional reconstructions
    may be helpful in special situations, such as the evaluation of medial clavicular physeal fractures or sternoclavicular fracture-dislocations.

    2011 American Academy of Orthopaedic Surgeons

    A classification system for clavicle fractures based


    solely on the anatomic location of the fracture (lateral,
    medial, or midshaft) has been proposed, and lateral end
    fractures have been classified as nondisplaced (type I)
    or displaced (type II). Displaced lateral fractures can be
    further subclassified according to the integrity of the
    conoid and trapezoid ligaments (Figure 2). The Edinburgh classification has been used to subclassify shaft
    fractures according to displacement and degree of comminution.1 This classification scheme has acceptable
    levels of interobserver and intraobserver variation. Medial and lateral end fractures are subclassified with the
    Edinburgh system according to their displacement and
    articular involvement.

    Midshaft Fractures
    Fractures of the middle third of the clavicle usually proceed to bony union uneventfully without the need for
    surgery. Studies have reported that significant risk factors for nonunion include age, female sex, fracture displacement, and comminution; shortening of the fracture (> 20 mm) is also a risk factor for the development
    of nonunion.3
    Previous studies have reported a nonunion rate of
    only 0.13% to 0.8%. Shortcomings of these studies are
    inclusion of the pediatric population and absence of

    3: Upper Extremity

    Dr. Abboud or an immediate family member serves as a


    board member, owner, officer, or committee member of
    the American Academy of Orthopaedic Surgeons Multimedia subcommittee; is a member of a speakers bureau
    or has made paid presentations on behalf of DePuy, and
    serves as a paid consultant to or is an employee of
    DePuy. Dr. Boardman or an immediate family member is
    a member of a speakers bureau or has made paid presentations on behalf of GlaxoSmithKline, DePuy, and
    Merck and serves as a paid consultant to or is an employee of DePuy.

    Classification

    Figure 1

    AP radiograph showing a displaced segmental


    midshaft clavicle fracture.

    Orthopaedic Knowledge Update 10

    271

    Section 3: Upper Extremity

    are either dynamic compression or locking plates. Sitespecific precontoured locking plates have become increasingly popular and may be less prominent after
    healing, leading to lower rates of hardware removal after union.6
    If nonsurgical treatment of the fracture leads to
    symptomatic malunion or nonunion, surgical management, including plate fixation with autologous bone
    grafting, can be considered. In 47 patients treated with
    superior plating for clavicular nonunions, 93% of the
    fracture nonunions united after one surgery.8 The authors reported that treating patients with a superiorly
    applied plate without a distant autogenous bone graft
    was efficacious in obtaining fracture union.

    Figure 2

    Lordotic radiographic view of the clavicle showing a type II displaced lateral third clavicle
    fracture.

    modern methods for assessing functional outcomes. It


    is generally accepted that midshaft clavicle fractures
    will heal in most adults. The standard of care is initial
    immobilization in either a sling or figure-of-8 bandage,
    with immobilization discontinued when the level of
    pain allows.
    Until recently, there was little evidence available to
    suggest that early surgical treatment of displaced clavicle fractures conferred a functional benefit when compared with the results of initial nonsurgical treatment.
    A recent multicenter trial comparing nonsurgical treatment with primary plate fixation for displaced fractures
    in 132 patients reported better functional outcomes,
    lower rates of malunion and nonunion, and a shorter
    time to union in the latter group.4 However, the group
    treated with primary plate fixation had a complication
    rate of 34% and a reoperation rate of 18%, although
    most reoperations were for hardware removal. In a retrospective review of 30 patients who had been treated
    nonsurgically for displaced midshaft clavicle fractures,
    a higher prevalence of patient dissatisfaction was reported when shortening was greater than 2 cm, which
    corroborates previous reports.5

    3: Upper Extremity

    Plate Fixation
    Plate fixation provides immediate rigid stabilization
    and pain relief and facilitates early mobilization. Most
    commonly, the plate is implanted on the superior aspect
    of the clavicle; biomechanical studies have shown this
    to be advantageous, especially in the presence of inferior cortical comminution.6 Superior plating techniques
    have greater load to failure and bending failure stiffness
    than anterior inferior plating.7 Despite the biomechanical advantages, the superior approach is associated
    with a greater risk of injury to the underlying neurovascular structures during fracture manipulation and drilling. In addition, plate prominence with the superior approach may require hardware removal in symptomatic
    patients. Currently, the implants most commonly used
    272

    Orthopaedic Knowledge Update 10

    Intramedullary Nailing
    Intramedullary nailing is another option in the surgical
    treatment of clavicle fractures. Intramedullary repair of
    midshaft clavicle fractures with a titanium elastic nail
    can be safe and minimally invasive;9 however, implantrelated complications can include medial perforations,
    lateral penetrations, nail breakage, and hardware irritations.10 More studies are needed to fully define the role
    of intramedullary nail fixation in clavicular fractures.

    Distal Third Fractures


    Lateral third clavicle fractures can be classified based
    on the location relative to the coracoclavicular ligaments. Type I fractures are interligamentous and only
    minimally displaced, as both the proximal and distal
    fragments continue to be stabilized by the coracoclavicular ligaments. For these injuries, nonsurgical management is the treatment of choice, and the protocol is similar to that of shaft fractures. Type II fractures occur
    medial to the coracoclavicular ligaments. Deforming
    forces, such as the weight of the arm and muscular attachments, lead to inferior and medial displacement of
    the distal fragment via its ligamentous attachments.
    These fracture patterns are associated with delayed
    union and nonunion. Type III fractures extend into the
    articular surface of the acromioclavicular joint with no
    ligamentous injury and are generally stable.
    Although several retrospective studies have reported
    high rates of nonunion after nonsurgical treatment of
    displaced lateral end fractures, a recent study showed a
    low incidence of nonunion after nonsurgical treatment.3 In addition, high complication rates have been
    reported with surgical fixation.11 Because most of these
    injuries occur in middle-aged and elderly patients, nonunion is often tolerated, with few patients requiring delayed surgical intervention.3,11 In the small number of
    patients in whom substantial arthritis develops, resection of the lateral segment may result in a functional
    shoulder.2
    Many primary surgical techniques have been described for the treatment of type II fractures and many
    surgical techniques used to treat displaced lateral end
    fractures have been adapted from those used to treat
    acromioclavicular separations. Treatment options include coracoclavicular screws, hook-plate fixation,

    2011 American Academy of Orthopaedic Surgeons

    Chapter 22: Shoulder Trauma: Bone

    locking plates, Kirschner wire fixation, and suture techniques.


    Intra-articular fractures (type III) carry an increased
    risk of late acromioclavicular osteoarthritis, which may
    require further treatment. Type III fractures are generally adequately managed nonsurgically, although open
    reduction and internal fixation (ORIF) may be indicated if a large fragment resulting in significant articular step-off is present. Delayed distal clavicle resection
    is the procedure of choice if symptomatic degenerative
    disease occurs.2

    Medial Third Clavicle Fractures


    Medial third clavicle fractures are rare, and most are
    extra-articular and minimally displaced.1 Often, these
    fractures are physeal fracture-dislocations, usually in a
    posterior direction. Stability depends on the integrity of
    the costoclavicular ligaments. If the ligaments are ruptured, the lateral fragment displaces anteriorly and may
    overlap the medial fragment. These fractures are usually managed nonsurgically, unless fracture displacement produces mediastinal compromise. In such circumstances, an emergent attempt at closed reduction
    should be made, with open reduction performed next if
    that is unsuccessful. If surgical stabilization of this fracture is required, a thoracic surgeon should be available.
    A variety of internal fixation techniques, including use
    of the modified Balser plate and use of polyester fiber
    suture or other strong braided interosseous sutures,
    have been described.12 However, supporting evidence is
    limited for each technique, and there is a lack of consensus regarding the optimal treatment of fractures that
    require surgical treatment.

    General Complications of
    Clavicular Fracture Fixation
    The main intraoperative complication in clavicular
    fracture fixation is injury to the subclavian artery or
    vein at the time of fracture mobilization or from drill
    penetration. As with any ORIF, postoperative wound
    complications, scar dysesthesia, infection, fixation failure, and nonunion can occur and may require revision
    surgery.

    Proximal Humerus Fractures

    2011 American Academy of Orthopaedic Surgeons

    AP radiograph of the shoulder showing a valgusimpacted four-part proximal humerus fracture.

    sult from falls and involve osteoporotic bone, these


    fractures can occur secondary to high-energy mechanisms in younger patients, who often sustain more severe trauma with concomitant soft-tissue and neurovascular injuries.

    Presentation
    In a patient with a proximal humerus fracture, the
    shoulder is often swollen and tender to palpation.
    There is abundant ecchymosis that progresses down the
    arm and into the forearm and chest. Because most patients are elderly, the etiology of the fall should be discerned and associated injuries evaluated. The presence
    of associated peripheral nerve injury has typically been
    underappreciated. It has been shown that 67% of all
    patients with proximal humerus fractures have acute
    neurologic injury most commonly affecting the axillary
    nerve and/or the suprascapular nerve.13

    Vascularity
    Blood supply to the proximal humerus is important in
    determining survival of the humeral head. The anterior
    humeral circumflex artery contributes the major blood
    supply to the humeral head through the ascending anterolateral branch, which enters the proximal aspect of
    the bicipital groove. Other vascular contributors include vessels entering the tuberosities through the rotator cuff insertions and direct branches of the circumflex
    vessels.
    An emphasis on the importance of the vascularity of
    the proximal humerus has led surgeons to try to ascertain a deeper understanding of fracture configuration
    because it relates to perfusion of the articular segment.
    Recently, patients treated with hemiarthroplasty re-

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Fractures of the proximal humerus are common injuries, representing 4% to 6% of all fractures. There is a
    2:1 female to male distribution, and increasing age has
    been shown to correlate with an increasing fracture risk
    in women, suggesting an association with osteoporosis.
    Fractures of the proximal humerus represent the third
    most common fracture in elderly patients, with hip
    fractures and distal radius fractures being more common. Approximately 85% of proximal humerus fractures are minimally displaced; however, there is a fairly
    significant amount of controversy over the diagnosis
    and treatment of the remaining 15% of patients (Figure
    3). Although proximal humerus fractures frequently re-

    Figure 3

    273

    Section 3: Upper Extremity

    ceived tetracycline labeling to measure humeral head


    viability after three- or four-part proximal humerus
    fractures. It was found that the vascular supply was
    preserved in both three- and four-part fractures of the
    proximal humerus and that patient age was inversely
    proportional to the amount of vascularity in the area.14
    In a recent report, intraoperative assessment of humeral head perfusion was performed by means of bore
    hole drillings, laser Doppler flowmetry, or both.15 Osteonecrosis did not develop in 8 of 10 humeral heads
    that were initially ischemic at the time of surgery; this
    finding led the authors to believe that revascularization
    can occur and that the rate of osteonecrosis may not be
    as high as traditionally believed. As a result of these
    findings, osteosynthesis with preservation of the humeral head may be considered when adequate reduction and stable fixation, which are optimal conditions
    for revascularization, can be obtained. A recent study
    analyzed a proximal humerus fracture classification
    scheme and outlined factors that predicted the likelihood of humeral head ischemia.16 Such factors included
    disruption of the medial periosteal hinge, medial metadiaphyseal extension less than 8 mm, increasing fracture complexity, and displacement greater than 10 mm
    or angulation greater than 45.

    Radiographic Evaluation and Classification

    3: Upper Extremity

    The trauma series of radiographs, consisting of AP,


    scapular Y, and axillary views, is the standard for evaluating proximal humerus fractures. CT with threedimensional reconstruction is useful for evaluating the
    size and displacement of fracture fragments. The classification of proximal humerus fractures is commonly
    based on the four-part system of Neer. This scheme is
    based on the identification of the four anatomic fragments (humeral head, greater tuberosity, lesser tuberosity, and humeral shaft) and the determination of displacement and angulation between these parts greater
    than 1 cm or 45, respectively. Another classification
    scheme assesses predictors of ischemia, including medial hinge disruption greater than 2 mm and metaphyseal head extension less than 8 mm.17 A third scheme,
    the AO/Orthopaedic Trauma Association (OTA) system, classifies fractures into types A, B, and C. Type A
    is a two-part extracapsular fracture with an intact vascular supply, type B is a three-part partially intracapsular fracture with possible vascular compromise, and
    type C is a four-part intracapsular fracture with a likelihood of vascular compromise.16
    A recent study evaluated the impact of stereovisualization of three-dimensional volume-rendering CT
    datasets on the interobserver and intraobserver reliability of the AO/OTA and Neer classification systems in
    the assessment of proximal humerus fractures.18 Both
    classification systems showed moderate interobserver
    reliability with plain radiographs and two-dimensional
    CT. Three-dimensional volume-rendered CT improved
    interobserver reliability to good for both classification
    systems, and the intraobserver reliability for the threedimensional scans improved to good for the AO/OTA
    274

    Orthopaedic Knowledge Update 10

    classification and to excellent for the Neer classification.

    Nonsurgical Treatment
    The treatment of proximal humerus fractures is based
    on many factors, including patient age, bone quality,
    medical comorbidities, concurrent injuries, and fracture
    type. Nonsurgical treatment with early passive motion
    remains the treatment of choice for minimally displaced
    or nondisplaced fractures. Open treatment is reserved
    for displaced fractures that cannot be reduced with
    closed means. A recent study found that immediate
    physiotherapy after a minimally displaced proximal humerus fracture resulted in a faster recovery with maximum functional benefits being achieved at 1 year.19 The
    authors of a recent study reported that nonsurgical
    treatment of proximal humerus fractures is safe and effective, specifically in AO/OTA fracture types A and B,
    but can also be extended to three-part fractures.20 Of
    the fractures regarded suitable for conservative treatment, few required later surgical stabilization. When
    complex proximal humerus fractures are managed nonsurgically, there is usually some degree of malunion,
    and osteonecrosis leading to collapse of the humeral
    head may occur. As mentioned previously, this osteonecrosis appears to occur at lower rates than have been
    described previously.21

    Surgical Treatment
    When the humeral head is amenable to fixation, many
    methods are available. Fractures considered for ORIF
    include displaced greater tuberosity fractures with more
    than 5 mm of displacement, lesser tuberosity fractures
    with involvement of the articular surface, displaced or
    unstable surgical neck fractures, displaced anatomic
    fractures in young patients, and displaced reconstructible three- and four-part fractures.
    Fractures amenable to closed reduction and percutaneous pinning include two-part fractures of the surgical
    neck, greater tuberosity, and lesser tuberosity; threepart surgical neck fractures with involvement of the
    greater or lesser tuberosity; and valgus-impacted fourpart fractures. Closed reduction and percutaneous pinning is a demanding surgical technique (Figure 4). For
    this technique to be used successfully, several conditions are required: (1) a stable closed reduction; (2)
    good bone stock; (3) minimal comminution, particularly involving the tuberosity; (4) an intact medial calcar; and (5) a cooperative patient. It has been shown
    that the posteromedial hinge is a mechanical structure
    that provides support for percutaneous reduction and
    stabilization of a proximal humerus fracture by ligamentotaxis.22 If acceptable alignment cannot be obtained, the technique should be abandoned in favor of
    more traditional open reduction.
    Greater Tuberosity Fractures
    Two-part fractures of the greater tuberosity commonly
    occur in the setting of a glenohumeral dislocation. After
    closed reduction of the glenohumeral dislocation, the tu-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 22: Shoulder Trauma: Bone

    Figure 5
    Figure 4

    AP postoperative radiographs after percutaneous


    pinning of an unstable two-part proximal humerus fracture.

    berosity should be assessed for displacement. If superior


    and posterior displacement greater than 5 mm to 10 mm
    persists, ORIF of the tuberosity fragment is considered.
    Untreated residual displacement greater than 5 mm may
    cause impingement of the superiorly displaced greater tuberosity against the acromion. Fixation of the tuberosity
    is often achieved with intraosseous sutures incorporating the cuff insertion. If the tuberosity is a single large
    piece, screw fixation can be used.

    2011 American Academy of Orthopaedic Surgeons

    humeral joint.24 The authors reported that the surgical


    treatment of displaced proximal humerus fractures
    with use of a proximal humeral plate can lead to good
    functional outcomes provided that the correct surgical
    technique is used. Accurate length measurements and
    the selection of shorter screws were recommended to
    prevent primary screw perforation. Awareness of the
    need to obtain anatomic reduction of the tubercles and
    restoration of medial support should reduce the incidence of secondary screw penetrations even in osteoporotic bone (Figure 5).
    New Techniques in Fixation
    Several new techniques being introduced for fixation of
    proximal humerus fractures include the humeral block
    system, the block-bridge, and the use of helix wire.25,26
    Because there is a paucity of information regarding the
    outcomes of treatment with these modalities, they
    should be considered with care.

    3: Upper Extremity

    ORIF With Precontoured Locking Plates


    Short-term outcomes of precontoured locking plates for
    fixation of displaced proximal humerus fractures have
    recently been described. In a study of 187 patients with
    acute proximal humerus fractures who were treated
    with ORIF with a locking proximal humeral plate, 62
    complications occurred in 52 patients at 1-year followup.23 Twenty-five complications (40%) were related to
    incorrect surgical technique and were present at the end
    of the surgical procedure. The most common complication, reported in 21 of 155 patients, was intraoperative
    screw perforation of the humeral head.
    In a study using a proximal humerus internal locking
    system plate (Philos, Synthes, Oberdorf, Switzerland) in
    the treatment of displaced proximal humerus fractures
    in 157 patients (158 fractures), the complication rate
    was relatively high (35%), particularly because of primary and secondary screw perforation into the gleno-

    AP radiograph of a left shoulder showing precontoured plate fixation used in the treatment of a
    displaced three-part proximal humerus fracture.
    Note the inferior placement of the plate relative to the top of the greater tuberosity as well
    as the purposeful placement of the screws in
    the humeral head well short of the subchondral
    surface.

    Hemiarthroplasty
    Hemiarthroplasty is an option for fractures involving
    young or middle-aged patients with a nonreconstructible articular surface, severe head splits, or extruded anatomic neck fractures, and elderly patients

    Orthopaedic Knowledge Update 10

    275

    Section 3: Upper Extremity

    throplasty for proximal humerus fractures with a minimum 5-year follow-up, satisfactory results were reported in 27 patients and unsatisfactory results in 30
    patients.29 The study data suggest that patients treated
    with arthroplasty for an acute fracture of the proximal
    humerus may achieve satisfactory long-term pain relief.
    However, the result for overall shoulder motion is less
    predictable. Based on these results, it has been suggested that the current indications, surgical technique,
    and postoperative treatment of these fractures be reevaluated.

    Figure 6

    AP radiograph of a right shoulder showing a cemented hemiarthroplasty for a shoulder fracture. Note the reduction of the tuberosities is
    nearly anatomic.

    3: Upper Extremity

    with markedly comminuted severely osteoporotic threeand four-part fractures as well as three- and four-part
    fracture-dislocations. Primary hemiarthroplasty for
    fracture of the proximal humerus can result in good patient satisfaction and pain relief. Intraoperative restoration of the anatomic humeral height, version, and tuberosity reconstruction have been identified as
    important factors in the improvement of outcomes after arthroplasty for shoulder fractures (Figure 6). Humeral length reconstruction and centering of the prosthetic head in hemiarthroplasty for proximal humerus
    fractures using the pectoralis major as a reference point
    were evaluated in a 2008 study.27 In 21 of 30 patients,
    the humeral length reconstruction was performed using
    the pectoralis major tendon as a reference; in 9 patients
    this reference was not used. Patients appeared to have
    improved outcomes when the pectoralis major tendon
    was used as a reference point.
    In a recent study, 82 patients treated with primary
    hemiarthroplasty for a severely displaced proximal humerus fracture were evaluated at an average follow-up
    of 4.4 years.28 Primary hemiarthroplasty generally prevented shoulder pain, but most patients had only moderate function and poor strength. The reduced function
    appeared to be related to lack of rotator cuff integrity.
    In a 2008 review of 50 patients treated with hemiar276

    Orthopaedic Knowledge Update 10

    Reverse Arthroplasty
    With the increasing use of reverse shoulder arthroplasty, indications for this procedure have been extended to the treatment of comminuted fractures in elderly patients. Forty-three consecutive patients with a
    mean age of 78 years who sustained three- and fourpart proximal humerus fractures were evaluated after
    reverse shoulder arthroplasty.30 This group had a postoperative mean active forward elevation of 97 and
    mean active external rotation of 30. The study authors
    concluded that compared with conventional hemiarthroplasty, satisfactory mobility was obtained despite
    frequent migration of the tuberosities at short-term
    follow-up.
    Twenty-nine patients were treated with reverse arthroplasty after failure of primary hemiarthroplasty for
    fracture treatment.31 In patients treated with revision
    from a hemiarthroplasty for fracture to a reverse shoulder prosthesis, the average forward flexion improved
    from 38 to 73 and abduction improved from 34 to
    70. In these instances, the reverse shoulder prosthesis
    offered a salvage-type solution to the complication of
    failed hemiarthroplasty because of glenoid arthrosis
    and rotator cuff deficiency following tuberosity failure.
    The study authors caution that long-term results are required before reverse shoulder arthroplasty can be recommended as a routine procedure in treating complex
    fractures of the proximal humerus in elderly patients.
    Proximal Humeral Nonunion and Malunion
    Although rare, proximal humeral nonunion tends to involve the surgical neck or the greater tuberosity.
    Malunion tends to occur as a result of failure of the primary surgical procedure or as a sequelae of nonsurgical
    treatment. Shoulder arthroplasty in the setting of a
    malunited proximal humerus fracture has been performed with caution because of the higher rate of complications and unpredictable functional results.32 Patients with surgical neck nonunions may be candidates
    for revision ORIF with bone grafting.33 Greater tuberosity nonunions are often not amenable to revision
    ORIF or anatomic shoulder arthroplasty. For severe
    nonunions, particularly those affecting the tuberosities,
    there are increasing data to support the use of reverse
    shoulder arthroplasty, although this approach should
    be carefully considered on an individual basis.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 22: Shoulder Trauma: Bone

    Scapular Fractures
    Scapular fractures account for approximately 4% of all
    shoulder girdle fractures. Because of the extensive softtissue coverage from the rotator cuff musculature and
    the thoracic cavity, significant forces are required to
    fracture the scapula. As such, most scapular fractures
    (11% to 25%) occur secondary to high-energy injuries.34

    Presentation
    In the setting of high-energy trauma, the context in
    which scapular fractures typically occur, the patient
    should be assessed using the Advanced Trauma Life
    Support protocol. Scapular fractures also can occur secondary to low-energy mechanisms, such as a fall onto
    outstretched hands. In the awake patient, palpation of
    the scapula as well as abduction of the arm causes pain.
    The arm is typically held in the adducted position and
    the forearm is held against the chest wall. Pseudorupture of the rotator cuff may be seen with intramuscular
    hemorrhage and consequent muscular dysfunction.35

    Associated Injuries
    The high incidence (35% to 98%) of associated injuries
    mandates a thorough evaluation of the patient with a
    scapular fracture. In a retrospective review, the incidence of associated injuries was reported as follows: rib
    fractures, 52%; pulmonary contusion, 41%; spinal
    fractures, 29%; clavicular fractures, 25%; and pneumothorax, 32%.36 Patients with a brachial plexus injury and a scapular fracture have a 57% chance of arterial injury.37

    Radiographic Evaluation
    Scapular fractures are seen only 57% of the time on initial chest radiographs.38 A true AP radiograph of the
    scapula, a scapular Y view, and an axillary view should
    be obtained. A Stryker notch view (AP radiography
    with the beam centered over the coracoid process directed 10 cephalad) can also be obtained to visualize
    coracoid fractures. CT is helpful in evaluating the glenoid and the coracoid, and may show body fractures
    not initially seen with plain imaging.

    Classification

    2011 American Academy of Orthopaedic Surgeons

    Treatment
    Scapular Body Fractures
    Nonsurgical treatment of scapular body fractures, the
    most common scapular fractures, generally yields good
    outcomes in most patients. Early pendulum, passive,
    and active-assisted exercises should preferably begin
    soon after the injury. In a study of 123 scapular body
    fractures, 106 (86%) had either good or excellent results.40 Patient dissatisfaction with treatment was
    caused by weakness, crepitus, or pain. Patients with
    isolated scapular body fractures usually regain good
    function; however, multiple trauma patients tend to
    have poorer outcomes.
    Acromial Fractures
    Fractures of the acromion process usually result either
    from a direct blow to the shoulder or from an indirect
    blow through the humerus. Stress fractures also have
    been reported in advanced-stage rotator cuff tear arthropathy, and recently have been seen following reverse total shoulder arthroplasty. It may be difficult to
    differentiate between an acromial fracture and os acromiale, the latter occurring bilaterally in up to 60% of
    patients.41,42 MRI of the shoulder should be obtained to
    rule out a rotator cuff tear if superior displacement of
    the humeral head is present. Acromial fractures that do
    not cause subacromial impingement are amenable to
    nonsurgical treatment. An abduction orthosis may help
    decrease the pull of the deltoid on the acromion to prevent an increase in fracture displacement. If subacromial impingement occurs, the acromion process fracture can be repaired with figure-of-8 wiring, cannulated
    screws, plating, or if the fragment is small, surgical
    excision.43-45
    Coracoid Fractures
    Direct blows, avulsion injury, anterior shoulder dislocation, acromioclavicular dislocation, superior escape of
    the humerus, and coracoclavicular taping have all been
    implicated as causes of coracoid fractures. These fractures most commonly occur at the coracoid base and
    are usually minimally displaced because of multiple
    soft-tissue attachments. Surgical fixation has been advocated for avulsion injuries in athletes as well as those
    who perform heavy labor. However, even with marked
    displacement, nonsurgical management has produced
    excellent results and is the mainstay of treatment.46,47
    Fracture healing generally occurs in 6 weeks with nonsurgical treatment.

    3: Upper Extremity

    Scapular fractures are divided into the following types:


    body, acromion, coracoid, glenoid neck, and intraarticular glenoid fractures (glenoid fossa). Acromial
    fractures are further subdivided into minimally displaced, displaced without subacromial impingement,
    and displaced with subacromial impingement. Coracoid fractures are classified by the location of the fracture, either proximal (type 1) or distal (type 2) to the
    coracoclavicular ligaments. Extra-articular glenoid
    neck fractures are differentiated by the presence or absence of a clavicle fracture or acromioclavicular separation (such as the presence or absence of the so-called
    floating shoulder). The Ideberg fracture classification
    for intra-articular glenoid fractures was modified into

    six types.39 Type I is a fracture of the glenoid rim, type


    II a transverse fracture through the fossa with a subluxated humeral head, types III-V include scapular body
    fractures, and type VI has severe glenoid fossa comminution.

    Glenoid Neck Fractures


    A glenoid neck fracture is the second most common
    pattern of scapular fracture. True glenoid neck fractures exit along the lateral scapular border as well as

    Orthopaedic Knowledge Update 10

    277

    Section 3: Upper Extremity

    superiorly, either medial or lateral to the coracoid base.


    The major deforming force is the long head of the triceps. More than 90% of all glenoid neck fractures are
    minimally displaced and can be treated nonsurgically
    with good to excellent functional results. An intact
    clavicle and acromioclavicular joint enhance fracture
    stability, and healing usually occurs in the position documented at the primary examination.
    Surgical treatment has been recommended for patients with greater than 40 of angulation or greater
    than 1 cm of medial translation.48 Study results of 113
    patients showed that nonsurgical treatment of these
    fractures resulted in continued pain in 50% of the patients, weakness with exertion in 40%, persistent mechanical symptoms in 25%, and decreased range of
    shoulder motion in 20%.48 Greater loss of shoulder abduction was associated with increased medialization of
    the glenoid. The surgical approach to the glenoid neck
    is typically posterior, with preservation of the deltoid
    origin.
    Glenoid Fossa Fractures
    Most (90%) of all glenoid fossa fractures are minimally
    displaced and can be treated nonsurgically. In addition
    to standard scapular imaging, a Stryker notch view and
    CT are often helpful in assessing the fracture for displacement and joint congruity.
    Type I
    Glenoid rim fractures occur when the humeral head eccentrically loads the glenoid cavity. Surgical management should be considered in patients with persistent
    subluxation, with fracture displacement of more than
    10 mm, or with 25% anterior or 33% posterior fracture involvement.49 The approach to these fractures is
    dictated by fracture locationanterior via a deltopectoral approach or posterior.
    Types II-V
    Surgery is indicated in patients with more than 5 mm of
    step-off of the articular surface, continued humeral
    head subluxation, or severe separation of the glenoid
    fragments.50 The approach may require a combination
    of multiple surgical approaches (anterior, posterior,
    and/or superior).

    3: Upper Extremity

    Type VI
    Severely comminuted glenoid cavity fractures are best
    treated with early motion. Surgery may disrupt softtissue support, potentially hastening chondral damage.

    The Floating Shoulder


    The superior shoulder suspensory complex is an osseous and soft-tissue structure that maintains a stable relationship between the axial skeleton and upper extremity. The components of the superior shoulder
    suspensory complex form a ring composed of the acromion, glenoid, coracoid, coracoclavicular ligaments,
    distal clavicle, and acromioclavicular joint with its respective ligaments. Injuries involving the disruption of
    278

    Orthopaedic Knowledge Update 10

    a single component of the superior shoulder suspensory


    complex are stable, whereas a disruption of two or
    more components leads to instability.51
    The classic floating shoulder has a fracture to both
    the glenoid neck and the clavicle. Management of these
    injuries continues to be controversial. Nonsurgical care
    consists of a period of immobilization followed by
    physical therapy. Nonsurgical outcomes are good to excellent for fractures with minimal displacement; however, there is debate on the degree of acceptable displacement. In nonsurgically treated patients with more
    than 10 mm of clavicular displacement and more than
    5 mm of scapular displacement, outcomes were comparable to those of patients with nondisplaced fractures.52
    Patients with glenoid medialization of more than 30
    mm fared better with surgery.
    Fixation of the clavicle and/or glenoid neck also has
    been debated. In the absence of coracoclavicular disruption, fixation of the clavicle lengthens the soft tissues, neutralizes deforming forces, prevents displacement and malrotation of the glenoid, allows earlier
    physical therapy, and is a relatively uncomplicated procedure. Good to excellent results have been consistently
    achieved.53,54 Proponents for surgical fixation of the
    glenoid argue that it facilitates postoperative rehabilitation and provides greater stability to the humerus. Although several approaches have been used, surgical fixation of the clavicle is generally addressed first. An
    intraoperative evaluation of the glenoid should occur;
    fixation should be done if necessary.

    Humeral Shaft Fractures


    Humeral shaft fractures account for approximately 4%
    of all fractures and occur in a bimodal distribution,
    with the first peak occurring in males in the third decade of life (largely secondary to high-energy trauma).
    The second peak occurs in the seventh decade of life,
    with an increased incidence in females, typically resulting from falls. Appropriate recognition of the mechanism of injury and patient characteristics are important
    for treatment.

    Presentation
    Patients with fractures of the humeral shaft will typically present with pain and deformity of the affected
    extremity. A thorough examination of the skin and
    neurovascular status must be performed as an integral
    component of the evaluation. Radial nerve palsy is the
    most common nerve injury seen with humeral shaft
    fractures, with a reported incidence of 3% to 34%.55,56
    This rate increases with open fractures, multiple
    trauma, vascular injury, and multiple ipsilateral fractures.

    Radiographic Evaluation
    The initial radiographic evaluation of humerus fractures should include orthogonal plain radiographs. In
    addition, dedicated views of both the ipsilateral shoul-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 22: Shoulder Trauma: Bone

    Figure 8

    Figure 7

    AP view of the humeral shaft demonstrating a


    midshaft fracture in acceptable alignment
    treated with a Sarmiento brace.

    der and elbow should be obtained (Figure 7). Angiography should be considered for fractures with apparent
    associated vascular injury. CT may provide benefit
    acutely in the evaluation of fracture extension into joint
    surfaces, and later in the evaluation of humeral rotational malunions.

    Nonsurgical treatment with functional bracing is an


    important mainstay in the treatment of midshaft humerus fractures, permitting early range of motion, patient comfort, and cost containment (Figure 8). Time to
    union varies from 3 to 40 weeks, with closed fractures
    averaging 10.7 weeks. The nonunion rate has been reported at 5.5% (79 of 1,428 fractures).57 Malunion
    represents one of the potential disadvantages of functional bracing, with varus angulation the most common
    deformity. However, varus angulation in excess of 10
    has been reported to occur in less than 15% of patients
    treated with functional bracing. In a recent study of

    2011 American Academy of Orthopaedic Surgeons

    452 fractures, an average sagittal angulation of 3.7


    was reported, and only 2% of patients had more than
    20 of angulation in the sagittal plane.57 No studies reported shortening exceeding 2 cm. Alignment is considered acceptable for fractures that heal with up to 20 of
    anterior angulation, 30 of varus angulation, and/or
    3 cm of shortening.
    Although excellent clinical results have been reported with nonsurgical management, there are several
    indications for the surgical treatment of humeral shaft
    fractures. These indications include open fractures,
    fractures with vascular injury, associated ipsilateral upper extremity fractures, multiple trauma, and fractures
    with intra-articular extension.
    Surgical options include plate osteosynthesis, intramedullary nailing, and external fixation. Whereas
    functional bracing is the mainstay for nonsurgical treatment, plate osteosynthesis remains the gold standard
    for surgical treatment. Union rates in the 93% to 96%
    range have been consistently reported. Low complication rates also have been reported, including radial
    nerve palsy (2%), infection (2%), and refracture
    (1%).58 The surgical approach (anterolateral, lateral, or
    posterior) is largely dictated by the surgeons preference
    as well as the fracture site. As a rule, middle to proximal shaft fractures are amenable to an anterolateral approach, whereas more distal fractures may benefit from

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Management

    Scapular Y view of the humeral shaft, 1 year after


    injury, demonstrating fracture union in acceptable alignment.

    279

    Section 3: Upper Extremity

    a posterior approach. A 3.5- or 4.5-mm dynamic compression plate with three screws proximal and distal to
    the fracture site is preferred, with lag screw placement
    when possible. Fractures with comminution, poor
    screw purchase, or poor bone quality may require more
    robust fixation and the use of a fixed-angle locking
    plate.
    Intramedullary nailing has not shown the same success rates in the upper extremity as seen in the lower
    extremity. Antegrade, retrograde, and lateral antegrade
    insertion entry points have been devised to permit nail
    placement. In a meta-analysis of more than 155 patients, humeral nailing had higher rates of reoperation,
    radial nerve injury, chronic subacromial pain, and iatrogenic fracture compared with compression plating.59
    However, intramedullary nailing of the humerus plays a
    role in the treatment of pathologic fractures, morbidly
    obese patients, and fractures with soft-tissue compromise that preclude a safe surgical approach for plate
    fixation.
    External fixation traditionally has been used as a
    temporizing measure in the context of contaminated
    wounds, infected nonunions, or the need for quick stabilization in unstable patients or those with vascular injury. Constant motion from the shoulder and elbow in
    the presence of a large soft-tissue envelope has led to
    complications, including delayed union, pin tract irritation, and infection.

    tures, high-energy injuries, impaired blood supply, infection, unstable fracture patterns, obesity, osteoporosis, patient noncompliance, smoking, and malnutrition.
    Humeral shaft fracture nonunion should be treated
    with excision of the nonunion site, opening of the humeral canal, bone graft application, and dynamic compression plating. Union is achievable in 83% to 100%
    of nonunion cases.67-69 If an intramedullary nail has
    been placed, the nail must be removed. In a retrospective study, nine of nine intramedullary nailed nonunions healed after plating.70 Union rates of 88% to
    95% have been reported with irrigation, dbridement,
    intravenous antibiotics, and an external fixator for infected nonunions.71 Free fibular grafting offers a viable
    treatment
    option
    for
    recalcitrant,
    atrophic
    nonunions.72-74

    Annotated References
    1.

    Robinson CM: Fractures of the clavicle in the adult: Epidemiology and classification. J Bone Joint Surg Br
    1998;80(3):476-484.

    2.

    Khan LA, Bradnock TJ, Scott C, Robinson CM: Fractures of the clavicle. J Bone Joint Surg Am 2009;91(2):
    447-460.
    Nonsurgical treatment of displaced shaft fractures may
    be associated with a higher rate of nonunion and functional deficits than previously reported. However, it remains difficult to predict which patients will have these
    complications.

    3.

    Robinson CM, Court-Brown CM, McQueen MM,


    Wakefield AE: Estimating the risk of nonunion following nonoperative treatment of a clavicular fracture.
    J Bone Joint Surg Am 2004;86(7):1359-1365.

    4.

    Canadian Orthopaedic Trauma Society: Nonoperative


    treatment compared with plate fixation of displaced
    midshaft clavicular fractures: A multicenter, randomized
    clinical trial. J Bone Joint Surg Am 2007;89(1):1-10.
    The authors concluded that primary plate fixation of
    completely displaced midshaft clavicular fractures in active adults is an acceptable treatment method.

    5.

    McKee MD, Pedersen EM, Jones C, et al: Deficits following nonoperative treatment of displaced midshaft
    clavicular fractures. J Bone Joint Surg Am 2006;88(1):
    35-40.

    6.

    Iannotti MR, Crosby LA, Stafford P, Grayson G, Goulet R: Effects of plate location and selection on the stability of midshaft clavicle osteotomies: A biomechanical
    study. J Shoulder Elbow Surg 2002;11(5):457-462.

    7.

    Robertson C, Celestre P, Mahar A, Schwartz A: Reconstruction plates for stabilization of mid-shaft clavicle
    fractures: Differences between nonlocked and locked
    plates in two different positions. J Shoulder Elbow Surg
    2009;18(2):204-209.

    Radial Nerve Palsy

    3: Upper Extremity

    Radial nerve palsy in the setting of humerus fractures


    requires special mention. As previously noted, the incidence of radial nerve palsy associated with humeral
    shaft fractures is 3% to 34%.60 In a recent metaanalysis, the most frequently reported fracture location
    with a radial nerve injury was the distal third of the humerus (23.6%), followed by the middle third (15.2%),
    and the proximal third (1.8%).61 Most of these radial
    nerve injuries are neurapraxias with a good chance for
    recovery of nerve function. In a study of 1,045 patients
    with humerus fractures and radial nerve palsy, 921 recovered nerve function.56,62-65 However, patients with
    open fractures recovered nerve function less frequently
    (85.7%) than those with closed fractures (97.1%). The
    mean time to onset of recovery was 7.3 weeks. If no recovery is apparent, a baseline nerve conduction velocity
    study and electromyography should be obtained at approximately 3 to 4 weeks after injury. If there is no return of nerve function, repeat electrodiagnostic studies
    should be obtained at approximately 4 to 6 months after injury and before surgery is considered. If a transected nerve is involved, surgical repair or tagging of
    the nerve for a delayed repair should be performed.

    Nonunion
    Nonunion occurs in 2% to 10% of nonsurgically
    treated fractures and in up to 15% of fractures treated
    with internal fixation, more often occurring with intramedullary nailing than with plating.66 An increased
    incidence of nonunion is associated with open frac280

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 22: Shoulder Trauma: Bone

    tetracycline hydrochloride. Humeral head biopsies were


    taken from four predetermined locations intraoperatively. The authors concluded that the vascular supply is
    preserved in displaced three- and four-part proximal humerus fractures, especially in younger patients in the anterosuperior aspect of the humeral head.

    The authors present an evaluation of the biomechanical


    stability of locking and nonlocking clavicle reconstruction plates for treating midshaft transverse fractures,
    comparing anterior-inferior to superior plate position.
    Level of evidence: I.
    8.

    9.

    10.

    11.

    Endrizzi DP, White RR, Babikian GM, Old AB: Nonunion of the clavicle treated with plate fixation: A review of forty-seven consecutive cases. J Shoulder Elbow
    Surg 2008;17(6):951-953.
    Forty-seven patients were treated with superior plating
    for clavicular nonunions. Distant autogenous bone graft
    is usually not necessary to obtain union. Level of evidence: III.
    Mueller M, Rangger C, Striepens N, Burger C: Minimally invasive intramedullary nailing of midshaft clavicular fractures using titanium elastic nails. J Trauma
    2008;64(6):1528-1534.
    Thirty-one midshaft clavicular fractures were treated
    with intramedullary nailing with a titanium elastic nail.
    Nonunion was not observed. No patient sustained a refracture after nail removal. Medial migration of the titanium elastic nail in seven patients and iatrogenic perforation of the lateral cortex in one patient required
    secondary shortening on five occasions. Nail breakage
    after fracture healing was observed twice. Level of evidence: III.
    Frigg A, Rillmann P, Perren T, Gerber M, Ryf C: Intramedullary nailing of clavicular midshaft fractures
    with the titanium elastic nail: Problems and complications. Am J Sports Med 2009;37(2):352-359.
    Thirty-four patients were treated with intramedullary
    nailing. A standard titanium elastic nail was used in 19
    patients and a titanium elastic nail with an end cap in
    15 patients. A short incision at the fracture site was
    made for open reduction if needed. In 62% of patients,
    open reduction was necessary independent of fracture
    type, flattening of the titanium elastic nail, or transverse
    fragments. In 70% of patients, complications occurred.
    Level of evidence: IV.
    Robinson CM, Cairns DA: Primary nonoperative treatment of displaced lateral fractures of the clavicle. J Bone
    Joint Surg Am 2004;86(4):778-782.
    Franck WM, Siassi RM, Hennig FF: Treatment of posterior epiphyseal disruption of the medial clavicle with a
    modified Balser plate. J Trauma 2003;55(5):966-968.

    13.

    Visser CP, Coene LN, Brand R, Tavy DL: Nerve lesions


    in proximal humeral fractures. J Shoulder Elbow Surg
    2001;10(5):421-427.

    14.

    Crosby LA, Finnan RP, Anderson CG, Gozdanovic J,


    Miller MW: Tetracycline labeling as a measure of humeral head viability after 3- or 4-part proximal humerus fracture. J Shoulder Elbow Surg 2009;18(6):851858.
    Nineteen patients were treated with hemiarthroplasty as
    definitive treatment of 20 displaced three- and four-part
    proximal humerus fractures after receiving 500 mg of

    2011 American Academy of Orthopaedic Surgeons

    Bastian JD, Hertel R: Initial post-fracture humeral head


    ischemia does not predict development of necrosis.
    J Shoulder Elbow Surg 2008;17(1):2-8.
    The authors evaluated the functional outcome and the
    occurrence of osteonecrosis in 51 consecutive patients
    (26 women) with intracapsular fractures of the proximal humerus treated with ORIF. Osteosynthesis with
    preservation of the humeral head warrants consideration when adequate reduction and stable conditions for
    revascularization can be obtained. Level of evidence: II.

    16.

    Robinson BC, Athwal GS, Sanchez-Sotelo J, Rispoli


    DM: Classification and imaging of proximal humerus
    fractures. Orthop Clin North Am 2008;39(4):393-403.
    Understanding the particular proximal humeral fracture
    pattern in each case is complicated. Three-dimensional
    reconstructions based on CT currently available in most
    institutions allow a better understanding of complex
    fractures. Level of evidence: IV.

    17.

    Hertel R, Hempfing A, Stiehler M, Leunig M: Predictors


    of humeral head ischemia after intracapsular fracture of
    the proximal humerus. J Shoulder Elbow Surg 2004;
    13(4):427-433.

    18.

    Brunner A, Honigmann P, Treumann T, Babst R: The


    impact of stereo-visualisation of three-dimensional CT
    datasets on the inter- and intraobserver reliability of the
    AO/OTA and Neer classifications in the assessment of
    fractures of the proximal humerus. J Bone Joint Surg Br
    2009;91(6):766-771.
    The authors evaluated the impact of stereovisualization
    of three-dimensional volume-rendering CT datasets on
    the interobserver and intraobserver reliability assessed
    by kappa values on the AO/OTA and Neer classifications in the assessment of proximal humeral fractures.
    Level of evidence: I.

    19.

    Hodgson SA, Mawson SJ, Saxton JM, Stanley D: Rehabilitation of two-part fractures of the neck of the humerus (two-year follow-up). J Shoulder Elbow Surg
    2007;16(2):143-145.
    The 2-year results of a randomized, prospective, controlled trial of minimally displaced proximal humeral
    fractures treated either by immediate physiotherapy or
    after 3 weeks of immobilization are reported. Delayed
    rehabilitation by 3 weeks of shoulder immobilization
    produces a slower recovery, which continues for at least
    2 years after the time of injury. Level of evidence: I.

    20.

    Hanson B, Neidenbach P, de Boer P, Stengel D: Functional outcomes after nonoperative management of fractures of the proximal humerus. J Shoulder Elbow Surg
    2009;18(4):612-621.
    Patients older than 18 years presenting with a closed
    proximal humeral fracture who were considered suit-

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    12.

    15.

    281

    Section 3: Upper Extremity

    Seventy-six patients older than 70 years with three- or


    four-part fractures were treated with percutaneous reduction and internal fixation using the Humerusblock
    (Synthes, Salzburg, Austria) This technique can provide
    a comfortable and mobile shoulder in elderly patients
    and is a satisfactory alternative to replacement and traditional techniques of internal fixation. Level of evidence: IV.

    able for functional treatment by the surgeon in charge


    were enrolled in a prospective, externally monitored,
    observational study. This study may provide reference
    values for future investigations; it stresses ceiling effects
    that will make it difficult to demonstrate a significant
    advantage of surgical over nonsurgical treatment in patients with proximal humeral fractures. Level of evidence: IV.
    21.

    22.

    23.

    3: Upper Extremity

    24.

    25.

    282

    Edelson G, Safuri H, Salami J, Vigder F, Militianu D:


    Natural history of complex fractures of the proximal
    humerus using a three-dimensional classification system.
    J Shoulder Elbow Surg 2008;17(3):399-409.
    The natural history of 63 patients with complex fractures of the proximal humerus was followed prospectively for 2 to 9 years with a nonrandomized protocol.
    Status comparable to a successful surgical shoulder fusion was achieved in most cases (termed natures fusion). Osteonecrosis, even in severely displaced injuries,
    is rare. Level of evidence: II.
    Kralinger F, Unger S, Wambacher M, Smekal V,
    Schmoelz W: The medial periosteal hinge, a key structure in fractures of the proximal humerus: A biomechanical cadaver study of its mechanical properties.
    J Bone Joint Surg Br 2009;91(7):973-976.
    The authors investigated the biomechanical properties
    of the medial periosteum in fractures of the proximal
    humerus using a standard model in 20 fresh-frozen cadaver specimens comparable in age, sex, and bone mineral density. Periosteal rupture started at a mean displacement of 2.96 mm with a mean load of 100.9 N. A
    statistically significant but low correlation between bone
    mineral density and the maximum load uptake was observed. Level of evidence: I.
    Konrad GG, Mehlhorn A, Khle J, Strohm PC, Sdkamp NP: Proximal humerus fractures: Current treatment options. Acta Chir Orthop Traumatol Cech 2008;
    75(6):413-421.
    Nondisplaced fractures and fractures with minimal displacement and adequate stability are usually successfully
    treated nonsurgically. Recently invented implants with
    angular stability provide better biomechanical properties and enhanced anchorage, especially in the osteoporotic bone. These implants have the potential for
    achieving better results in the treatment of these complex injuries.
    Brunner F, Sommer C, Bahrs C, et al: Open reduction
    and internal fixation of proximal humerus fractures using a proximal humeral locked plate: A prospective
    multicenter analysis. J Orthop Trauma 2009;23(3):163172.
    One hundred fifty-seven patients with 158 fractures
    were treated with ORIF with a Philos plate. The authors
    concluded that a good functional outcome can be expected. However, complication incidence proportions
    are high. Level of evidence: II.
    Bogner R, Hbner C, Matis N, Auffarth A, Lederer S,
    Resch H: Minimally-invasive treatment of three- and
    four-part fractures of the proximal humerus in elderly
    patients. J Bone Joint Surg Br 2008;90(12):1602-1607.

    Orthopaedic Knowledge Update 10

    26.

    Russo R, Visconti V, Lombardi LV, Ciccarelli M, Giudice G: The block-bridge system: A new concept and
    surgical technique to reconstruct articular surfaces and
    tuberosities in complex proximal humeral fractures.
    J Shoulder Elbow Surg 2008;17(1):29-36.
    The block-bridge system is a new technique for the reconstruction of the proximal humerus around a
    triangular-shaped bone block positioned inside the head
    and the metaphysis. The results were excellent or good
    in 23 patients. The mean active anterior elevation was
    160 and all patients were pain free and returned to
    their preoperative activities, including sports. One patient had a symptomatic osteonecrosis that was treated
    with a hemiarthroplasty. Level of evidence: IV.

    27.

    Greiner SH, Kb MJ, Krning I, Scheibel M, Perka C:


    Reconstruction of humeral length and centering of the
    prosthetic head in hemiarthroplasty for proximal humeral fractures. J Shoulder Elbow Surg 2008;17(5):709714.
    This study analyzed clinical outcome, reconstruction of
    humeral length, centering of the prosthetic head in the
    glenoid, and tuberosity positioning and healing, using
    the pectoralis major tendon as a reference intraoperatively. Clinical outcome depended significantly on
    greater tuberosity healing and centering of the prosthetic head in the glenoid. Level of evidence: III.

    28.

    Grnhagen CM, Abbaszadegan H, Rvay SA,


    Adolphson PY: Medium-term results after primary
    hemiarthroplasty for comminute proximal humerus
    fractures: A study of 46 patients followed up for an average of 4.4 years. J Shoulder Elbow Surg 2007;16(6):
    766-773.
    This study evaluated 82 patients treated with primary
    hemiarthroplasty for a severely displaced proximal humerus fracture. The mean Constant score for all patients
    was 42 of 100 points. Radiologic evaluation showed
    that 24 prostheses had migrated superiorly, ectopic bone
    developed in 25 patients, 16 had glenoid erosion, and 5
    had displaced tuberosities. Level of evidence: IV.

    29.

    Antua SA, Sperling JW, Cofield RH: Shoulder hemiarthroplasty for acute fractures of the proximal humerus:
    A minimum five-year follow-up. J Shoulder Elbow Surg
    2008;17(2):202-209.
    The study data suggest that patients undergoing arthroplasty as treatment of an acute fracture of the proximal
    humerus may achieve satisfactory long-term pain relief;
    however, the result for overall shoulder motion is less
    predictable. All efforts should be aimed at reconstructing the tuberosities anatomically and delaying aggressive
    physical therapy until there is radiographic evidence of
    tuberosity healing.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 22: Shoulder Trauma: Bone

    30.

    31.

    Bufquin T, Hersan A, Hubert L, Massin P: Reverse


    shoulder arthroplasty for the treatment of three- and
    four-part fractures of the proximal humerus in the elderly: A prospective review of 43 cases with a short-term
    follow-up. J Bone Joint Surg Br 2007;89(4):516-520.
    Reverse shoulder arthroplasty was used in 43 patients
    with a three- or four-part fracture of the proximal humerus. Complications included three patients with reflex sympathetic dystrophy and five with neurologic
    complications; most of these complications resolved.
    One patient had an anterior dislocation. Level of evidence: II.

    39.

    Goss TP: Fractures of the glenoid cavity. J Bone Joint


    Surg Am 1992;74(2):299-305.

    40.

    Gosens T, Speigner B, Minekus J: Fracture of the scapular body: Functional outcome after conservative treatment. J Shoulder Elbow Surg 2009;18(3):443-448.

    Levy JC, Virani N, Pupello D, Frankle M: Use of the reverse shoulder prosthesis for the treatment of failed
    hemiarthroplasty in patients with glenohumeral arthritis
    and rotator cuff deficiency. J Bone Joint Surg Br 2007;
    89(2):189-195.
    The authors report on the reverse shoulder prosthesis in
    the revision of a failed shoulder hemiarthroplasty in 19
    shoulders in 18 patients with severe pain and loss of
    function. Statistically significant improvements were
    seen in pain and functional outcome. There were six
    prosthesis-related complications in six shoulders (32%),
    five of which had severe bone loss of the glenoid, proximal humerus, or both. Level of evidence: IV.

    41.

    Liberson F: Os acromiale: A contested anomaly. J Bone


    Joint Surg Am 1937;19:683-689.

    42.

    Sammarco VJ: Os acromiale: Frequency, anatomy, and


    clinical implications. J Bone Joint Surg Am 2000;82(3):
    394-400.

    43.

    Wong-Pack WK, Bobechko PE, Becker EJ: Fractured


    coracoid with anterior shoulder dislocation. J Can Assoc Radiol 1980;31(4):278-279.

    44.

    Mick CA, Weiland AJ: Pseudoarthrosis of a fracture of


    the acromion. J Trauma 1983;23(3):248-249.

    45.

    Gorczyca JT, Davis RT, Hartford JM, Brindle TJ: Open


    reduction internal fixation after displacement of a previously nondisplaced acromial fracture in a multiply injured patient: Case report and review of literature. J Orthop Trauma 2001;15(5):369-373.

    46.

    Asbury S, Tennent TD: Avulsion fracture of the coracoid process: A case report. Injury 2005;36(4):567-568.

    47.

    Zlowodzki M, Bhandari M, Zelle BA, Kregor PJ, Cole


    PA: Treatment of scapula fractures: Systematic review of
    520 fractures in 22 case series. J Orthop Trauma 2006;
    20(3):230-233.

    48.

    Ada JR, Miller ME: Scapular fractures: Analysis of 113


    cases. Clin Orthop Relat Res 1991;269:174-180.

    49.

    DePalma A, ed: Surgery of the Shoulder, ed 3. Philadelphia, PA, JB Lippincott; 1983.

    50.

    Soslowsky LJ, Flatow EL, Bigliani LU, Mow VC: Articular geometry of the glenohumeral joint. Clin Orthop
    Relat Res 1992;285:181-190.

    51.

    Goss TP: Double disruptions of the superior shoulder


    suspensory complex. J Orthop Trauma 1993;7(2):99106.

    52.

    Egol KA, Connor PM, Karunakar MA, Sims SH, Bosse


    MJ, Kellam JF: The floating shoulder: Clinical and functional results. J Bone Joint Surg Am 2001;83(8):11881194.

    53.

    DeFranco MJ, Patterson BM: The floating shoulder.


    J Am Acad Orthop Surg 2006;14(8):499-509.

    32.

    Boileau P, Trojani C, Walch G, Krishnan SG, Romeo A,


    Sinnerton R: Shoulder arthroplasty for the treatment of
    the sequelae of fractures of the proximal humerus.
    J Shoulder Elbow Surg 2001;10(4):299-308.

    33.

    Walch G, Badet R, Nov-Josserand L, Levigne C: Nonunions of the surgical neck of the humerus: Surgical
    treatment with an intramedullary bone peg, internal fixation, and cancellous bone grafting. J Shoulder Elbow
    Surg 1996;5(3):161-168.
    McGahan JP, Rab GT: Fracture of the acromion associated with an axillary nerve deficit: A case report and review of the literature. Clin Orthop Relat Res 1980;147:
    216-218.

    35.

    Neviaser JS: Traumatic lesions: Injuries in and about the


    shoulder joint. Instr Course Lect 1956;13:187-216.

    36.

    Baldwin KD, Ohman-Strickland P, Mehta S, Hume E:


    Scapula fractures: A marker for concomitant injury? A
    retrospective review of data in the National Trauma Database. J Trauma 2008;65(2):430-435.
    The authors studied whether there was a relationship
    between scapula fractures and concomitant injury and
    determined that injuries to the upper extremity and pelvic ring and thoracic injuries were associated with
    greater frequency in patients with scapular fracture.

    37.

    Folman Y, el-Masri W, Gepstein R, Messias R: Fractures of the scapula associated with traumatic paralysis:
    A pathomechanical indicator. Injury 1993;24(5):306308.

    38.

    Harris RD, Harris JH Jr: The prevalence and significance of missed scapular fractures in blunt chest
    trauma. AJR Am J Roentgenol 1988;151(4):747-750.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    34.

    Isolated scapular body fractures healed after nonsurgical


    treatment, leading to a functional shoulder score level
    equal to that of the general population and a range of
    motion equal to the uninjured shoulder. Multitrauma
    patients had a less favorable outcome.

    283

    Section 3: Upper Extremity

    64.

    Shaw JL, Sakellarides H: Radial-nerve paralysis associated with fractures of the humerus: A review of fortyfive cases. J Bone Joint Surg Am 1967;49(5):899-902.

    Tingstad EM, Wolinsky PR, Shyr Y, Johnson KD: Effect


    of immediate weightbearing on plated fractures of the
    humeral shaft. J Trauma 2000;49(2):278-280.

    65.

    Postacchini F, Morace GB: Fractures of the humerus associated with paralysis of the radial nerve. Ital J Orthop
    Traumatol 1988;14(4):455-464.

    56.

    Ring D, Chin K, Jupiter JB: Radial nerve palsy associated with high-energy humeral shaft fractures. J Hand
    Surg Am 2004;29(1):144-147.

    66.

    Pugh DM, McKee MD: Advances in the management of


    humeral nonunion. J Am Acad Orthop Surg 2003;
    11(1):48-59.

    57.

    Papasoulis E, Drosos GI, Ververidis AN, Verettas DA:


    Functional bracing of humeral shaft fractures: A review
    of clinical studies. Injury 2010;41(7):e1-e7.

    67.

    Otsuka NY, McKee MD, Liew A, et al: The effect of comorbidity and duration of nonunion on outcome after
    surgical treatment for nonunion of the humerus.
    J Shoulder Elbow Surg 1998;7(2):127-133.

    68.

    Ring D, McKee MD, Perey BH, Jupiter JB: The use of a


    blade plate and autogenous cancellous bone graft in the
    treatment of ununited fractures of the proximal humerus. J Shoulder Elbow Surg 2001;10(6):501-507.

    69.

    Healy WL, White GM, Mick CA, Brooker AF Jr, Weiland AJ: Nonunion of the humeral shaft. Clin Orthop
    Relat Res 1987;219:206-213.

    70.

    McKee MD, Miranda MA, Riemer BL, et al: Management of humeral nonunion after the failure of locking
    intramedullary nails. J Orthop Trauma 1996;10(7):492499.

    71.

    Patel VR, Menon DK, Pool RD, Simonis RB: Nonunion


    of the humerus after failure of surgical treatment: Management using the Ilizarov circular fixator. J Bone Joint
    Surg Br 2000;82(7):977-983.

    72.

    Healy WL, Jupiter JB, Kristiansen TK, White RR: Nonunion of the proximal humerus: A review of 25 cases.
    J Orthop Trauma 1990;4(4):424-431.

    73.

    Chhabra AB, Golish SR, Pannunzio ME, Butler TE Jr,


    Bolano LE, Pederson WC: Treatment of chronic nonunions of the humerus with free vascularized fibula
    transfer: A report of thirteen cases. J Reconstr Microsurg 2009;25(2):117-124.
    The authors reviewed 13 cases of chronic nonunion of
    the humerus treated with vascularized fibula transfer
    and found that healing occurred in 12 of the 13 patients
    after an average of 18 weeks.

    74.

    Jupiter JB: Complex non-union of the humeral diaphysis: Treatment with a medial approach, an anterior
    plate, and a vascularized fibular graft. J Bone Joint Surg
    Am 1990;72(5):701-707.

    54.

    Owens BD, Goss TP: The floating shoulder. J Bone


    Joint Surg Br 2006;88(11):1419-1424.

    55.

    The authors conducted a literature review to determine


    the efficacy of functional bracing and found that humeral shaft fractures heal in an average of 10.7 weeks
    after treatment and proximal third and AO type A fractures have a higher nonunion rate. Residual deformity
    and joint stiffness are the main disadvantages of this
    treatment.
    58.

    59.

    60.

    McKee MD: Fractures of the shaft of the humerus, in


    Bucholz RW, Heckman JD, Brown CC, eds: Rockwood
    and Greens Fractures in Adults, ed 6. Philadelphia, PA,
    Lippincott Williams & Wilkins, 2006, vol 1, pp 11171159.
    Bhandari M, Devereaux PJ, McKee MD, Schemitsch
    EH: Compression plating versus intramedullary nailing
    of humeral shaft fractures: A meta-analysis. Acta Orthop 2006;77(2):279-284.
    Hak DJ: Radial nerve palsy associated with humeral
    shaft fractures. Orthopedics 2009;32(2):111.

    3: Upper Extremity

    The authors discussed the need for surgical exploration


    in patients with radial nerve palsy associated with humeral shaft fractures.

    284

    61.

    Shao YC, Harwood P, Grotz MR, Limb D, Giannoudis


    PV: Radial nerve palsy associated with fractures of the
    shaft of the humerus: A systematic review. J Bone Joint
    Surg Br 2005;87(12):1647-1652.

    62.

    Larsen LB, Barfred T: Radial nerve palsy after simple


    fracture of the humerus. Scand J Plast Reconstr Surg
    Hand Surg 2000;34(4):363-366.

    63.

    Pollock FH, Drake D, Bovill EG, Day L, Trafton PG:


    Treatment of radial neuropathy associated with fractures of the humerus. J Bone Joint Surg Am 1981;63(2):
    239-243.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 23

    Shoulder Reconstruction
    Anand M. Murthi, MD

    Jesse A. McCarron, MD

    Glenohumeral Degenerative Joint Disease

    Dr. Murthi or an immediate family member serves as a


    paid consultant to or is an employee of Zimmer and Ascension Orthopaedics and has received research or institutional support from Arthrex, DePuy, and Synthes. Dr.
    McCarron or an immediate family member is a member
    of a speakers bureau or has made paid presentations
    on behalf of Mitek, serves as a paid consultant to or is
    an employee of Wyeth, and has received research or institutional support from Wyeth.

    2011 American Academy of Orthopaedic Surgeons

    3: Upper Extremity

    Glenohumeral degenerative joint disorders are caused


    by numerous disease processes and injury patterns.
    Common disease processes include osteoarthritis (OA),
    rheumatoid (inflammatory) arthritis, osteonecrosis,
    posttraumatic arthritis, rotator cuff arthropathy, and
    postoperative or iatrogenic arthropathy. Each of these
    entities has associated symptomatology, examination
    findings, radiographic changes, and therapeutic interventions.
    Primary OA is a disease of cartilage and, as such, is
    the most common degenerative process in the shoulder.
    Classic physical findings include painful loss of motion,
    early morning stiffness, and loss of strength. Radiographic findings include osteophyte formation, loss of
    joint space, and subchondral sclerosis (Figure 1). A late
    finding is posterior glenoid wear, which is important in
    planning surgical reconstruction and potential glenoid
    resurfacing.
    Rheumatoid arthritis is a synovial fluidbased disease that more commonly occurs in older women.
    Physical findings are similar to those of OA, although
    range of motion may not be as limited. Classic radiographic findings include central glenoid wear, osteopenia, subchondral cysts, and bony erosions. When considering surgical reconstruction and arthroplasty,
    pathologic abnormality of the rotator cuff is very common and must be evaluated.
    Osteonecrosis is a less frequently occurring disease
    process that can manifest as significant deep-seated
    shoulder pain, although the patient is often able to
    maintain motion and strength. Stiffness occurs during
    late stages, with complete loss of the humeral head architecture. Osteonecrosis is caused by disruption of the
    vascular supply to the humeral head, which can lead to
    cartilage death and collapse. Osteonecrosis is character-

    ized by early radiographic sclerosis, then humeral head


    collapse, and later glenoid changes. Common causes include steroid intake, alcoholism, and trauma. A careful
    diagnosis with radiography or MRI to determine the
    presence of humeral head collapse will guide the choice
    of surgical treatment from core decompression to total
    shoulder replacement.
    Posttraumatic arthritis presents in many forms, from
    proximal humerus malunions and subsequent irregular
    glenoid contact stresses to intra-articular glenoid fractures leading to glenohumeral arthroses. Previous
    trauma or fracture may predispose a patient to this disorder. Numerous case reports and small series have
    shown that rapid chondrolysis may be an issue in
    young patients presenting with painful, stiff shoulders
    after arthroscopic surgery.1-3 Chondrolysis may result
    from pain pump insertion, infection, and/or thermal
    procedures. Although there has been no definitive correlation, rapid chondrolysis along with infection should
    be considered in the differential diagnosis of the rapid
    loss of joint space.

    Figure 1

    True AP radiographic view of a shoulder with OA.

    Orthopaedic Knowledge Update 10

    285

    Section 3: Upper Extremity

    Postoperative arthropathy is difficult to diagnose accurately and develop a treatment strategy for, especially
    in a shoulder treated with stabilization or capsulorrhaphy. For example, in a common scenario, a 50-yearold man presents with a stiff, painful, arthritic shoulder
    many years after undergoing open subscapularis shortening and/or a disruptive procedure (such as Putti-Platt,
    Magnuson-Stack, or Bristow-Latarjet). The eccentric
    forces placed on the glenoid lead to severe arthritis
    (posterior glenoid wear) and extreme loss of external
    rotation. These shoulders require complex treatments,
    especially when performing arthroplasty procedures,
    because regaining motion can be difficult when softtissue balancing is needed to provide stability and motion.
    Understanding the many origins of degenerative
    shoulder disease permits proper surgical planning and
    the best chance for a successful outcome because each
    disease process lends itself to various treatment modalities.

    Nonsurgical Treatment

    3: Upper Extremity

    Nonsurgical treatment in the form of activity modification, pharmacotherapy, and physical therapy remains
    the first-line treatment option for patients with glenohumeral arthritis, although the effectiveness of these
    modalities is inconclusive. Nonsurgical, multimodality
    therapies should be tried in all patients (especially
    younger patients) before surgical treatment is considered.
    Physical therapy is often prescribed for mild or moderate glenohumeral arthritis to preserve motion and optimize function, but its efficacy has not been
    established.4-6 Determining the efficacy of physical therapy for glenohumeral arthritis has been complicated by
    the failure of most studies and systematic reviews to
    distinguish between different etiologies of shoulder
    pain and by the lack of consistency in the type of therapy prescribed. Similarly, acupuncture and transcutaneous electrical nerve stimulation are reasonable treatment options for the arthritic shoulder; however, no
    studies have evaluated the specific efficacy of these modalities in the management of glenohumeral arthritis.
    Symptomatic improvement with these modalities likely
    results in large part from the alleviation of neck and
    upper back pain often associated with shoulder dysfunction; these treatments have shown great efficacy in
    relieving such pain.7-10
    Acetaminophen, nonsteroidal anti-inflammatory
    drugs (NSAIDs), and narcotic medications are frequently prescribed for arthritis-related shoulder pain
    and have demonstrated efficacy in reducing symptoms.
    However, all of these medications can have deleterious
    side effects that must be taken into consideration. A
    meta-analysis of randomized controlled trials suggests
    that NSAIDs are more effective than acetaminophen
    for treating pain related to OA, but are also associated
    with a higher risk of complications.11 Patients with an
    increased risk of gastrointestinal complications are best
    treated with either a cyclooxygenase-2 selective NSAID
    286

    Orthopaedic Knowledge Update 10

    or a nonselective NSAID with coprescription of a proton pump inhibitor.4 Although the risk of gastrointestinal and renal complications is considered lower with
    acetaminophen than with NSAIDs, a new focus on the
    potential for liver toxicity with acetaminophen or medications that contain acetaminophen (including many
    narcotics) emphasizes the need to consider these risk
    factors when prescribing these medications.
    Glenohumeral steroid injections are commonly used
    for shoulder arthritis to reduce pain, but there are no
    studies showing the efficacy of these injections in the
    shoulder and their effectiveness is inconclusive. Generally, the administration of glenohumeral steroid injections is likely to be more effective when treating an inflammatory synovitis component of the pain, which
    may accompany many forms of arthritis. Pain that is
    related to the strenuous use of the arm or caused by
    mechanical problems, such as pain at the extremes of
    motion caused by capsular tightness or osteophytes, is
    less likely to be successfully treated by steroid injections. Guidelines at this time are based on level V evidence.
    Viscosupplementation for joints affected by OA has
    a delayed onset but improved duration in relieving pain
    when compared with steroid injections or placebo.4,12
    The only multicenter randomized controlled trial to
    evaluate viscosupplementation for shoulder arthritis
    showed modest but statistically significant improvements in pain (2 to 8 points better than placebo on a
    100-point visual analog scale) over a 26-week period.12

    Nonprosthetic Joint-Sparing Techniques


    Surgical options for the treatment of shoulder OA that
    avoid hemiarthroplasty or total shoulder arthroplasty
    include glenohumeral dbridement, lavage and microfracture, autologous chondrocyte implantation, osteochondral autologous transplantation, and capsular release. The effectiveness of treating OA by these means
    remains inconclusive.
    Arthroscopic glenohumeral dbridement, with removal of loose debris and resection of unstable cartilage flaps back to a stable edge, is considered a reasonable treatment option for a patient who does not have
    end-stage arthritis or diffuse full-thickness cartilage defects and has been unsuccessfully managed with nonsurgical treatment. In two case reports and in one limited retrospective review, it was shown that in a young
    patient with focal, full-thickness, cartilage lesions, dbridement and lavage with microfracture of the fullthickness cartilage defects can yield good short-term
    and midterm outcomes compared with the patients
    preoperative condition.13-15 These outcomes are equivalent to those of patients with lesser (Outerbridge grade
    2 or 3) chondral lesions at 12- to 33-month followups.15 Patients with bipolar lesions (involving both the
    glenoid and humeral sides of the joint) did significantly
    worse than patients with unipolar lesions.
    More involved treatment strategies involving autologous chondrocyte implantation, osteochondral autograft transplantation, or osteochondral allografting

    2011 American Academy of Orthopaedic Surgeons

    Chapter 23: Shoulder Reconstruction

    procedures for focal, full-thickness articular cartilage


    defects are intended to regenerate or replace lost cartilage as opposed to creating a fibrocartilage scar, which
    is associated with the microfracture technique. There is
    only one case report in the literature involving the use
    of autologous chondrocyte implantation in the shoulder. The procedure resulted in a good patient outcome
    at 3 months postoperatively, but no long-term
    follow-up was available.16 Osteochondral autografting
    for the treatment of full-thickness cartilage defects of
    the shoulder has been reported in a group of seven patients.17 All patients showed improved function, decreased pain, and good range of motion at a mean
    follow-up of 9-years; however, the procedure did not
    prevent the radiographic progression of glenohumeral
    OA.
    Dbridement with capsular release of full-thickness
    cartilage defects has achieved mixed results.18-20 Although good pain relief and improved function has
    been reported in some patient groups at a mean 34month follow-up,18 other reports have suggested more
    modest results with the return of pain within 1 year of
    surgery (after an initial pain-free period),19 and a 30%
    failure rate requiring conversion to hemiarthroplasty.20
    The initial success and durability of the results for these
    types of procedures are likely highly dependent on appropriate patient selection and management of expectations, with less favorable outcomes in younger patients
    with higher demands and those with larger, more diffuse chondral lesions.

    Shoulder Resurfacing Arthroplasty

    2011 American Academy of Orthopaedic Surgeons

    Hemiarthroplasty
    Historically, hemiarthroplasty or humeral head replacement has been indicated for most degenerative shoulder
    conditions, including OA, inflammatory arthritis, posttraumatic sequelae (osteochondral defects, malunions,
    and chondrolysis), osteonecrosis, and certain cuff tear
    arthropathies.24,26-28 Although the recent trend has been
    to use total shoulder arthroplasty to treat the arthritic
    shoulder with an intact rotator cuff, glenoid loosening
    must still be regarded as a source of potential failure in
    shoulder arthroplasty. Humeral head replacement continues to be an option in select, physiologically
    younger, active patients.28 Proper patient selection is
    paramount for success, and is considerably dependent
    on understanding glenoid morphology and wear patterns. Selecting patients with a centralized glenoid wear
    pattern without posterior wear or static subluxation
    should lead to improved outcomes. Soft-tissue balancing and appropriate capsular releases with subscapularis mobilization are required, just as with a total
    shoulder arthroplasty, to optimize results. A recent
    study indicated that concentric reaming with humeral
    head replacement, as performed during the ream and
    run procedure, may also benefit younger, active patients with degenerative arthritis.28
    The current literature has described a spectrum of
    results achieved in using humeral head replacement for
    degenerative joint disease.24,26-30 Guidelines indicate
    that obtaining proper height, version, and offset to balance the shoulder is essential to improve function. This
    theory of anatomic replacement allows proper tensioning in both the rotator cuff and deltoid to allow an in-

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Recent information has shown that select patients with


    pathologic conditions of the shoulder may benefit from
    shoulder resurfacing arthroplasty.20-23 Degenerative
    conditions such as inflammatory arthritis, OA, osteonecrosis, posttraumatic conditions, and focal articular defects have benefited from shoulder resurfacing arthroplasty. Short- and long-term improvements in pain and
    function have been reported after treatment with this
    bone-preserving technique.20,24
    Prerequisites for shoulder resurfacing arthroplasty
    include adequate proximal humeral bone stock to contain the short peg and support the implant. Bone loss
    up to 25% has not precluded shoulder resurfacing arthroplasty according to one study.25 Technically, the
    starting position of the centrally placed guidewire remains the reference point in all designs to recreate the
    anatomic position and function of the shoulder. Obtaining the proper amount of lateral offset will position
    the rotator cuff to function properly. In patients with
    significant anatomic distortion (for example, surgical
    neck malunion) or long-stem total elbow replacements,
    humeral stem placement may not be possible, thus providing an indication for shoulder resurfacing arthroplasty.
    Advantages of the shoulder resurfacing arthroplasty
    design include the ability to replicate native anatomic
    humeral version, inclination, offset, and head size while
    preserving bone stock. In physiologically younger, ac-

    tive patients who may require future revision surgery,


    preservation of bone stock is beneficial. Although
    hemiarthroplasty may provide similar functional outcomes, revising stemmed implants results in potentially
    significant proximal bone loss and soft-tissue disruption. Complications with humeral stems, such as
    periprosthetic fracture, loosening, bone resorption, and
    deep infection, do not occur with shoulder resurfacing
    arthroplasty. When properly implanted, a shoulder resurfacing arthroplasty device provides a stable shoulder
    replacement option that can mirror native offset; allows proper soft-tissue balancing; and preserves the glenoid, thus preventing the risk of polyethylene glenoid
    failure (Figure 2). The caveat remains that an overstuffed, lateralized, improperly positioned shoulder resurfacing arthroplasty can lead to rapid progression of
    pain and stiffness and potential cuff rupture. Selecting
    patients with relatively preserved motion and minimal
    and centralized glenoid wear (without static posterior
    subluxation or biconcavity) can lead to good results.
    Several studies have shown shoulder resurfacing arthroplasty to be an appropriate choice for the younger patient who meets these criteria.20,21,23 Shoulder resurfacing arthroplasty, however, may not be appropriate for
    patients with end-stage degenerative stiff shoulder with
    posterior static subluxation because stability and tissue
    balancing will be a consideration.

    287

    Section 3: Upper Extremity

    Figure 2

    A, Preoperative AP radiograph shows a shoulder with degenerative arthritis. B, Postoperative AP radiograph of the
    shoulder after successful surface replacement arthroplasty.

    crease in motion and decrease in pain. Anatomic sizing


    and the proper level of humeral head osteotomy (resection) are often misunderstood, leading to either overstuffing or instability. Resection is based on the level of
    the rotator cuff insertion, which results in anatomic
    version (approximately 20), with retroversion usually
    ranging from 20 to 40. Technical complications include malpositioning and overstuffing the joint (using
    too large a head size) to compensate for instability.
    Complications may include stiffness, progressive glenoid wear, periprosthetic fracture, infection, and instability (subscapularis dysfunction). Revision or conversion to total shoulder arthroplasty is complex, difficult,
    and rarely provides results similar to those achieved
    with primary total shoulder arthroplasty.29

    Biologic Total Shoulder Arthroplasty

    3: Upper Extremity

    Humeral head hemiarthroplasty with soft-tissue resurfacing of the glenoid (biologic total shoulder arthroplasty) is an option for treating patients with glenohumeral arthritis if younger age or a higher activity level
    makes implantation of a polyethylene glenoid component less desirable. The objective of this procedure is to
    reduce the rate of progressive glenoid erosions, arthrosis, and glenoid-side pain that is often reported following hemiarthroplasty at midterm and longer-term
    follow-up, while avoiding the increased risk of polyethylene wear and traditional glenoid component failure
    associated with younger, active patients. The biomechanical justification for soft-tissue resurfacing of the
    glenoid was demonstrated in a cadaver model that
    showed that lateral meniscal interposition reduced
    mean glenoid contact pressures by 10% and transferred
    more load to the periphery of the glenoid and away
    288

    Orthopaedic Knowledge Update 10

    from the glenoid center.31 It is unclear if similar benefits


    would be derived from using other interposition materials. The role for glenoid recontouring (or glenoid
    reaming) in distributing forces across the glenoid also is
    unclear.
    Lateral meniscus or Achilles tendon allograft, fascia
    lata or anterior joint capsule autograft, and dermal extracellular matrix patches have been used for glenoid
    resurfacing. Only small series and case reports are
    available on the short-term and midterm outcomes
    with this procedure, and results have been highly variable. Studies have described the use of anterior joint
    capsule, autologous fascia lata, Achilles tendon allograft or GraftJacket (Wright Medical, Arlington, VA)
    as the interposition material, reporting 50% excellent,
    36% satisfactory, and 14% unsatisfactory results at a
    mean of 7 years (range, 2 to 15 years) after surgery.32,33
    Early techniques using anterior joint capsule or fascia
    lata resulted in persistent pain and glenoid erosions,
    which led to the more recent use of Achilles tendon, lateral meniscus, or dermal extracellular matrix devices.34
    A 92% failure rate (defined as persistent pain, glenoid erosions, and loss of the joint space on radiographs) was reported in 13 shoulders treated with humeral hemiarthroplasty and Achilles tendon allograft
    glenoid resurfacing.35 Other investigators have reported
    short-term (12- to 18-month) outcomes with mixed results using lateral meniscus allografts. Complication
    rates as high as 17% have been reported, with loss of
    graft fixation, mechanical symptoms, graft failure, recurrent pain, or progressive glenoid bone erosions
    sighted as the most common causes of failure.36,37 Several reports, at 2- to 5-year follow-up, showed good
    functional outcomes and patient satisfaction with the

    2011 American Academy of Orthopaedic Surgeons

    Chapter 23: Shoulder Reconstruction

    Figure 3

    A, AP radiograph showing good joint space 2 weeks after hemiarthroplasty and glenoid resurfacing with anterior
    joint capsule. An opening wedge coracoid osteotomy also was done. B, AP radiograph 6 months postoperatively.
    C, AP radiograph 18 months postoperatively showing areas of glenoid erosion and loss of joint space despite a
    good clinical outcome.

    procedure; however, progressive joint-space narrowing


    and glenoid erosion were reported, which raises concerns about the ability of this procedure to serve as a
    durable treatment option for the glenoid and to prevent
    progressive glenoid bone loss.38,39 (Figure 3).
    Despite these unresolved questions, hemiarthroplasty with glenoid soft-tissue resurfacing is still considered a reasonable treatment option for a young patient
    with end-stage arthritis. Current recommendations to
    minimize the risk of complications are to avoid the use
    of anterior joint capsule or fascia lata, appropriately
    prepare the glenoid surface to create a healing environment for the graft, delay range-of-motion exercises, and
    select fewer high-demand patients for the procedure.

    Total Shoulder Arthroplasty

    2011 American Academy of Orthopaedic Surgeons

    3: Upper Extremity

    Total shoulder arthroplasty has consistently achieved


    good pain relief and improved function in patients with
    glenohumeral posttraumatic arthritis, inflammatory arthritis, and OA with short-term, midterm, and longterm follow-up; however, functional outcomes are usually more modest in patients with posttraumatic and
    inflammatory arthritis than in those with OA. Both cemented and press-fit humeral components have shown
    good longevity and a low incidence of loosening.40,41
    Glenoid component wear and glenoid loosening continue to present a clinical challenge and are the main
    source of failures, recurrent pain, and the need for revision surgery after total shoulder arthroplasty.
    Several clinical studies have recently reported the
    presence of progressive radiolucent lines around the
    glenoid component and/or glenoid component settling
    in 50% of patients as early as 3 to 4 years after total
    shoulder arthroplasty.40,42 The presence of radiographic
    glenoid lucencies or glenoid seating did not correlate
    with poor patient functional outcomes or pain at 3- to
    7-year follow-up.
    Recent data suggest that pegged glenoid designs instead of keeled designs, and cross-linked ultra-high
    molecular-weight polyethylene may reduce the rate of
    glenoid failure and improve the survivorship of total

    shoulder arthroplasties. In cyclic mechanical testing,


    cross-linked ultra-highmolecular-weight polyethylene
    demonstrated an 85% reduction in the glenoid polyethylene wear rate compared with a conventional, non
    cross-linked glenoid component.43 With similar particulate size and morphology of the wear debris from both
    the cross-linked and noncross-linked components, the
    osteolytic potential should be similar on a per volume
    basis, resulting in a theoretic 85% reduction in clinically observed glenoid lucency secondary to polyethylene wear.
    A recent study evaluating the 5- to 15-year clinical
    and radiographic outcomes of total shoulder arthroplasty with different glenoid component designs
    showed the lowest failure rates at 5 years when using
    cemented peg glenoid designs (99% survival) compared
    with cemented keeled or metal-backed designs.44 Uncemented, metal-backed keeled glenoid designs have
    shown the highest rates of glenoid lucencies,45,46 which
    likely result from the combination of backside wear between the metal and the polyethylene, and the inferior
    mechanical stability of the keeled component design
    and the bone-component interface.47 Because pegged
    glenoid designs and cross-linked ultra-highmolecularweight polyethylene have only been used in shoulder
    arthroplasty in recent years, long-term follow-up is not
    yet available to determine if these advances will lead to
    reduced failure and revision rates.

    Rotator Cuff Tear Arthropathy


    Rotator cuff tear arthropathy (RCTA) is a pathoanatomic condition described during the 1800s.48 In 1983,
    Neer et al49 provided a thorough description of this entity, which included both mechanical and nutritional responses in the shoulder, leading to the subsequent development of arthritis in the setting of massive
    attritional rotator cuff tearing (Figure 4). The pathogenesis of this disorder is unknown despite previous
    theories. However, evidence suggests that RCTA is a

    Orthopaedic Knowledge Update 10

    289

    Section 3: Upper Extremity

    Figure 4

    A, Flow chart showing the effects of a tear on rotator cuff nutritional factors. These include loss of a so-called
    water-tight joint space with reduction in the pressure of the joint fluid required for the perfusion of nutrients to
    the articular cartilage. This contributes to disuse osteoporosis of the subchondral bone of the humeral head. B,
    Flow chart showing the mechanical effects of a tear on rotator cuff, including instability of the humeral head not
    only upward but also anteriorly and posteriorly. Upward instability escalates wear into the anterior part of the
    acromion and the acromioclavicular joint. (Reproduced with permission from Neer CS II, Craig EV, Fukuda H: Cufftear arthropathy. J Bone Joint Surg Am 1983;65(9):1232-1244.)

    3: Upper Extremity

    crystalline-induced arthropathy in which synovial fluidbased matrix degradation proteins act to degrade
    tendons and cartilage. Calcium phosphate crystal deposition has been reported in end-stage disease. Characteristics of RCTA include massive chronic rotator cuff
    tears, glenohumeral cartilage destruction, subchondral
    bone osteoporosis, and humeral head collapse. This
    disease process usually occurs in the dominant shoulder, with a mean patient age of 69 years and a 3:1 female predominance. Classic physical findings include
    shoulder effusions, painful arcs of motion, spinati atrophy, and weakness in rotation; late-stage findings include pseudoparalysis with the inability to raise the
    arm. Radiographic findings include acromial acetabularization, femoralization of the humeral head, eccentric superior glenoid wear, lack of typical peripheral osteophytes of OA, osteopenia, subarticular sclerosis
    (snowcap sign), and loss of the coracoacromial arch
    (anterosuperior escape). MRI is not routinely necessary
    for the diagnosis.
    A classification scheme has been developed50 to categorize the various radiographic stages of RCTA,
    which are described in Table 1. This classification
    scheme may guide the surgeon in the proper selection
    of arthroplasty reconstruction. A type II shoulder may
    not improve with humeral head replacement because it
    has lost coracoacromial arch support and is unstable
    and uncompensated.
    Treatment of RCTA includes nonsurgical modalities
    such as rest, anti-inflammatory drugs, corticosteroid injections, and therapy to strengthen the deltoid. Arthroscopic treatments include extensive dbridement
    (greater tuberosity tuberoplasty) with concomitant biceps tenotomy and/or tenodesis. Although useful, these
    options achieve unpredictable results.
    290

    Orthopaedic Knowledge Update 10

    When nonsurgical treatments fail, shoulder arthroplasty may be necessary. The objectives of reconstruction
    are to decrease discomfort and improve shoulder motion.
    The two arthroplasty options are hemiarthroplasty and
    reverse shoulder replacement. Traditional unconstrained
    total shoulder arthroplasty is contraindicated because of
    evidence of early glenoid loosening. Hemiarthroplasty is
    recommended for younger patients with RCTA who
    have relatively active lifestyles. Better results are achieved
    with maintained elevation (greater than 90) and intact
    force couples.51 An intact subscapularis appears to be key
    in maintaining postoperative elevation and rotation. Anatomic sizing is important to prevent joint-line lateralization and subsequent deltoid stretching. Soft-tissue balancing and repair of any residual posterior superior
    rotator cuff may lead to improved results. Surgical techniques include maintaining the anterior cuff and working through the superior cuff defect. The deltoid insertion and coracoacromial arch and/or ligament must be
    maintained to prevent anterior-superior escape. Results
    may deteriorate over time, with loss of motion and pain
    from superior glenoid erosion.52 Specially designed
    hooded and/or extended coverage prostheses built to articulate with the acromion with less friction may provide
    improved pain relief and function; however, few wellcontrolled studies are available for comparison. Rehabilitation is slow, with the focus on deltoid strengthening
    and limited-goals outcomes.
    Reverse shoulder arthroplasty is reserved for the
    physiologically older patient with a painful pseudoparalytic shoulder from RCTA.53-55 Relative indications include glenohumeral arthritis with cuff tearing, failed
    previous cuff surgery, a massive rotator cuff tear without arthritis, proximal humerus malunions and/or nonunions, and acute four-part fractures in an elderly pa-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 23: Shoulder Reconstruction

    Table 1

    Radiographic Classification of Cuff Tear Arthropathy


    Type IA
    Centered Stable

    Type IB
    Centered Medialized

    Type IIA
    Type IIB
    Decentered Limited Stable Decentered Unstable

    Intact anterior restraints


    Minimal superior migration
    Dynamic joint stabilization
    Acetabularization of
    coracoacromial arch and
    femoralization of humeral
    head

    Intact anterior restraints


    Force couple intact/
    compensated
    Minimal superior migration
    Compromised dynamic joint
    stabilization
    Medial erosion of the glenoid
    Acetabularization of
    coracoacromial arch
    Femoralization of humeral
    head

    Compromised anterior
    restraints
    Compromised force couple
    Superior translation
    Insufficient dynamic joint
    stabilization
    Minimum stabilization by
    coracoacromial arch
    Superior-medial erosion
    Extensive acetabularization of
    coracoacromial arch
    Femoralization of humeral
    head

    Incompetent anterior
    structures
    Anterior superior escape
    Absent dynamic joint
    stabilization
    No stabilization by
    coracoacromial arch
    Deficient anterior structures

    (Adapted with permission from Visotsky JL, Basamania C, Seebauer L, et al: Cuff tear arthropathy. J Bone Joint Surg Am 2004;86:35-40.)

    Figure 5

    tient with osteoporosis. Reverse shoulder arthroplasty is


    another treatment option for the patient with failed
    shoulder arthroplasty, especially those with dysfunctional rotator cuffs and humeral and/or glenoid bone
    loss. Prerequisites for surgery include a functional deltoid, adequate glenoid bone stock for base plate implantation, and specific patient expectations. Contraindica-

    2011 American Academy of Orthopaedic Surgeons

    3: Upper Extremity

    Center of rotation and position of the humerus and deltoid muscles with the arm at the side (A) and in abduction
    (B) in normal shoulder anatomy. C and D, Reverse total shoulder arthroplasty medializes the center of rotation,
    distalizes the humerus, and elongates the deltoid. The lever arm of the deltoid muscle (dotted line) is lengthened
    so that for any given angular displacement of the humerus, shortening of the deltoid is greater than with total
    shoulder arthroplasty. F = deltoid line of action. (Reproduced from Gerber C, Pennington SD, Nyffeler RW: Reverse
    total shoulder arthroplasty. J Am Acad Orthop Surg 2009;17:284-295.)

    tions include deltoid dysfunction, chronic infection, and


    poor glenohumeral bone stock. With the semiconstrained reverse shoulder prosthesis, the center of rotation is moved inferior and medial onto the scapula to
    assist the deltoid fulcrum in raising the arm (Figure 5).
    Early results in European and American studies are very
    promising for improved elevation and pain relief.53-55

    Orthopaedic Knowledge Update 10

    291

    Section 3: Upper Extremity

    Table 2

    AAOS Clinical Practice Guideline on the Treatment of Glenohumeral Arthritis


    Strength of
    Recommendation

    Recommendation
    Recommend for or against physical therapy for the initial treatment of patients with osteoarthritis of the
    glenohumeral joint.
    Recommend for or against the use of pharmacotherapy in the initial treatment of patients with
    glenohumeral joint osteoarthritis.
    Recommend for or against the use of injectable corticosteroids when treating patients with glenohumeral
    joint osteoarthritis.

    Inconclusive

    The use of injectable viscosupplementation as an option when treating patients with glenohumeral joint
    osteoarthritis.
    Recommend for or against the use of arthroscopic treatments for patients with glenohumeral joint
    osteoarthritis. These treatments include dbridement, capsular release, chondroplasty, microfracture,
    removal of loose bodies, and biologic and interpositional grafts, subacromial decompression, distal
    clavicle resection, acromioclavicular joint resection, biceps tenotomy or tenodesis, and labral repair or
    advancement.
    Recommend for or against open dbridement and/or nonprosthetic or biologic interposition arthroplasty
    in patients with glenohumeral joint osteoarthritis. These treatments include allograft, biologic and
    interpositional grafts, and autograft.

    Weak

    Recommend for total shoulder arthroplasty and hemiarthroplasty as options when treating patients with
    glenohumeral joint osteoarthritis.

    Weak

    Recommend for total shoulder arthroplasty over hemiarthroplasty when treating patients with
    glenohumeral joint osteoarthritis.
    An option for reducing immediate postoperative complication rates is for patients to avoid shoulder
    arthroplasty by surgeons who perform fewer than two shoulder arthroplasties per year.

    Moderate

    In the absence of reliable evidence, it is the opinion of this work group that physicians use perioperative
    mechanical and/or chemical venous thromboembolism prophylaxis for shoulder arthroplasty patients.
    The use of either keeled or pegged all-polyethylene cemented glenoid components are options when
    performing total shoulder arthroplasty.
    In the absence of reliable evidence, it is the opinion of this work group that total shoulder arthroplasty
    not be performed in patients with glenohumeral osteoarthritis who have an irreparable rotator cuff
    tear.

    Consensus

    Recommend for or against biceps tenotomy or tenodesis when performing shoulder arthroplasty in
    patients who have glenohumeral joint osteoarthritis.
    Recommend for or against a subscapularis trans-tendonous approach or a lesser tuberosity osteotomy
    when performing shoulder arthroplasty in patients who have glenohumeral joint osteoarthritis.
    Recommend for or against a specific type of humeral prosthetic design or method of fixation when
    performing shoulder arthroplasty in patients with glenohumeral joint osteoarthritis.
    Recommend for or against physical therapy following shoulder arthroplasty

    Inconclusive

    Inconclusive
    Inconclusive

    Inconclusive

    Inconclusive

    Weak

    Weak
    Consensus

    Inconclusive
    Inconclusive
    Inconclusive

    (AAOS Evidence-Based Clinical Practice Guidelines: American Academy of Orthopaedic Surgeons web site. http://www.aaos.org/research/guidelines/guide.asp. Accessed
    August 4, 2010.)

    3: Upper Extremity

    Complications include instability, component failure,


    infection, and scapular notching (which may predispose
    the patient to base plate failure). With improved component design and postoperative rehabilitation, recent
    evidence suggests decreased complication rates and the
    maintenance of good functional outcomes (Figure 6).

    Clinical Practice Guidelines


    The American Academy of Orthopaedic Surgeons
    (AAOS) work group on the treatment of glenohumeral
    OA has provided a summary of clinical practice guide292

    Orthopaedic Knowledge Update 10

    lines based on available evidence. A summary of these


    recommendations is provided in Table 2.

    Future Directions
    Advances in medical therapies, such as immune modulatory drugs for the treatment of inflammatory arthritis, selective cyclooxygenase-2 inhibitors, viscosupplementation, and other nonsurgical treatment options,
    are preventing or delaying the need for surgery. At the
    same time, less invasive and minimally invasive treatment strategies, including arthroscopic dbridement

    2011 American Academy of Orthopaedic Surgeons

    Chapter 23: Shoulder Reconstruction

    The authors discuss two patients with bilateral shoulder


    chondrolysis after arthroscopy.

    Figure 6

    Zhang W, Moskowitz RW, Nuki G, et al: OARSI recommendations for the management of hip and knee osteoarthritis: Part II. OARSI evidence-based, expert consensus guidelines. Osteoarthritis Cartilage 2008;16(2):
    137-162.
    This study presents the systematic review of current
    guidelines and literature related to the management of
    lower extremity arthritis performed by 16 experts from
    four disciplines (rheumatology, orthopaedics, primary
    care, and evidence-based medicine).

    5.

    Burbank KM, Stevenson JH, Czarnecki GR, Dorfman J:


    Chronic shoulder pain: Part II. Treatment. Am Fam
    Physician 2008;77(4):493-497.
    Review of general practice guidelines for initial nonsurgical treatment of common causes of shoulder pain.

    6.

    Smidt N, de Vet HC, Bouter LM, et al; Exercise Therapy Group: Effectiveness of exercise therapy: A bestevidence summary of systematic reviews. Aust J Physiother 2005;51(2):71-85.

    7.

    Kelly RB: Acupuncture for pain. Am Fam Physician


    2009;80(5):481-484.
    A syystematic literature review on the use of acupuncture for treatment of musculoskeletal pain and pain syndromes is presented. The authors analysis of available
    literature suggests some potential benefits may be seen
    with the use of acupuncture to treat shoulder pain, although definitive data are lacking.

    8.

    Wang ZL, Chen LF, Zhu WM: Observation on the transient analgesic effect of abdominal acupuncture TENS
    on pain of neck, shoulder, loin and legs. Zhongguo
    Zhen Jiu 2007;27(9):657-659.
    One hundred twenty patients with neck, shoulder, or leg
    pain were randomized into four groups to receive different modalities of combined acupuncture and transcutaneous electrical nerve stimulation (TENS) treatment for
    musculoskeletal pain. Visual analog scores were measured before and after treatment. Patients receiving abdominal acupuncture and TENS treatment saw significantly better transient reductions in pain as compared to
    other acupuncture/TENS treatment modalities.

    9.

    Vas J, Ortega C, Olmo V, et al: Single-point acupuncture and physiotherapy for the treatment of painful
    shoulder: A multicentre randomized controlled trial.
    Rheumatology (Oxford) 2008;47(6):887-893.
    A randomized controlled trial evaluating the efficacy of
    acupuncture in the treatment of shoulder pain arising
    from the subacromial space is described. The authors
    found that acupuncture was effective in reducing pain
    and the consumption of analgesic medication.

    10.

    Vance CG, Radhakrishnan R, Skyba DA, Sluka KA:


    Transcutaneous electrical nerve stimulation at both high
    and low frequencies reduces primary hyperalgesia in
    rats with joint inflammation in a time-dependent manner. Phys Ther 2007;87(1):44-51.

    A, Preoperative AP radiograph of classic RCTA.


    B, Postoperative AP radiograph of a reverse
    shoulder arthroplasty.

    and osteochondral autografts, are allowing intervention


    at an earlier stage in the disease process to preserve the
    native tissues before nonrecoverable damage is done.
    When end-stage glenohumeral arthritis requires reconstructive procedures, many prosthetic designs and treatment strategies are available depending on the nature
    of the disorder. Current trends suggest that future approaches will use more extensive preoperative planning
    through the use of surgical simulators and advanced
    imaging techniques,56,57 and intraoperative procedures
    will use computer-assisted navigation to optimize implant placement.58-60 Although still in its nascent stages,
    the field of bioengineering will likely shift the focus of
    treatment strategies for end-stage shoulder pathology
    away from reconstructive procedures, which replace
    damaged tissue with inert composite materials, and toward regenerative strategies intended to restore lost or
    degenerated tissues through biologics.

    Annotated References
    1.

    2.

    3.

    Levy JC, Virani NA, Frankle MA, Cuff D, Pupello DR,


    Hamelin J: Young patients with shoulder chondrolysis
    following arthroscopic shoulder surgery treated with total shoulder arthroplasty. J Shoulder Elbow Surg 2008;
    17(3):380-388.
    Total shoulder arthroplasty has been shown to improve
    pain and function in patients with shoulder chondrolysis
    after arthroscopic surgery.
    Levy JC, Frankle M: Bilateral shoulder chondrolysis following arthroscopy: A report of two cases. J Bone Joint
    Surg Am 2008;90(11):2546-2547.
    The authors discuss two patients with bilateral shoulder
    chondrolysis after arthroscopy.
    Greis PE, Legrand A, Burks RT: Bilateral shoulder
    chondrolysis following arthroscopy. A report of two
    cases. J Bone Joint Surg Am 2008;90(6):1338-1344.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    4.

    293

    Section 3: Upper Extremity

    The authors studied Sprague-Dawley rats with intraarticular injection and chemically induced knee inflammation as a model for joint pain. Sham TENS application, low-frequency (4-Hz) TENS, and high-frequency
    (100-Hz) TENS were applied to the affected knee at
    4 hours, 24 hours, and 2 weeks after injection. Lowand high-frequency TENS application both reduced the
    withdrawl from pain response at 24 hours and 2 weeks
    as compared to placebo (sham) treatment.
    11.

    Zhang W, Jones A, Doherty M: Does paracetamol (acetaminophen) reduce the pain of osteoarthritis? A metaanalysis of randomised controlled trials. Ann Rheum
    Dis 2004;63(8):901-907.

    12.

    Blaine T, Moskowitz R, Udell J, et al: Treatment of persistent shoulder pain with sodium hyaluronate: A randomized, controlled trial. A multicenter study. J Bone
    Joint Surg Am 2008;90(5):970-979.
    The authors present the results of a randomized controlled trial of three or five hyaluronate injections versus
    placebo to treat arthritic pain, adhesive capsulitis, or rotator cuff pathology. Hyaluronate injections were effective in reducing pain for patients with arthritis but not
    for those with adhesive capsulitis or rotator cuff pathology.

    13.

    3: Upper Extremity

    14.

    15.

    294

    Gogus A, Ozturk C: Osteochondritis dissecans of the


    glenoid cavity: A case report. Arch Orthop Trauma
    Surg 2008;128(5):457-460.
    A case report of a 60-year-old woman with shoulder
    pain and an articular cartilage flap overlying a cystic
    glenoid lesion who was treated with arthroscopic debridement of the loose flap and microfracture of the glenoid is presented. At 4 years after surgery, the patient
    reported full motion and no pain. Level of evidence: IV.
    Koike Y, Komatsuda T, Sato K: Osteochondritis dissecans of the glenoid associated with the nontraumatic,
    painful throwing shoulder in a professional baseball
    player: A case report. J Shoulder Elbow Surg 2008;
    17(5):e9-e12.
    The authors discuss a case report of a 22-year-old male
    baseball pitcher who underwent joint dbridement and
    microfracture of a full-thickness glenoid cartilage defect.
    The patient returned to training 4 months after surgery.
    Japan Shoulder Society and Constant scores improved
    from 43 to 88 and from 86 to 98, respectively. Further
    follow-up and ability to return to competitive pitching
    was not reported. Level of evidence: IV. ain. Level of evidence: IV.
    Kerr BJ, McCarty EC: Outcome of arthroscopic dbridement is worse for patients with glenohumeral arthritis of both sides of the joint. Clin Orthop Relat Res
    2008;466(3):634-638.
    The authors describe their retrospective review of 19 patients (20 shoulders) with shoulder arthritis who were
    treated arthroscopically. The patients were age 55 years
    or younger. Focal, full-thickness defects are effectively
    managed with dbridement and microfracture; however,
    patients with involvement of both sides of the joint have
    worse outcomes. Level of evidence: IV.

    Orthopaedic Knowledge Update 10

    16.

    Romeo AA, Cole BJ, Mazzocca AD, Fox JA, Freeman


    KB, Joy E: Autologous chondrocyte repair of an articular defect in the humeral head. Arthroscopy 2002;18(8):
    925-929.

    17.

    Kircher J, Patzer T, Magosch P, Lichtenberg S, Habermeyer P: Osteochondral autologous transplantation for


    the treatment of full-thickness cartilage defects of the
    shoulder: Results at nine years. J Bone Joint Surg Br
    2009;91(4):499-503.
    Reported outcomes at 8 years postoperatively of seven
    patients treated with osteochondral autologous transplantation for full-thickness cartilage defects of the
    shoulder are presented. Assessments were made using
    the Constant score, radiographs, and MRI.

    18.

    Cameron BD, Galatz LM, Ramsey ML, Williams GR,


    Iannotti JP: Non-prosthetic management of grade IV osteochondral lesions of the glenohumeral joint. J Shoulder Elbow Surg 2002;11(1):25-32.

    19.

    Richards DP, Burkhart SS: Arthroscopic debridement


    and capsular release for glenohumeral osteoarthritis. Arthroscopy 2007;23(9):1019-1022.
    The authors present a case-series of eight patients with a
    diagnosis of glenohumeral arthritis treated with arthroscopic capsular release and joint dbridement. The
    mean postoperative range of motion improved by 22 of
    forward flexion, 16 of external rotation, and 31 of internal rotation. Patients also reported decreased pain. The
    surgical technique is described. Level of evidence: IV.

    20.

    Bailie DS, Llinas PJ, Ellenbecker TS: Cementless humeral resurfacing arthroplasty in active patients less
    than fifty-five years of age. J Bone Joint Surg Am 2008;
    90(1):110-117.
    A review of young patients with arthritis treated with
    hemiarthroplasty and multiple other ancillary procedures is presented. Good outcomes with regard to function and pain were reported at 3-year follow-up.

    21.

    Uribe JW, Botto-van Bemden A: Partial humeral head


    resurfacing for osteonecrosis. J Shoulder Elbow Surg
    2009;18(5):711-716.
    Partial humeral head resurfacing had successful results
    in advanced focal osteonecrosis in patients with a mean
    age of 56 years and average follow-up of 30 months.

    22.

    Levy O, Copeland SA: Cementless surface replacement


    arthroplasty (Copeland CSRA) for osteoarthritis of the
    shoulder. J Shoulder Elbow Surg 2004;13(3):266-271.

    23.

    Raiss P, Kasten P, Baumann F, Moser M, Rickert M,


    Loew M: Treatment of osteonecrosis of the humeral
    head with cementless surface replacement arthroplasty.
    J Bone Joint Surg Am 2009;91(2):340-349.
    Cementless surface replacement arthroplasty provides
    good functional results as a bone-preserving procedure
    in humeral heads with osteonecrosis and up to 31%
    bone loss.

    24.

    Lo IK, Litchfield RB, Griffin S, Faber K, Patterson SD,


    Kirkley A: Quality-of-life outcome following hemiar-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 23: Shoulder Reconstruction

    throplasty or total shoulder arthroplasty in patients


    with osteoarthritis: A prospective, randomized trial.
    J Bone Joint Surg Am 2005;87(10):2178-2185.
    25.

    Raiss P, Aldinger PR, Kasten P, Rickert M, Loew M:


    Total shoulder replacement in young and middle-aged
    patients with glenohumeral osteoarthritis. J Bone Joint
    Surg Br 2008;90(6):764-769.
    The authors evaluated the outcome of total shoulder replacement in young and middle-aged patients with glenohumeral arthritis and found a low rate of complications and excellent results.

    26.

    Pfahler M, Jena F, Neyton L, Sirveaux F, Mol D: Hemiarthroplasty versus total shoulder prosthesis: Results of
    cemented glenoid components. J Shoulder Elbow Surg
    2006;15(2):154-163.

    27.

    Wirth MA, Tapscott RS, Southworth C, Rockwood CA


    Jr: Treatment of glenohumeral arthritis with a hemiarthroplasty: A minimum five-year follow-up outcome
    study. J Bone Joint Surg Am 2006;88(5):964-973.

    28.

    Lynch JR, Franta AK, Montgomery WH Jr, Lenters TR,


    Mounce D, Matsen FA III: Self-assessed outcome at two
    to four years after shoulder hemiarthroplasty with concentric glenoid reaming. J Bone Joint Surg Am 2007;
    89(6):1284-1292.

    Burkhead WZ Jr, Krishnan SG, Lin KC: Biologic resurfacing of the arthritic glenohumeral joint: Historical review and current applications. J Shoulder Elbow Surg
    2007;16(5, suppl)S248-S253.
    A historical review of the use of interposition resurfacing arthroplasties in orthopaedics is presented, as well
    as current surgical techniques for soft-tissue resurfacing
    of the glenoid. Clinical outcomes from 5- to 13-year
    follow-up from a select case series are reported. Level of
    evidence: IV.

    33.

    Krishnan SG, Nowinski RJ, Harrison D, Burkhead WZ:


    Humeral hemiarthroplasty with biologic resurfacing of
    the glenoid for glenohumeral arthritis: Two to fifteenyear outcomes. J Bone Joint Surg Am 2007;89(4):727734.
    A case series is discussed describing the surgical technique and outcomes of 36 patients treated with humeral
    hemiarthroplasty and biologic glenoid resurfacing for a
    diagnosis of glenohumeral arthritis. Three different glenoid resurfacing materials were investigated: anterior
    joint capsule (19%), fascia lata (31%), and Achilles tendon allograft (50%). Pain relief was excellent or good in
    86% of patients, and increased activity levels and range
    of motion were reported at most recent follow-up (minimum 2 years). Poor outcomes were associated with use
    of anterior joint capsule as an interposition material.

    34.

    Krishnan SG, Reineck JR, Nowinski RJ, Harrison D,


    Burkhead WZ: Humeral hemiarthroplasty with biologic
    resurfacing of the glenoid for glenohumeral arthritis:
    Surgical technique. J Bone Joint Surg Am 2008;90(suppl
    2, pt 1):9-19.
    The surgical technique and concepts used when performing hemiarthroplasty and biologic glenoid resurfacing are described.

    35.

    Elhassan B, Ozbaydar M, Diller D, Higgins LD, Warner


    JJ: Soft-tissue resurfacing of the glenoid in the treatment
    of glenohumeral arthritis in active patients less than
    fifty years old. J Bone Joint Surg Am 2009;91(2):419424.
    The authors retrospectively reviewed 13 shoulders in
    patients with a mean age of 34 years treated with hemiarthroplasty and biologic resurfacing of the glenoid. A
    92% failure rate was reported.

    36.

    Nicholson GP, Goldstein JL, Romeo AA, et al: Lateral


    meniscus allograft biologic glenoid arthroplasty in total
    shoulder arthroplasty for young shoulders with degenerative joint disease. J Shoulder Elbow Surg 2007;16(5,
    suppl)S261-S266.
    In a case series, 30 patients (ages 18 to 52 years) underwent humeral hemiarthroplasty and glenoid resurfacing
    with lateral meniscus allograft for treatment of multiple
    etiologies of glenohumeral arthrosis. Ninety-four percent of patients said they would have the procedure
    again. Average American Shoulder and Elbow Surgeons
    score increased from 38 to 69 points. A 17% complication rate was reported during the first year, all of which
    required re-operation. Duration of postoperative
    follow-up was not given. Level of evidence: IV.

    Patients with a mean age of 57 years treated with hemiarthroplasty with concentric glenoid reaming showed
    improved self-assessment shoulder scores for comfort
    and function at a minimum 2-year follow-up. Twentytwo of 37 patients maintained radiographic joint space.
    29.

    30.

    Carroll RM, Izquierdo R, Vazquez M, Blaine TA,


    Levine WN, Bigliani LU: Conversion of painful hemiarthroplasty to total shoulder arthroplasty: Long-term results. J Shoulder Elbow Surg 2004;13(6):599-603.
    Radnay CS, Setter KJ, Chambers L, Levine WN, Bigliani LU, Ahmad CS: Total shoulder replacement compared with humeral head replacement for the treatment
    of primary glenohumeral osteoarthritis: A systematic review. J Shoulder Elbow Surg 2007;16(4):396-402.
    This systematic review provides evidence that total
    shoulder replacement significantly improves pain relief,
    range of motion, and patient satisfaction and has a
    lower rate of revision surgery when compared with
    hemiarthroplasty.

    31.

    Creighton RA, Cole BJ, Nicholson GP, Romeo AA, Lorenz EP: Effect of lateral meniscus allograft on shoulder
    articular contact areas and pressures. J Shoulder Elbow
    Surg 2007;16(3):367-372.
    The authors present a cadaver biomechanical study of
    the influence of lateral meniscus transplant on glenoid
    contact area and contact pressures under compressive
    loads of 220N and 440N. A statistically significant decrease in total force was seen at 220N and 440N of
    loading, and decreased contact area was seen at 220N
    loading when comparing glenoid loading with meniscal
    allograft to glenoid loading without glenoid allograft.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    32.

    295

    Section 3: Upper Extremity

    37.

    38.

    39.

    40.

    3: Upper Extremity

    41.

    42.

    296

    Ellenbecker TS, Bailie DS, Lamprecht D: Humeral resurfacing hemiarthroplasty with meniscal allograft in a
    young patient with glenohumeral osteoarthritis. J Orthop Sports Phys Ther 2008;38(5):277-286.
    In this case report, a 36-year-old male manual laborer
    underwent humeral hemiarthroplasty and meniscal allograft glenoid resurfacing for postinstability glenohumeral arthritis. A detailed description of the postoperative rehabilitation program is presented. American
    Shoulder and Elbow Surgeons scores improved from 17
    preoperation to 85 at 1 year postoperation but decreased to 68 at 2-year follow-up. Level of evidence: IV.
    Lee KT, Bell S, Salmon J: Cementless surface replacement arthroplasty of the shoulder with biologic resurfacing of the glenoid. J Shoulder Elbow Surg 2009;
    18(6):915-919.
    In this retrospective case series, 18 patients (mean age,
    55 years) were treated with humeral head surface replacement and biologic glenoid resurfacing. At a mean
    follow-up of 4.8 years, 83% of patients were satisfied
    with their results. Radiographic examination demonstrated moderate to severe glenoid erosions in 55% of
    shoulders. Level of evidence: IV.
    Wirth MA: Humeral head arthroplasty and meniscal allograft resurfacing of the glenoid. J Bone Joint Surg Am
    2009;91(5):1109-1119.
    In this case series, 27 patients were followed for a minimum of 2 years (mean, 3 years) following humeral
    hemiarthroplasty and meniscal allograft glenoid resurfacing for treatment of glenohumeral arthritis. Function
    and pain were significantly improved from their preoperative status at last follow-up. Progressive glenoid joint
    space narrowing but no glenoid erosions were observed
    radiographically. Level of evidence: IV.
    Raiss P, Aldinger PR, Kasten P, Rickert M, Loew M:
    Total shoulder replacement in young and middle-aged
    patients with glenohumeral osteoarthritis. J Bone Joint
    Surg Br 2008;90(6):764-769.
    A review of 21 patients treated with total shoulder arthroplasty at a mean age of 55 years old is presented.
    The authors report good functional outcomes and pain
    relief; however, there was a 48% rate of glenoid lucent
    lines at 51-month follow-up.
    Cil A, Veillette CJ, Sanchez-Sotelo J, Sperling JW,
    Schleck C, Cofield RH: Revision of the humeral component for aseptic loosening in arthroplasty of the shoulder. J Bone Joint Surg Br 2009;91(1):75-81.
    Thirty-eight humeral components were revised for loosening over a 28-year period at a high-volume shoulder
    reconstruction service. Revision humeral stems were cemented in 29 and press-fit in 9. Humeral component
    survivorship was 89% at 10 years after revision, with
    one humeral component demonstrating recurrent loosening. Level of evidence: III.
    Levy JC, Virani NA, Frankle MA, Cuff D, Pupello DR,
    Hamelin JA: Young patients with shoulder chondrolysis
    following arthroscopic shoulder surgery treated with total shoulder arthroplasty. J Shoulder Elbow Surg 2008;
    17(3):380-388.

    Orthopaedic Knowledge Update 10

    Eleven shoulders with chondrolysis were reviewed to


    evaluate the etiology and assess functional and radiographic outcomes after total shoulder arthroplasty.
    Functional outcomes were good at 3 years, but high
    rates of glenoid lucency and seating were observed.
    43.

    Wirth MA, Klotz C, Deffenbaugh DL, McNulty D,


    Richards L, Tipper JL: Cross-linked glenoid prosthesis:
    A wear comparison to conventional glenoid prosthesis
    with wear particulate analysis. J Shoulder Elbow Surg
    2009;18(1):130-137.
    Biomechanical testing of cross-linked and conventional
    glenoid polyethylene was performed. Cross-linked glenoid polyethylene showed an 85% reduction in volume
    of particulate debris generated, with similar particulate
    size and morphology compared with conventional glenoid components.

    44.

    Fox TJ, Cil A, Sperling JW, Sanchez-Sotelo J, Schleck


    CD, Cofield RH: Survival of the glenoid component in
    shoulder arthroplasty. J Shoulder Elbow Surg 2009;
    18(6):859-863.
    The authors present the results of a retrospective review
    of 1,542 total shoulder arthroplasties performed with
    several different glenoid component designs between
    1984 and 2004. Cemented, all-polyethylene, and pegged
    glenoid components had the lowest rate of revision surgery for glenoid failure.

    45.

    Taunton MJ, McIntosh AL, Sperling JW, Cofield RH:


    Total shoulder arthroplasty with a metal-backed, boneingrowth glenoid component: Medium to long-term results. J Bone Joint Surg Am 2008;90(10):2180-2188.
    Retrospective review of 83 total shoulder arthroplasties
    performed with metal-back, press-fit ingrowth glenoid
    components. Mean clinical follow-up was 9.5 years.
    Five-year glenoid survival rate was 71.6%, and 10-year
    survival rate was 51.9%. Excessive polyethylene and
    metal wear with glenoid loosening was the common
    cause of failure. Level of evidence: III.

    46.

    Tammachote N, Sperling JW, Vathana T, Cofield RH,


    Harmsen WS, Schleck CD: Long-term results of cemented metal-backed glenoid components for osteoarthritis of the shoulder. J Bone Joint Surg Am 2009;
    91(1):160-166.
    Retrospective review of 95 total shoulder arthroplasties
    performed with cemented metal-backed glenoid components. At minimum follow-up of 2 years, two glenoids
    were revised for loosening, and one was revised for
    periprothestic lucency. Eighty-three percent of shoulders
    demonstrated radiographic evidence of periprosthetic
    glenoid lucency. Level of evidence: III.

    47.

    Pelletier MH, Langdown A, Gillies RM, Sonnabend


    DH, Walsh WR: Photoelastic comparison of strains in
    the underlying glenoid with metal-backed and allpolyethylene implants. J Shoulder Elbow Surg 2008;
    17(5):779-783.
    A biomechanical study comparing cortical glenoid shear
    strain measurements with uncemented, keeled metalbacked glenoid components and cemented, allpolyethylene pegged glenoid components was performed.
    Loading was performed in 0, 30, 60, and 90 of ab-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 23: Shoulder Reconstruction

    duction. Uncemented, keeled metal-backed components


    demonstrated higher cortical strains than cemented allpolyethylene pegged components.
    48.

    Frankle MA, ed: Rotator Cuff Deficiency of the Shoulder. New York, NY, Thieme, 2008.
    This comprehensive text covers the pathomechanics and
    pathophysiology, and diagnostic and treatment options
    for rotator cuff pathology. Level of evidence: V.

    49.

    Neer CS II, Craig EV, Fukuda H: Cuff-tear arthropathy.


    J Bone Joint Surg Am 1983;65(9):1232-1244.

    50.

    Visotsky JL, Basamania C, Seebauer L, Rockwood CA,


    Jensen KL: Cuff tear arthropathy: Pathogenesis, classification, and algorithm for treatment. J Bone Joint Surg
    Am 2004;86(suppl 2):35-40.

    51.

    Goldberg SS, Bell JE, Kim HJ, Bak SF, Levine WN, Bigliani LU: Hemiarthroplasty for the rotator cuff-deficient
    shoulder. J Bone Joint Surg Am 2008;90(3):554-559.
    Hemiarthroplasty for arthritic, cuff-deficient shoulders
    can provide good long-term results, especially in those
    with maintained elevation of more than 90. A low
    complication rate was noted in the 34 shoulders reviewed.

    52.

    Sanchez-Sotelo J, Cofield RH, Rowland CM: Shoulder


    hemiarthroplasty for glenohumeral arthritis associated
    with severe rotator cuff deficiency. J Bone Joint Surg
    Am 2001;83(12):1814-1822.

    53.

    Wall B, Nov-Josserand L, OConnor DP, Edwards TB,


    Walch G: Reverse total shoulder arthroplasty: A review
    of results according to etiology. J Bone Joint Surg Am
    2007;89(7):1476-1485.
    The authors showed, in a large cohort of 191 patients,
    that reverse shoulder arthroplasty can produce good
    functional results for multiple complex shoulder disorders in addition to RCTA. Higher complication rates
    were reported in the revision arthroplasty group and in
    patients with posttraumatic arthritis. The mean
    follow-up was 39.9 months.

    54.

    Werner CM, Steinmann PA, Gilbart M, Gerber C:


    Treatment of painful pseudoparesis due to irreparable
    rotator cuff dysfunction with the Delta III reverse-balland-socket total shoulder prosthesis. J Bone Joint Surg
    Am 2005;87(7):1476-1486.

    2011 American Academy of Orthopaedic Surgeons

    Hoenecke HR Jr, Hermida JC, Dembitsky N, Patil S,


    DLima DD: Optimizing glenoid component position
    using three-dimensional computed tomography reconstruction. J Shoulder Elbow Surg 2008;17(4):637-641.
    Computer-based virtual implantation of 3 glenoid implant designs (keel, standard pegs, and modified pegs)
    was performed into 40 glenoid vault CT scans. The ability to implant the glenoid component without perforation of the glenoid vault and still correct for glenoid retroversion was greatest with a modified peg design.
    Retroverted glenoid components were well tolerated.

    57.

    Scalise JJ, Codsi MJ, Bryan J, Iannotti JP: The threedimensional glenoid vault model can estimate normal
    glenoid version in osteoarthritis. J Shoulder Elbow Surg
    2008;17(3):487-491.
    Preoperative templating using CT scanbased threedimensional reconstruction in a surgical simulator allows accurate assessment of glenoid version and bone
    loss.

    58.

    Kircher J, Wiedemann M, Magosch P, Lichtenberg S,


    Habermeyer P: Improved accuracy of glenoid positioning in total shoulder arthroplasty with intraoperative
    navigation: A prospective-randomized clinical study.
    J Shoulder Elbow Surg 2009;18(4):515-520.
    In a small, prospective randomized clinical study, two
    groups (10 patients in each group) were assessed. Intraoperative navigation resulted in greater correction of
    glenoid retroversion at the time of total shoulder arthroplasty based on preoperative and postoperative CT.
    Level of evidence: II.

    59.

    Nguyen D, Ferreira LM, Brownhill JR, et al: Improved


    accuracy of computer assisted glenoid implantation in
    total shoulder arthroplasty: An in-vitro randomized
    controlled trial. J Shoulder Elbow Surg 2009;18(6):907914.
    Sixteen paired cadaver shoulders were randomized to
    two groups and underwent glenoid component implantation either with or without computer-assisted navigation. Computer-navigated glenoid implantation was
    more accurate at reproducing the planned glenoid position determined during preoperative templating. Nonnavigated glenoid implantation trended toward increased glenoid retroversion.

    60.

    Edwards TB, Gartsman GM, OConnor DP, Sarin VK:


    Safety and utility of computer-aided shoulder arthroplasty. J Shoulder Elbow Surg 2008;17(3):503-508.
    The authors discuss a case series of 27 patients who underwent implantation of total shoulder arthroplasty using an image-free navigation system. No navigationrelated complications were reported. The navigation
    system was safe and provided real-time information on
    the patient-specific anatomy and angles of resection and
    reaming. Level of evidence: IV.

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    55.

    Boileau P, Gonzalez JF, Chuinard C, Bicknell R, Walch


    G: Reverse total shoulder arthroplasty after failed rotator cuff surgery. J Shoulder Elbow Surg 2009;18(4):600606.
    Reverse shoulder arthroplasty provided improved functional results in 40 patients after failed rotator cuff surgery. The mean follow-up was 50 months, with a 12%
    complication rate.

    56.

    297

    Chapter 24

    Shoulder Instability and Rotator


    Cuff Tears
    Charles L. Getz, MD

    Jonathan E. Buzzell, MD

    Sumant G. Krishnan, MD

    Shoulder Instability
    The pathologic increase in glenohumeral motion is a
    common disorder in physically active patients. Diagnosis and treatment of patients with shoulder instability
    continues to evolve with a better understanding of pathology and treatment outcomes.

    Anatomy
    Shoulder stability is the end result of the shoulder stabilizing structures working properly together. The constraints on shoulder motion can be divided into static
    stabilizers and dynamic stabilizers (Table 1).
    Static stability is chiefly maintained by joint congruency, the labrum, and the shoulder ligaments. The glenohumeral joint is a ball and shallow socket joint with
    a constant mismatch between the radii of curvatures.
    The unconstrained bony relationship allows the shoulder to obtain a large excursion and range of motion.
    The glenoid socket is deepened by the glenoid labrum,

    2011 American Academy of Orthopaedic Surgeons

    Biomechanics
    The ligaments of the shoulder limit the extremes of motion. The labrum acts as a wedge to limit sliding and increases the wall height to prevent dislocation.4 When
    the arm is abducted and externally rotated, the anteroinferior glenohumeral ligament is stretched. An anterior
    dislocation can occur with a failure of the anterior stabilizing structures, from the anterior glenoid rim,
    labrum, capsule (ligaments), or humeral insertion.
    With the arm in the adducted, forward flexed position, a force applied to the arm stresses the posterior
    glenoid, posterior labrum, and posterior capsule. Posterior dislocation or subluxation of the joint results in an
    injury to one or more of these structures. Repetitive
    submaximal stress to the ligaments can produce a
    pathologic increase in joint range of motion. The subsequent atraumatic instability pattern often is associated with generalized laxity, instability in multiple
    planes, abnormal proprioception, and scapulohumeral
    rhythm dysfunction.

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Dr. Getz or an immediate family member has received


    research or institutional support from Zimmer, Smith &
    Nephew, Johnson & Johnson, and Biomet. Dr. Krishnan
    or an immediate family member serves as a board member, owner, officer, or committee member of the American Shoulder and Elbow Surgeons and the Arthroscopy
    Association of North America; has received royalties
    from Innovation Sports, Tornier, and TAG Medical; is a
    member of a speakers bureau or has made paid presentations on behalf of Mitek and Tornier; serves as a paid
    consultant to or is an employee of Tornier and TAG
    Medical; has received research or institutional support
    from Wolters Kluwer HealthLippincott Williams &
    Wilkins, Mitek, Tornier, and TAG Medical; has stock or
    stock options held in Johnson & Johnson, Pfizer, and
    Merck; and has received nonincome support (such as
    equipment or services), commercially derived honoraria,
    or other nonresearch-related funding (such as paid
    travel) from Mitek and Tornier. Neither Dr. Buzzell nor
    any immediate family member has received anything of
    value from or owns stock in a commercial company or
    institution related directly or indirectly to the subject of
    this chapter.

    which is made of fibrocartilage. The labrum serves as


    the attachment site for the glenohumeral capsule and biceps tendon, and decreases the glenoid radius of curvature to more closely match the humeral curvature. Discrete thickening of the capsule in consistent locations
    form the glenohumeral ligaments (Figure 1). The glenohumeral capsule connects to the humerus at the rotator
    cuff insertion and inferiorly onto the humeral neck.1
    The main dynamic stabilizers are the rotator cuff,
    scapulothoracic rhythm, and the long head of the biceps. The neurologic feedback that connects the dynamic stabilizers to each other and to the static stabilizers is called proprioception. A dysfunction of any of the
    stabilizers can lead to instability, dysfunction, and pain
    in the shoulder. The rotator cuff consists of four muscles (subscapularis, supraspinatus, infraspinatus, and
    teres minor) whose tendons coalesce to dynamically
    stabilize the humeral head in the center of the glenoid
    cavity throughout the full range of shoulder motion by
    generating force couples in the coronal and transverse
    planes of the glenohumeral joint.2,3 Loss of the coronal
    plane force couple results in superior head migration,
    but not necessarily loss of function. Disruption of the
    transverse force couple can result in pain and loss of
    function.

    299

    Section 3: Upper Extremity

    Table 1

    Static and Dynamic Constraints to Joint


    Instability
    Type

    Subtypes

    Static
    Osteochondral

    Proximal humerus: articular


    surface (Hill-Sachs lesion,
    posttraumatic defect,
    osteonecrosis), abnormal
    humeral version
    Glenoid: articular surface; bony
    defect, fracture, or erosion;
    abnormal morphology
    (dysplasia); abnormal glenoid
    version

    Capsulolabral complex

    Glenoid labrum
    Glenohumeral ligaments
    Coracohumeral ligament

    Coracoacromial ligament
    Negative intra-articular
    pressure
    Synovial fluid
    adhesion-cohesion
    Rotator cuff
    Dynamic
    Rotator cuff
    Long head of biceps
    Scapulothoracic rhythm
    Concavity-compression
    Proprioception
    (Reproduced from Costouros JG, Warner JP: Classification, clinical assessment, and
    imaging of glenohumeral instability, in Galatz, LM, ed: Orthopaedic Knowledge
    Update: Shoulder and Elbow 3. Rosemont, IL, American Academy of
    Orthopaedic Surgeons, 2008, pp 67-81.)

    3: Upper Extremity

    The role of glenoid bone loss in patients with recurrent anterior instability has received considerable recent
    attention. Anterior glenoid bone loss of up to 25% was
    classically treated with open soft-tissue repair.5 Reports
    of higher rates of recurrent instability after arthroscopic repairs in patients with substantial bone loss
    has heightened interest in this problem.6 A biomechanical study has shown a significant decrease in anterior
    shoulder stability with bone loss of at least 21% of the
    glenoid.7
    The type of anterior glenoid bone loss may also play
    a role in treatment. Patients with recent onset of recurrent dislocations will likely have identifiable bone at
    the time of repair. Patients with long-standing instability will likely have resorption of the bone and blunting
    of the glenoid margin.8 Humeral bone loss from a HillSachs lesion or reverse Hill-Sachs lesion can contribute
    to instability because the glenoid can fall into the humeral head defect. The location and size of these engaging lesions and the importance of the lesions in regard
    300

    Orthopaedic Knowledge Update 10

    Figure 1

    The anterior glenohumeral ligaments are shown


    in a cadaver specimen.

    to anterior bone loss continues to be explored.


    As previously stated, the rotator cuff provides dynamic shoulder stability by generating force couples in
    the coronal and transverse planes of the glenohumeral
    joint (Figure 2). A force couple is composed of two
    equal but oppositely directed forces that act simultaneously on opposite sides of an axis of rotation. Translational forces are cancelled out, linear motion is eliminated, and torque is produced. Loss of the coronal
    plane force couple results in superior head migration,
    but not necessarily loss of function. The transverse
    force couple is composed of the subscapularis anteriorly and the infraspinatus/teres minor posteriorly, and
    provides anterior-posterior glenohumeral stability
    throughout active elevation. Disruption of the transverse force couple results in loss of concavity compression, a pathologic increase in translation or subluxation
    of the humeral head toward the cuff deficiency, and decreased active abduction.
    The functions of the long head of the biceps tendon,
    described as the fifth tendon of the rotator cuff,9 are
    proposed to involve shoulder flexion, abduction, and
    glenohumeral joint stabilization during rotation. One
    study provided radiographic evidence of the superior
    stabilizing effect of the biceps tendon,10 and another
    study evaluated biceps activity electromyographically
    during 10 basic shoulder motions and reported very little biceps activity.11 Although its functional contributions are debated, painful lesions of the biceps tendon
    can coexist with rotator cuff tears.12

    Classification
    Instability can be classified into categories based on
    timing, etiology, and the direction of instability. Instability can be acute or insidious in onset, can occur after

    2011 American Academy of Orthopaedic Surgeons

    Chapter 24: Shoulder Instability and Rotator Cuff Tears

    Figure 2

    Illustration showing force couples of the shoulder. O = center of rotation, S = subscapularis, D = deltoid, I = infraspinatus, and RC = rotator cuff.

    a single traumatic event, or can be the result of repetitive microtraumas. Instability can occur in a single
    plane or in multiple directions. An understanding of the
    spectrum of disorders that result from shoulder instability can help in diagnosing and treating patients.

    Anterior Instability

    Treatment
    When a shoulder dislocation is diagnosed, closed reduction of the joint is attempted. The patient typically
    is given pain medication and muscle relaxants for
    closed reduction in the emergency department. The patient should be evaluated for rotator cuff tears and neurologic injury after the shoulder is reduced. Inability to
    reduce the shoulder dislocation can result from chronic
    dislocation, interposed soft tissue, and buttonholing of
    the humerus under the conjoined tendon. If the shoul-

    2011 American Academy of Orthopaedic Surgeons

    Natural History
    The role of nonsurgical treatment in young, active patients with anterior instability continues to be defined.
    Physical therapy does not decrease dislocation recurrence rates except in a very tightly controlled population. Immobilization in external rotation can reduce the
    labrum back to a more anatomic position compared
    with traditional immobilization in internal rotation.15
    There appears to be a clinically significant reduction in
    recurrent dislocation if the shoulder is immobilized for
    3 weeks in external rotation. In contrast, one study reported no difference in instability when comparing traditional to external rotation immobilization after an
    anterior dislocation in a young active population.16
    Several large cohorts of first-time dislocators were
    evaluated with variable incidences of recurrent instability ranging from 8% to 75%.17-19 These studies reported lower rates of recurrent instability compared
    with smaller studies with patient-based outcomes.17,20,21
    A 2007 study reported on a cohort of patients with
    dislocations and associated large (> 5 mm) and displaced (> 2 mm) fractures of the anteroinferior glenoid
    rim. Patients were followed for an average of 5.6
    years.22 Nonsurgical treatment was used only in patients with a concentrically reduced joint. No patient in
    the cohort had a dislocation, and the average outcome
    score was excellent.
    Fifty percent to 80% of patients younger than 20
    years at the time of the initial dislocation have a recurrent dislocation. The rate of recurrent instability declines with age.18,23 Patients older than 40 years appear
    to be at increased risk for rotator cuff tears and neuro-

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    The most common direction of dislocation is anterior,


    that is, the humeral head comes to lie anterior to the
    glenoid. A subluxation event can occur that may not
    produce a dislocation but can result in continued instability.13
    When an anterior dislocation occurs, a lesion to the
    anterior stabilizing structures has occurred. The injury
    can take the form of a labral detachment from the glenoid (Bankart lesion), bone and labral detachment
    (bony Bankart lesion), ligament stretching or tearing,
    or detachment of the capsule/ligament from the humerus. When the Bankart lesion heals along the medial
    glenoid neck, it is often referred to as an anterior periosteal sleeve avulsion.14 The anterior periosteal sleeve
    avulsion lesion highlights the fact that healing of a Bankart lesion does not stabilize the shoulder; the labrum
    must be in the proper location on the glenoid edge to
    stabilize the shoulder.
    MRI may be helpful in determining the presence of
    anterior glenoid rim fractures, labral tears, the size of
    humeral defects, and rotator cuff tears. CT provides
    better detail of the bony defects compared with MRI,
    but does not allow visualization of the soft tissues.

    der remains dislocated, the patient should be treated


    with closed reduction while under general anesthesia.
    Open reduction is also a possibility. Consideration
    should be given to advanced imaging before surgical reduction (if it can be obtained expeditiously) because the
    studies may show an interposed rotator cuff, large
    losses of humeral bone, or associated fractures; these
    findings may alter surgical treatment.

    301

    Section 3: Upper Extremity

    and rates of recurrence.30 In two studies that systematically reviewed the literature,31,32 the authors reported
    that when modern suture anchor techniques were used,
    outcome scores were similar or appeared to favor arthroscopic repair over open repair.

    Figure 3

    The Latarjet procedure involves a transfer of the


    coracoid process to the medial glenoid via a
    split of the subscapularis. The coracoid provides
    for glenohumeral stability by augmenting the
    anterior glenoid rim, whereas the conjoined
    tendon acts as a stabilizer with the arm abducted and externally rotated. (Reproduced
    from Burns JP, Snyder SJ: Shoulder instability, in
    Fischgrund JS, ed: Orthopaedic Knowledge Update 9. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2008, pp 301-311.)

    logic injury.24
    For young and active patients, the recurrence of instability is an indication for either open or arthroscopic
    stabilization. With the high recurrence rates reported
    after nonsurgical treatment in young, active patients,
    some authors recommend surgical repair for these patients at the time of the first shoulder dislocation. A
    randomized controlled trial compared arthroscopic stabilization with joint lavage alone after a primary dislocation. In the group of patients with arthroscopically
    stabilized shoulders, there was an 82% risk reduction
    for recurrent instability and a 76% risk reduction for
    dislocation 2 years after the initial injury.25

    3: Upper Extremity

    Arthroscopic Versus Open Repair


    Patients with recurrent anterior shoulder instability can
    be treated using open or arthroscopic repair. Multiple
    studies have reported excellent results for open repair,
    with an approximate 5% rate of recurrent instability
    after surgery. With older arthroscopic repair techniques, results are less reliable, with recurrent instability rates of 15% to 33%.9,23,26 With improvement in arthroscopic repair techniques, results have approached
    those of open repair, with successful outcomes in 90%
    to 96% of patients.27-29
    In a randomized controlled trial comparing open
    and arthroscopic repair for recurrent anterior shoulder
    instability, the two groups had similar outcome scores
    302

    Orthopaedic Knowledge Update 10

    Recurrent Instability After Repair


    When instability occurs after shoulder repair, multiple
    potential sources can be considered, including excessive
    bone loss from the anterior glenoid or humerus, capsular laxity, failure of labrum healing, medialization of
    the labrum, and unrepaired humeral avulsion of the inferior glenohumeral ligament. An 89% instability recurrence rate was reported for contact athletes when
    the anterior bony deficiency of 20% to 30% of the
    joint surface was treated with soft-tissue repair only.9
    Significant bone lesions can be treated arthroscopically
    by incorporating the lesions into the repair. A 93% success rate was reported in patients with an average defect measuring 24% of the joint surface.33 However, the
    quality of the bony fragments may be an important
    consideration because a significantly higher instability
    recurrence rate was identified in patients with attritional fragments.11 An association of recurrent instability with attritional bone loss on the glenoid has been reported.26
    For defects of the anterior glenoid covering more
    than 25% to 30% of the joint surface, an open or arthroscopic coracoid transfer procedure (Figure 3) or
    structural iliac crest graft can be used. This technique
    can also be considered in the primary setting. A 4.4%
    instability recurrence rate was reported in patients with
    significant anterior glenoid bone loss who were treated
    with the Latarjet procedure.34 The use of structural iliac
    crest has been supported by reports of high rates of patient satisfaction;35,36 however, concerns regarding humeral head articulation on the graft, which leads to degenerative changes, have been raised.37
    Large Hill-Sachs lesions (> 25% of the joint surface)
    can be considered for osteochondral allograft,38 remplissage,39 or infraspinatus transfer into the defect. There
    appears to be a biomechanical correlation between the
    size and location of a Hill-Sachs lesion and the ability
    of the humeral head to track on the glenoid.40 Bone
    grafting of defects larger than 37.5% of the joint surface has been recommended based on biomechanical
    testing.41

    Posterior Instability
    Although posterior shoulder dislocations are less common than anterior dislocations, posterior dislocations
    are commonly missed. Mechanisms involved in posterior dislocations include trauma to the anterior aspect
    of the shoulder, an indirect force applied through an
    adducted or flexed arm, seizure, and electrocution.
    Acute Posterior Dislocation
    Unlike anterior instability, posterior instability does not
    lead to frequent recurrent dislocations. Once the dislocation is reduced, a short period of immobilization in

    2011 American Academy of Orthopaedic Surgeons

    Chapter 24: Shoulder Instability and Rotator Cuff Tears

    external rotation is recommended, followed by physical


    therapy and range-of-motion exercises. The diagnosis
    of a posterior dislocation can be difficult. Diagnostic
    modalities such as CT can be a valuable adjunct in establishing the diagnosis.
    Surgical Treatment
    Patients with recurrent posterior shoulder instability or
    those with continued pain with loading of the arm in
    the forward flexed position (bench press or football
    pass blocking) are candidates for surgical posterior
    shoulder stabilization. Stabilization can be performed
    through an open posterior approach or arthroscopically. The goal of any repair is to address the posterior
    labral detachment, repair any capsular tears, and/or reduce the volume of the posterior capsule. Success has
    been reported with both open and arthroscopic approaches. Results for open surgery have been successful
    in 80% to 85% of patients at 5- to 7-year followups.42,43 With shorter follow-ups, arthroscopic repairs
    have been reported to have similar results.44,45
    Chronic Posterior Dislocation
    After several weeks of posterior dislocation, the bone
    of the humeral head and the glenoid begins to erode. If
    left untreated, destruction of the humerus and glenoid
    can occur. After 2 to 3 weeks, a closed reduction is unlikely to achieve a reduction of a posterior dislocation;
    an open repair will be required.
    Prior to proceeding with open reduction, CT can
    help determine the extent and location of bone loss. After reduction, the shoulder can be assessed for stability.
    Options to improve stability include subscapularis or
    lesser tuberosity transfer into the reverse Hill-Sachs lesion, osteochondral bone grafting, segmental humeral
    head replacement, and humeral head replacement. For
    glenoid bone loss, iliac crest bone graft can be used to
    restore bone stock.
    As the dislocation becomes more chronic, the bone
    of the humeral head becomes osteoporotic and arthritic. If humeral head arthritis is extensive, if the head
    collapses during reduction, or if bone loss is more than
    50% of the articular surface, humeral head replacement is needed to restore stability and treat the arthritis. Total shoulder replacement can be considered when
    significant glenoid arthritis is present.

    When instability occurs in more then one plane, the


    term multidirectional instability (MDI) is used. Patients
    with MDI often have generalized shoulder laxity, have
    had no acute trauma, and do not have a true dislocation of the joint. MDI can result from poor technique
    during athletic activities, genetics (Ehlers-Danlos syndrome), poor scapulohumeral mechanics, and rotator
    cuff dysfunction.
    Comparison with the unaffected side will help to
    identify instability and increased motion in multiple
    planes. Provocative testing for anterior or posterior instability as described previously can be positive, and in-

    2011 American Academy of Orthopaedic Surgeons

    Nonsurgical Treatment
    Treatment for MDI is nonsurgical and includes prolonged abstinence from the sporting activity that provoked the symptoms. Results of nonsurgical treatment
    have been variable, with success rates reported as high
    as 80%.46 One report outlined significant dysfunction
    after nonsurgical treatment, with one third of patients
    with poor outcomes at 8-year follow-up.47
    Surgical Treatment
    Moderate success in treating MDI has been achieved
    with open capsular shift, with the goal of reducing the
    capsular volume of the shoulder. Open techniques can
    be performed from an anterior or posterior approach,
    with some surgeons choosing the approach based on
    the direction of primary instability. An 88% success
    rate was reported following inferior capsular shift surgery.48 Similarly, techniques have been developed to accomplish volume reduction during arthroscopy. Early
    results for arthroscopic plication have been promising,
    with success rate reported from 85% to 88%.49,50

    Rotator Cuff Disorders


    The understanding, evaluation, and treatment of rotator cuff tears have evolved since the 1934 publication
    of Codmans landmark text, The Shoulder.51 Codman
    proposed that cuff tears have a traumatic origin, described the fundamental pathology and pathophysiology of the rotator cuff, and detailed the associated clinical findings and treatment options. In 1937, the theory
    of outlet impingement was introduced and it was proposed that rotator cuff tears occur secondary to
    chronic, repetitive contact between the greater tuberosity and the acromion.52 A later study introduced the
    three stages of outlet impingement (Table 2), which
    represent the spectrum of disease severity, and described the technique of anterior acromioplasty designed to remove the offending structures that contribute to symptomatic outlet impingement of the rotator
    cuff tendon.53 It is likely that all of these theories of rotator cuff tear etiology are correct, and that one simplified mechanism does not apply to all situations.
    An age-dependent increase in the incidence of fullthickness rotator cuff tears has been reported in patients older than 50 years.54,55 A 22% to 23% rate of
    asymptomatic tears was reported in two studies with a
    combined total of 999 patients; the incidence of asymptomatic full-thickness tears increased dramatically for
    each decade after 50 years of age.54,55

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Multidirectional Instability

    ferior instability may be present. Inferior instability is


    characterized by a positive sulcus test and a sulcus that
    does not reduce with external rotation; both are signs
    of rotator interval injury. MRI with intra-articular administration of gadolinium can be helpful to determine
    the presence of labral tears. In most patients with MDI,
    no labral pathology is present and the capsular volume
    is increased.

    303

    Section 3: Upper Extremity

    Table 2

    Neer Stages of Impingementa


    Stage

    Patient Age
    (years)

    Findings

    Treatment

    Younger than 25

    Reversible edema, hemorrhage

    Conservative

    II

    25-40

    Irreversible tendon fibrosis,


    tendinosis

    Conservative, surgical

    III

    Older than 40

    Rotator cuff tear

    Subacromial decompression/acromioplasty and rotator cuff


    repair

    The Neer stages of impingement progress from reversible changes to irreversible tendonosis, and finally to full-thickness rotator cuff tears. As the severity of staging
    increases, the likelihood of successful conservative therapy decreases.
    (Reproduced with permission from Neer CS: Impingement lesions. Clin Orthop Relat Res 1983;173:70-77.

    Table 3

    Patient Factors Associated With Poor Healing


    After Rotator Cuff Repaira
    Age older than 65 years
    Female sex
    Smoking
    Duration of symptoms
    Medical comorbidities
    Inability to elevate > 100
    Weak elevation and external rotation
    a

    Patient factors that have been associated with diminished tendon healing after
    cuff repair must be considered in conjunction with tear characteristics (fatty
    infiltration, retraction, atrophy) when determining treatment options.

    The spectrum of rotator cuff disease occurs in a wide


    range of patients, from the young, elite, overhead athlete who presents with a partial-thickness rotator cuff
    tear to the elderly patient with a massive, irreparable
    tear.

    History and Physical Examination

    3: Upper Extremity

    A thorough history and physical examination is the


    first step in evaluating a patient with shoulder pain. Patient factors associated with poor healing after rotator
    cuff repair, when considered individually, may not preclude an attempt at repair (Table 3). The examination
    of a patient with a suspected rotator cuff tear begins
    with the cervical spine, which must be ruled out as the
    source of the patients symptoms. The shoulder girdle is
    then inspected in both shoulders. The deltoid is evaluated for atrophy, detachment, swelling, and/or evidence
    of anterosuperior escape. The supraspinatus and infraspinatus fossae are inspected for evidence of muscular atrophy. Tenderness to palpation over the acromioclavicular (AC) joint and the insertion of the
    supraspinatus on the greater tuberosity (the Codman
    point) should also be evaluated. Active and passive
    ranges of motion are compared, and rotator cuff
    strength is measured and compared with the normal
    contralateral side, if asymptomatic.
    304

    Orthopaedic Knowledge Update 10

    The supraspinatus is tested at 30 abduction and internal rotation, and the infraspinatus is tested in adduction with the elbows flexed to 90 and in maximal external rotation. Subscapularis strength is tested with the
    belly press test (upper subscapularis) and the lift-off
    test (lower subscapularis).56 The teres minor muscle is
    an external rotator that is tested with the shoulders in
    90 of abduction. At this point, a diagnostic subacromial injection of local anesthetic is used to determine if
    existing motion and/or strength deficits are caused by a
    rotator cuff tear or pain. Any differences in strength
    and/or motion are retested and the patient is evaluated
    for the presence of lag signs, which are indicative of
    full-thickness tears of the respective rotator cuff muscles shown in Table 4.

    Associated Lesions
    The biceps tendon, glenohumeral and AC joints, os acromiale, and the suprascapular nerve may be involved
    in the symptom complex of rotator cuff disease; each
    lesion should be identified during the workup phase
    and treated appropriately for the best outcome.
    AC joint arthritis is fairly common in patients with
    rotator cuff disease. Specific findings include radiographic degenerative changes, tenderness to palpation
    directly over the AC joint, and pain in the AC joint with
    cross-arm adduction and/or the active compression test.
    An os acromiale is found in approximately 8% of the
    population57 and should be recognized preoperatively.
    The potential for poorer outcomes after rotator cuff repair in patients with stable or unstable meso-os acromiale has been reported.58 Suprascapular nerve compression can cause shoulder pain and weakness that can
    mimic full-thickness supraspinatus and/or infraspinatus
    tears, or may be seen in conjunction with tears that include supraspinatus retraction of 2 cm or more.59
    It is important to evaluate the patient for associated
    symptomatic lesions so that the lesions may be appropriately treated. The use of diagnostic injections with
    1% plain lidocaine requires a small investment of time
    in the clinic, but provides a wealth of information for
    treatment planning.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 24: Shoulder Instability and Rotator Cuff Tears

    Table 4

    Lag Signs for Rotator Cuff Teara


    Muscle

    Test

    Positive Finding

    Supraspinatus

    Drop arm test

    Examiner places patients arm in 90 elevation; patient unable to maintain

    Infraspinatus

    External rotation lag


    test

    Examiner places patients arm in maximum external rotation with arm in


    adduction; patient unable to maintain

    Teres minor

    Hornblower sign

    Examiner places patients arm in 90 abduction, 90 external rotation; patient


    unable to maintain external rotation

    Upper subscapularis

    Belly press test

    Patient places hands on abdomen and must maintain elbows anterior to


    midsagittal plane of body

    Lower subscapularis

    Lift-off test

    Examiner lifts patients hand off lumbosacral spine; patient unable to


    maintain hand position

    The various lag signs are useful in determining the integrity of each muscle of the rotator cuff. Diagnostic injections help determine if weakness is caused by pain,
    full-thickness tearing, or both.

    Diagnostic Imaging

    Tear Classification
    Rotator cuff tears have been classified according to the
    depth (full- versus partial-thickness), etiology, age of

    2011 American Academy of Orthopaedic Surgeons

    Table 5

    Goutallier Classification of Fatty Infiltrationa


    Grade

    Finding

    No fat within the muscle

    Some fatty streaks

    Fat < muscle

    Fat = muscle

    Fat > muscle

    Fatty infiltration of the rotator cuff muscles was first based on CT, but is now more
    commonly evaluated on MRI studies. Fatty infiltration greater than grade 2 is
    associated with a higher rate of failure.
    (Reproduced with permission from Goutallier D, Postel JM, Bernageau J, Lavau L,
    Voisin MC. Fatty muscle infiltration in cuff ruptures: Pre- and postoperative
    evaluation by CT scan. Clin Orthop Relat Res 1994;304:78-83.)

    the tear, size, shape, number of tendons involved, and


    topography/trophicity of the tear. As such, there is no
    standard classification for rotator cuff tears. The Patte
    classification61 is the most elaborate system and includes anatomic and pathologic considerations that are
    important for defining an individual treatment plan for
    each patient (Table 6 and Figure 4).

    Treatment
    There are three arms of treatment for disorders of the
    rotator cuff: (1) preventive, (2) conservative, and (3)
    surgical. Prevention focuses on body mechanics, proper
    use and strengthening of core body and shoulder girdle
    musculature, and avoiding aggravating activities. When
    cuff symptoms develop in the absence of a fullthickness tear, conservative therapy, including rest, activity modification, gentle passive and active motion
    exercises, anti-inflammatory medication, and periodic
    subacromial corticosteroid injections, can provide relief.63 Therapeutic corticosteroid injections should be
    used with knowledge of the potential detrimental effects on the tendon and bone and decreased potential

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Plain radiographs are obtained in the plane of the scapula and include AP views in internal and external rotation, a scapular Y view (10 to 15 of caudal tilt in the
    lateral scapular plane), and an axillary lateral view.
    Greater tuberosity sclerosis and excrescences, subacromial spurs and/or sclerosis (sourcil sign), and narrowing of the acromiohumeral distance are indications of
    rotator cuff tears. Radiographs should also be evaluated for glenohumeral arthritis, which may preclude
    cuff repair.
    CT is useful in evaluating rotator cuff tears and is
    ideal for grading the severity of bone loss in severe cuff
    tear arthropathy. The Goutallier grading system (Table
    5) of rotator cuff muscle fatty infiltration is based on
    CT imaging and remains an important method for determining whether a tear is reparable.60 A higher degree
    of preoperative fatty infiltration on CT ( grade 3) is
    associated with recurrent tears and lower Constant
    scores.
    MRI is an excellent method to confirm the diagnosis
    of a rotator cuff tear because it shows the number of
    tendons involved, the degree of retraction, fatty infiltration, and muscle atrophy.61 This information is crucial
    for determining the potential for healing after repair.
    The addition of intra-articular contrast is particularly
    beneficial for detecting small, full-thickness tears and
    for improved prediction of the extent of partial
    articular-sided tears.
    Ultrasound is an accurate, noninvasive method of
    detecting rotator cuff tears, is less expensive than MRI
    or CT arthrography, but requires an experienced technician and may not provide the same degree of information for evaluating concomitant pathology. Some evidence indicates that ultrasound is comparable to MRI
    for assessing rotator cuff tears.62

    305

    Section 3: Upper Extremity

    Table 6

    Patte Classification of Rotator Cuff Tears


    Extent of Tear
    Group I: Partial tears or full-substance tears < 1 cm in sagittal
    diameter at bony detachment
    a. Deep, partial tears
    b. Superficial tears
    c. Small, full-substance tears
    Group II: Full-substance tears of entire supraspinatus
    Group III: Full-substance tears involving more than one
    tendon
    Group IV: Massive tears with secondary osteoarthritis
    Topography of Tear in Sagittal Plane
    Segment 1: Subscapularis tear
    Segment 2: Coracohumeral ligament tear
    Segment 3: Isolated supraspinatus tear
    Segment 4: Tear of entire supraspinatus and one half of
    infraspinatus
    Segment 5: Tear of supraspinatus and infraspinatus
    Segment 6: Tear of subscapularis, supraspinatus, and
    infraspinatus
    Topography of Tear in Frontal Plane
    Stage 1: Proximal stump close to bony insertion
    Stage 2: Proximal stump at level of humeral head
    Stage 3: Proximal stump at level of glenoid
    Quality of Muscle
    1. Minimal fatty streaking
    2. Less fat than muscle
    3. Equal fat and muscle
    4. More fat than muscle
    State of the Biceps Tendon
    1. Intact
    2. Subluxated
    3. Dislocated

    3: Upper Extremity

    for healing after repair.64,65 For patients whose symptoms are not relieved by conservative measures, or for
    those who have a full-thickness rotator cuff tear,66 surgical treatment is recommended.
    Surgical Treatment
    Surgical treatment of rotator cuff tears can be performed through open, arthroscopically assisted miniopen, or all-arthroscopic techniques.67-69 Acromioplasty
    and subacromial decompression have therapeutic and
    technical roles in rotator cuff surgery; the goal is to
    smooth the undersurface of the arch to relieve pressure
    on the cuff without disrupting the deltoid origin or destabilizing the coracoacromial arch.
    306

    Orthopaedic Knowledge Update 10

    Open Rotator Cuff Repair: Basic Principles


    Diagnostic arthroscopy results enable the surgeon to visualize and address concomitant pathology before proceeding with a rotator cuff repair. In large and massive
    tears, the degree of glenohumeral arthritis may be more
    severe than suggested by preoperative imaging; therefore, the treatment plan may be altered to exclude repair and proceed with arthroscopic dbridement, subacromial decompression, and biceps tenotomy or
    tenodesis as dictated by the pathology (Table 7).
    With open repair, portals should be closed and the
    shoulder reprepped and draped to prevent infection.70
    Skin incisions should be made with consideration for
    the current surgery and any potential revision surgery,
    particularly with open repair of large and massive
    tears. An oblique incision from the posterior edge of
    the AC joint to the anterolateral corner of the acromion that extends 2 to 3 cm distally over the raphe between the anterior and middle deltoid provides excellent visualization for cuff repair and allows
    anterosuperior access for revision surgery (reverse
    shoulder arthroplasty) through the same incision.
    Distal clavicle excision and two-step acromioplasty71
    improve access to the subacromial space without the
    need to extend the deltoid split (Figure 5). Subacromial
    bursectomy improves visualization and is facilitated by
    rotating the arm. The coracohumeral ligament is palpated in external rotation, adduction, and released if it
    is tight. This exposes the rotator cuff for evaluation,
    mobilization, and repair. Advances in arthroscopic surgery have made repair techniques (single-row, doublerow, transosseous, and transosseous equivalent) similar
    in arthroscopic and open surgery. Following repair, the
    deltoid is meticulously repaired.
    Arthroscopic Repair
    Arthroscopic rotator cuff surgery, which requires a methodic, stepwise approach for successful and timely
    completion of a sturdy repair, is becoming increasingly
    popular. Patient positioning depends on the surgeons
    preference. The beach chair position with an articulated arm holder can be used. This positioning allows
    for easy conversion to an open procedure if necessary,
    and the arm holder allows flexibility of arm positioning
    throughout the surgery. Two-step acromioplasty, as
    previously described, is performed. The coracoacromial
    ligament may be preserved in large and massive repairs.
    Partial-Thickness Tears
    Surgical treatment of partial-thickness tears includes
    dbridement, transtendinous in situ repair, or tear completion and repair.72 Tears that are at least 50% (6 mm)
    of the tendon thickness should be considered for repair
    because, over time, these tears may progress to fullthickness tears.73 Patient factors must be considered
    when evaluating treatment options. No prospective
    study compares in situ repair with tear completion and
    repair despite reported good and excellent results with
    both techniques.74,75 Tear completion allows for dbridement of the degenerative tendon, thorough tuber-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 24: Shoulder Instability and Rotator Cuff Tears

    Figure 4

    Patte classification of rotator cuff tears. A, Rotator cuff tear topography in the sagittal plane is divided into six segments: Anterosuperior tears (segments 1, 2, and 3), superior tears (segments 2, and 3), posterosuperior tears (segments 4 and 5), and total cuff tears (segment 6). B, The topography of tears in the frontal plane is divided into
    three stages. Stage 1: the proximal stump shows little retraction; stage 2: retracted to the level of the humeral
    head; stage 3: retracted to the level of the glenoid. (Reproduced with permission from Patte D: Classification of
    rotator cuff lesions. Clin Orthop Relat Res 1990;254:81-86.)

    osity preparation, and repair of healthy tendon to


    bone. The proposed benefit of transtendinous repair is
    avoiding the creation of a full-thickness tear.

    Transosseous and Transosseous Equivalent Repairs


    Transosseous and transosseous equivalent rotator cuff
    repair techniques produce low bone-tendon interface
    motion, excellent footprint restoration, a high number
    of cycles to failure, and favorable distribution of stress
    over the repair in biomechanical and clinical evaluations.85-88

    2011 American Academy of Orthopaedic Surgeons

    Biceps Pathology Indicating the Need for


    Tenodesis or Tenotomya
    Subluxation
    Fraying
    Tenosynovitis
    Insertional detachment
    Hypertrophy
    a

    The functional contributions of the long head of the biceps tendon are debated,
    but biceps pathology is well-recognized as a pain generator. Sometimes, only
    subtle changes are found at diagnostic arthroscopy and, if left untreated (with
    tenotomy or tenodesis), the biceps can be a source of postoperative pain.

    Repair Augmentation: Grafts and Patches


    Recurrent tears of the repaired rotator cuff occur more
    frequently with large and massive tears,89 with up to
    94% of these repairs failing by 1-year follow-up.90
    Augmentation of large and massive rotator cuff repairs
    with allograft or xenograft tissues is proposed to improve repair strength and provide a bioreplaceable collagen network in an effort to decrease failure rates.
    Commonly used materials for grafts include human
    dermal allograft, porcine dermis, and porcine smooth
    intestine submucosa. Based on a randomized trial of
    large and massive cuff repairs, the authors recommended against porcine smooth intestine submucosa
    augmentation for cuff repair because of adverse graft
    reactions and failure to demonstrate improved outcomes.91 There are no similar randomized trials evaluating if augmented repair with human dermal allograft
    is beneficial, but there are no reports of adverse graft
    reactions, and the potential benefit of mechanical and
    biologic augmentation are worthy of consideration in
    young patients with large or massive cuff tears.

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Single-Row Versus Double-Row Repair


    There is no clear consensus on whether single- or doublerow repair of rotator cuff tears is better.33,76 Double-row
    fixation is more costly, time-consuming, and technically
    more difficult when performed arthroscopically. Biomechanical studies comparing the two techniques have reported higher initial fixation strength and stiffness, improved footprint restoration, and decreased gap
    formation and strain with double-row fixation.77-79 Recent prospective randomized studies have failed to demonstrate a convincing difference in effectiveness between
    the two techniques, but tear size may prove to be a determining factor.80-82 At 2-year follow-up, higher American Shoulder and Elbow Surgeon and Constant scores
    were reported with double-row fixation in tears larger
    than 3 cm; however, cuff integrity was not evaluated with
    MRI at follow-up.83 In a nonrandomized retrospective
    comparison, a clinical difference was not found between
    repair techniques at 2 years, but improved healing for
    double-row compared with single-row fixation was
    shown with CT arthrography.84 These data suggest that
    double-row fixation may prove better for larger tears,
    whereas single-row fixation is probably adequate for
    smaller (< 3 cm) tears.

    Table 7

    307

    Section 3: Upper Extremity

    Figure 5

    The two-step modification of the Neer acromioplasty procedure includes an anterior acromionectomy (A) followed
    by an anteroinferior acromioplasty (B). When performed arthroscopically, the anterior deltoid origin must remain
    intact and determines the extent of anterior acromionectomy. C, The undersurface of the acromion is rendered
    smooth with a bone rasp (arrow) or arthroscopic shaver or burr. D, In an open procedure, the deltoid is meticulously repaired to bone; when performed arthroscopically, the deltoid is respected and left intact. (Reproduced
    with permission from Rockwood CA Jr, Lyons FR: Shoulder impingement syndrome: Diagnosis, radiographic evaluation, and treatment with a modified Neer acromioplasty. J Bone Joint Surg Am 1993;75:409-424.)

    3: Upper Extremity

    Tendon Transfers
    Irreparable large and massive tears are challenging to
    treat, especially in younger patients (60 years or
    younger) with higher functional demands. Tendon
    transfers are a viable option to reduce pain and restore
    function when the rotator cuff cannot be mobilized for
    repair. Latissimus dorsi tendon transfer is suited for irreparable posterosuperior cuff tears,92-94 and pectoralis
    major tendon transfer is designed for treating anterosuperior tears with an irreparable subscapularis tendon.95
    Study results support the recommendation of latissimus dorsi tendon transfer for patients with an intact
    subscapularis, an irreparable posterosuperior rotator
    cuff tear with external rotation deficit, and grade 2 or
    less fatty infiltration of the teres minor on preoperative
    imaging.92,94 In contrast, other authors have reported
    improved results in patients with posterosuperior tears
    associated with preoperative teres minor dysfunction.93
    Each of these studies report improvements in external
    rotation and forward elevation, as well as subjective
    improvements that support latissimus dorsi tendon
    transfer as a viable option for patients who have pain308

    Orthopaedic Knowledge Update 10

    ful, irreparable posterosuperior cuff tears and an external rotation deficit.


    The results of pectoralis major tendon transfer in 30
    shoulders were reviewed. The authors reported Constant scores improved from 47 to 70 points at an average follow-up of 32 months.95 The pectoralis major
    was transferred superficial to the conjoined tendon.
    Worse outcomes were observed in patients with concomitant irreparable supraspinatus tears, whereas a
    reparable supraspinatus tear did not affect the postoperative outcome. Pectoralis major tendon transfer underneath the conjoined tendon has been described in a
    group of 12 older patients (average age 65 years); the
    Constant score improved from 26.9 points preoperatively to 67.1 points at a mean of 28 months postoperatively.96 Dramatic improvement in pain scores was
    noted in addition to the reported functional gains.

    Postoperative Rehabilitation
    Postoperatively, patients are maintained in a shoulder
    sling and pillow that positions the arm in approximately 20 to 30 of abduction to take tension off the

    2011 American Academy of Orthopaedic Surgeons

    Chapter 24: Shoulder Instability and Rotator Cuff Tears

    repair. Traditionally, passive-assisted forward elevation


    and external rotation are started immediately. Internal
    rotation of the arm up the back is delayed 3 weeks (for
    small or medium tears) to 6 weeks (for large or massive
    tears). Active motion combined with terminal stretching commences at approximately 6 weeks, depending
    on the extent of the tear.97 Resistive motion is added according to each patients individual progress, usually at
    10 weeks. Despite advances in repair techniques, recurrent cuff defects remain a treatment challenge for the
    orthopaedic surgeon. As such, there is a trend toward
    decelerated postoperative rehabilitation that delays passive elevation and external rotation in an effort to improve tendon healing.

    cuff disease, in Burkhead WZ Jr, ed: Rotator Cuff Disorders. Baltimore, MD, Williams and Wilkins, 1996, pp
    142-159.
    10.

    Warner JJ, McMahon PJ: The role of the long head of


    the biceps brachii in superior stability of the glenohumeral joint. J Bone Joint Surg Am 1995;77(3):366-372.

    11.

    Yamaguchi K, Riew KD, Galatz LM, Syme JA, Neviaser


    RJ: Biceps activity during shoulder motion: An electromyographic analysis. Clin Orthop Relat Res 1997;
    336(336):122-129.

    12.

    Bioleau P, Baqu F, Valerio L, Ahrens P, Chuinard C,


    Trojani C: Isolated arthroscopic biceps tenotomy or tenodesis improves symptoms in patients with massive irreparable rotator cuff tears. J Bone Joint Surg Am 2007;
    89(4):747-757.
    Arthroscopic biceps tenotomy or tenodesis is an effective method to relieve pain and improve function in patients with massive irreparable cuff tears with no pseudoparalysis or glenohumeral arthritis. Patients with an
    intact teres minor have a better outcome. Level of evidence: IV.

    13.

    Owens BD, Duffey ML, Nelson BJ, DeBerardino TM,


    Taylor DC, Mountcastle SB: The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med 2007;35(7):11681173.
    Military cadets were followed prospectively for 9
    months and all instability episodes were recorded. Most
    instability events (85%) were subluxations without true
    dislocation. Level of evidence: I.

    Annotated References
    1.

    Turkel SJ, Panio MW, Marshall JL, Girgis FG: Stabilizing mechanisms preventing anterior dislocation of the
    glenohumeral joint. J Bone Joint Surg Am 1981;63(8):
    1208-1217.

    2.

    Inman VT, Saunder CM, Abbott LC: Observations on


    the function of the shoulder joint. J Bone Joint Surg Am
    1944;26:1-30.
    Saha AK: Dynamic stability of the glenohumeral joint.
    Acta Orthop Scand 1971;42(6):491-505.

    4.

    Howell SM, Galinat BJ: The glenoid-labral socket: A


    constrained articular surface. Clin Orthop Relat Res
    1989;243(243):122-125.

    5.

    Rowe CR, Patel D, Southmayd WW: The Bankart procedure: A long-term end-result study. J Bone Joint Surg
    Am 1978;60(1):1-16.

    14.

    Neviaser TJ: The anterior labroligamentous periosteal


    sleeve avulsion lesion: A cause of anterior instability of
    the shoulder. Arthroscopy 1993;9(1):17-21.

    6.

    Burkhart SS, De Beer JF: Traumatic glenohumeral bone


    defects and their relationship to failure of arthroscopic
    Bankart repairs: Significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy 2000;16(7):677-694.

    15.

    7.

    Itoi E, Lee SB, Berglund LJ, Berge LL, An KN: The effect of a glenoid defect on anteroinferior stability of the
    shoulder after Bankart repair: A cadaveric study. J Bone
    Joint Surg Am 2000;82(1):35-46.

    Itoi E, Hatakeyama Y, Sato T, et al: Immobilization in


    external rotation after shoulder dislocation reduces the
    risk of recurrence: A randomized controlled trial.
    J Bone Joint Surg Am 2007;89(10):2124-2131.
    A total of 198 patients with anterior dislocation of the
    shoulder were randomized to treatment with immobilization in internal rotation or external rotation for 3
    weeks. Immobilization in external rotation reduced the
    risk of recurrence and was beneficial in patients age 30
    years or younger.

    8.

    Mologne TS, Provencher MT, Menzel KA, Vachon TA,


    Dewing CB: Arthroscopic stabilization in patients with
    an inverted pear glenoid: Results in patients with bone
    loss of the anterior glenoid. Am J Sports Med 2007;
    35(8):1276-1283.
    In patients with postoperative instability with moderate
    anterior bone loss treated with arthroscopic repair, a
    14.2% rate of recurrent instability was found in those
    patients with attritional bone loss. No instability was reported when significant bone was incorporated into the
    repair.

    16.

    Finestone A, Milgrom C, Radeva-Petrova DR, et al:


    Bracing in external rotation for traumatic anterior dislocation of the shoulder. J Bone Joint Surg Br 2009;91(7):
    918-921.
    The authors found that bracing in external rotation may
    not be as effective as previously believed in the prevention of anterior dislocation of the shoulder because further dislocation occurred a mean 33.4 months after
    treatment.

    17.

    Jakobsen BW, Johannsen HV, Suder P, Sjbjerg JO: Primary repair versus conservative treatment of first-time
    traumatic anterior dislocation of the shoulder: A ran-

    9.

    Habermeyer P, Walch G: The biceps tendon and rotator

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    3.

    309

    Section 3: Upper Extremity

    domized study with 10-year follow-up. Arthroscopy


    2007;23(2):118-123.
    Patients were randomized to open Bankart repair versus
    nonsurgical treatment. At a minimum 2-year follow-up,
    the stabilization group had 3% recurrent instability
    compared with 56% in the cohort treated nonsurgically.
    Level of evidence: I.
    18.

    19.

    3: Upper Extremity

    20.

    Sachs RA, Lin D, Stone ML, Paxton E, Kuney M: Can


    the need for future surgery for acute traumatic anterior
    shoulder dislocation be predicted? J Bone Joint Surg Am
    2007;89(8):1665-1674.
    One hundred thirty-one patients were followed prospectively after an initial dislocation. Approximately one
    third of the patients experienced recurrent instability of
    the shoulder. Level of evidence: I.
    Kirkley A, Werstine R, Ratjek A, Griffin S: Prospective
    randomized clinical trial comparing the effectiveness of
    immediate arthroscopic stabilization versus immobilization and rehabilitation in first traumatic anterior dislocations of the shoulder: Long-term evaluation. Arthroscopy 2005;21(1):55-63.

    21.

    Kirkley S: Primary anterior dislocation of the shoulder


    in young patients. A ten-year prospective study. J Bone
    Joint Surg Am 1998;80(2):300-301.

    22.

    Maquieira GJ, Espinosa N, Gerber C, Eid K: Nonoperative treatment of large anterior glenoid rim fractures after traumatic anterior dislocation of the shoulder. J Bone Joint Surg Br 2007;89(10):1347-1351.
    Patients with large displaced Bankart lesions, a single
    dislocation, and a postreduction concentric humeral
    head were followed after nonsurgical treatment. No patients experienced recurrent instability.

    23.

    Arciero Ra, Wheeler JH, Ryan JB, McBride JT: Arthroscopic Bankart repair versus nonoperative treatment for acute, initial anterior shoulder dislocations.
    Am J Sports Med 1994;22(5):589-594.

    24.

    Neviaser RJ, Neviaser TJ, Neviaser JS: Concurrent rupture of the rotator cuff and anterior dislocation of the
    shoulder in the older patient. J Bone Joint Surg Am
    1988;70(9):1308-1311.

    25.

    310

    Hovelius L, Olofsson A, Sandstrm B, et al: Nonoperative treatment of primary anterior shoulder dislocation
    in patients forty years of age and younger: A prospective twenty-five-year follow-up. J Bone Joint Surg Am
    2008;90(5):945-952.
    The authors studied the results of nonsurgical treatment
    of primary anterior shoulder dislocation and found that
    half of the dislocations had not recurred or had stabilized over time.

    Robinson CM, Jenkins PJ, White TO, Ker A, Will E:


    Primary arthroscopic stabilization for a first-time anterior dislocation of the shoulder: A randomized, doubleblind trial. J Bone Joint Surg Am 2008;90(4):708-721.
    Patients with first-time anterior shoulder dislocations
    were randomized to arthroscopic stabilization versus

    Orthopaedic Knowledge Update 10

    joint lavage alone. Patients treated with stabilization


    had a risk reduction for instability of 82% and dislocation rate of 76%. Level of evidence: I.
    26.

    Bioleau P, Villalba M, Hry JY, Balg F, Ahrens P, Neyton L: Risk factors for recurrence of shoulder instability
    after arthroscopic Bankart repair. J Bone Joint Surg Am
    2006;88(8):1755-1763.

    27.

    Kim SH, Ha KI, Cho YB, Ryu BD, Oh I: Arthroscopic


    anterior stabilization of the shoulder: Two to six-year
    follow-up. J Bone Joint Surg Am 2003;85(8):15111518.

    28.

    Carreira DS, Mazzocca AD, Oryhon J, Brown FM,


    Hayden JK, Romeo AA: A prospective outcome evaluation of arthroscopic Bankart repairs: Minimum 2-year
    follow-up. Am J Sports Med 2006;34(5):771-777.

    29.

    Marquardt B, Witt KA, Liem D, Steinbeck J, Ptzl W:


    Arthroscopic Bankart repair in traumatic anterior
    shoulder instability using a suture anchor technique. Arthroscopy 2006;22(9):931-936.

    30.

    Bottoni CR, Smith EL, Berkowitz MJ, Towle RB,


    Moore JH: Arthroscopic versus open shoulder stabilization for recurrent anterior instability: A prospective randomized clinical trial. Am J Sports Med 2006;34(11):
    1730-1737.

    31.

    Hobby J, Griffin D, Dunbar M, Boileau P: Is arthroscopic surgery for stabilisation of chronic shoulder
    instability as effective as open surgery? A systematic review and meta-analysis of 62 studies including 3044 arthroscopic operations. J Bone Joint Surg Br 2007;89(9):
    1188-1196.
    The authors report on a systematic review with metaanalysis of articles from 1985 to 2006 dealing with
    open compared with arthroscopic Bankart repair. When
    older techniques were eliminated, no significant difference in outcomes was found.

    32.

    Lenters TR, Franta AK, Wolf FM, Leopold SS, Matsen


    FA III: Arthroscopic compared with open repairs for recurrent anterior shoulder instability: A systematic review and meta-analysis of the literature. J Bone Joint
    Surg Am 2007;89(2):244-254.
    A systematic literature review and meta-analysis found
    higher outcomes score for patients treated with modern
    arthroscopic technique compared with open repair.
    Higher instability scores were reported in patients
    treated with arthroscopic repairs. Level of evidence: II.

    33.

    Sugaya H, Moriishi J, Kanisawa I, Tsuchiya A: Arthroscopic osseous Bankart repair for chronic recurrent
    traumatic anterior glenohumeral instability. J Bone
    Joint Surg Am 2005;87(8):1752-1760.

    34.

    Burkhart SS, De Beer JF, Barth JR, et al: Results of modified Latarjet reconstruction in patients with anteroinferior instability and significant bone loss. Arthroscopy
    2007;23(10):1033-1041.
    In a therapeutic case series, the authors demonstrate the

    2011 American Academy of Orthopaedic Surgeons

    Chapter 24: Shoulder Instability and Rotator Cuff Tears

    for posterior instability of the shoulder: A prospective


    study of 100 shoulders. Am J Sports Med 2006;34(7):
    1061-1071.

    effectiveness of the modified Latarjet procedure in the


    treatment of patients with dramatic bone loss in whom
    open or arthroscopic soft-tissue reconstruction is not an
    option. Level of evidence: IV.
    35.

    36.

    Provencher MT, Bell SJ, Menzel KA, Mologne TS: Arthroscopic treatment of posterior shoulder instability:
    Results in 33 patients. Am J Sports Med 2005;33(10):
    1463-1471.

    46.

    Haaker RG, Eickhoff U, Klammer HL: Intraarticular


    autogenous bone grafting in recurrent shoulder dislocations. Mil Med 1993;158(3):164-169.

    Burkhead WZ Jr, Rockwood CA Jr: Treatment of instability of the shoulder with an exercise program. J Bone
    Joint Surg Am 1992;74(6):890-896.

    47.

    Misamore GW, Sallay PI, Didelot W: A longitudinal


    study of patients with multidirectional instability of the
    shoulder with seven- to ten-year follow-up. J Shoulder
    Elbow Surg 2005;14(5):466-470.

    48.

    Hamada K, Fukuda H, Nakajima T, Yamada N: The inferior capsular shift operation for instability of the
    shoulder: Long-term results in 34 shoulders. J Bone
    Joint Surg Br 1999;81(2):218-225.

    49.

    Gartsman GM, Roddey TS, Hammerman SM: Arthroscopic treatment of multidirectional glenohumeral
    instability: 2- to 5-year follow-up. Arthroscopy 2001;
    17(3):236-243.

    50.

    Treacy SH, Savoie FH III, Field LD: Arthroscopic treatment of multidirectional instability. J Shoulder Elbow
    Surg 1999;8(4):345-350.

    51.

    Codman EA: The Shoulder. Brooklyn, NY, G Miller &


    Company, 1934.

    52.

    Meyer AW: Chronic functional lesions of the shoulder.


    Arch Surg 1937;35:646-674.

    53.

    Neer CS: Impingement lesions. Clin Orthop Relat Res


    1983;173:70-77.

    54.

    Tempelhof S, Rupp S, Seil R: Age-related prevalence of


    rotator cuff tears in asymptomatic shoulders. J Shoulder
    Elbow Surg 1999;8(4):296-299.

    55.

    Yamaguchi K, Ditsios K, Middleton WD, Hildebolt CF,


    Galatz LM, Teefey SA: The demographic and morphological features of rotator cuff disease: A comparison of
    asymptomatic and symptomatic shoulders. J Bone Joint
    Surg Am 2006;88(8):1699-1704.

    56.

    Tokish JM, Decker MJ, Ellis HB, Torry MR, Hawkins


    RJ: The belly-press test for the physical examination of
    the subscapularis muscle: Electromyographic validation
    and comparison to the lift-off test. J Shoulder Elbow
    Surg 2003;12(5):427-430.

    37.

    Hindmarsh J, Lindberg A: Eden-Hybbinettes operation


    for recurrent dislocation of the humero-scapular joint.
    Acta Orthop Scand 1967;38(4):459-478.

    38.

    Gerber C, Lambert SM: Allograft reconstruction of segmental defects of the humeral head for the treatment of
    chronic locked posterior dislocation of the shoulder.
    J Bone Joint Surg Am 1996;78(3):376-382.

    39.

    Purchase RJ, Wolf EM, Hobgood ER, Pollock ME,


    Smalley CC: Hill-Sachs remplissage: An arthroscopic
    solution for the engaging Hill-Sachs lesion. Arthroscopy
    2008;24(6):723-726.
    The authors used arthroscopic capsulotenodesis of the
    posterior capsule and infraspinatus tendon to treat traumatic shoulder instability in patients with glenoid bone
    loss and a large Hill-Sachs lesion.

    40.

    41.

    Yamamoto N, Itoi E, Abe H, et al: Contact between the


    glenoid and the humeral head in abduction, external rotation, and horizontal extension: A new concept of glenoid track. J Shoulder Elbow Surg 2007;16(5):649-656.
    The authors used a custom device to test nine freshfrozen cadaver shoulders in an assessment of contact between the glenoid and humeral head.
    Sekiya JK, Wickwire AC, Stehle JH, Debski RE: HillSachs defects and repair using osteoarticular allograft
    transplantation: Biomechanical analysis using a joint
    compression model. Am J Sports Med 2009;37(12):
    2459-2466.
    The authors concluded that the size and orientation of
    humeral head defects greatly contributes to glenohumeral joint function. An increase in the size of the defect
    required less anterior translation before dislocation and
    decreased the stability ration. As a result, the risk of recurrent instability was increased.

    42.

    Hawkins RJ, Koppert G, Johnston G: Recurrent posterior instability (subluxation) of the shoulder. J Bone
    Joint Surg Am 1984;66(2):169-174.

    43.

    Pollock RG, Bigliani LU: Recurrent posterior shoulder


    instability: Diagnosis and treatment. Clin Orthop Relat
    Res 1993;291(291):85-96.

    57.

    Sammarco VJ: Os acromiale: Frequency, anatomy, and


    clinical implications. J Bone Joint Surg Am 2000;82(3):
    394-400.

    44.

    Bradley JP, Baker CL III, Kline AJ, Armfield DR,


    Chhabra A: Arthroscopic capsulolabral reconstruction

    58.

    Abboud JA, Silverberg D, Pepe M, et al: Surgical treatment of os acromiale with and without associated rota-

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    45.
    Warner JJ, Gill TJ, Ohollerhan JD, Pathare N, Millett
    PJ: Anatomical glenoid reconstruction for recurrent anterior glenohumeral instability with glenoid deficiency
    using an autogenous tricortical iliac crest bone graft.
    Am J Sports Med 2006;34(2):205-212.

    311

    Section 3: Upper Extremity

    open rotator cuff repair for full-thickness rotator cuff


    tears: Disease-specific quality of life outcome at an average 2-year follow-up. Am J Sports Med 2008;36(6):
    1043-1051.
    A randomized controlled trial comparing open acromioplasty and rotator cuff repair to arthroscopic acromioplasty and mini-open rotator cuff repair demonstrated
    significantly better quality of life and shoulder-specific
    outcome scores at 3 months in the mini-open group.
    However, at 1 and 2 years postoperatively there was no
    difference in outcome between the groups. Level of evidence: I.

    tor cuff tears. J Shoulder Elbow Surg 2006;15(3):265270.


    59.

    Albritton MJ, Graham RD, Richards RS II, Basamania


    CJ: An anatomic study of the effects on the suprascapular nerve due to retraction of the supraspinatus muscle
    after a rotator cuff tear. J Shoulder Elbow Surg 2003;
    12(5):497-500.

    60.

    Goutallier D, Postel JM, Gleyze P, Leguilloux P, Van


    Driessche S: Influence of cuff muscle fatty degeneration
    on anatomic and functional outcomes after simple suture of full-thickness tears. J Shoulder Elbow Surg
    2003;12(6):550-554.

    61.

    Patte D: Classification of rotator cuff lesions. Clin Orthop Relat Res 1990;254(254):81-86.

    62.

    Teefey SA, Rubin DA, Middleton WD, Hildebolt CF,


    Leibold RA, Yamaguchi K: Detection and quantification
    of rotator cuff tears: Comparison of ultrasonographic,
    magnetic resonance imaging, and arthroscopic findings
    in seventy-one consecutive cases. J Bone Joint Surg Am
    2004;86(4):708-716.

    63.

    64.

    65.

    3: Upper Extremity

    66.

    67.

    312

    Kuhn JE: Exercise in the treatment of rotator cuff impingement: A systematic review and a synthesized
    evidence-based rehabilitation protocol. J Shoulder Elbow Surg 2009;18(1):138-160.
    This review synthesizes a new gold standard rehabilitation program for rotator cuff impingement syndrome
    based on level I and II studies evaluating nonsurgical
    treatment of this disorder in an effort to standardize
    therapy for improved outcome comparisons. Level of
    evidence: I.
    Watson M: Major ruptures of the rotator cuff: The results of surgical repair in 89 patients. J Bone Joint Surg
    Br 1985;67(4):618-624.
    Mikolyzk DK, Wei AS, Tonino P, et al: Effect of corticosteroids on the biomechanical strength of rat rotator
    cuff tendon. J Bone Joint Surg Am 2009;91(5):11721180.
    A single dose of corticosteroids significantly weakened
    intact and injured rat rotator cuff tendons at 1 week.
    Decreased maximum load, stress, and stiffness returned
    to baseline after 3 weeks.
    Nho SJ, Brown BS, Lyman S, Adler RS, Altchek DW,
    MacGillivray JD: Prospective analysis of arthroscopic
    rotator cuff repair: Prognostic factors affecting clinical
    and ultrasound outcome. J Shoulder Elbow Surg 2009;
    18(1):13-20.
    Single-tendon tears were nine times more likely to heal
    after arthroscopic repair than tears involving more than
    one tendon. Early repair of full-thickness rotator cuff
    tears will prevent tear progression and will likely improve patient outcomes. Level of evidence: IV.
    Mohtadi NG, Hollinshead RM, Sasyniuk TM, Fletcher
    JA, Chan DS, Li FX: A randomized clinical trial comparing open to arthroscopic acromioplasty with mini-

    Orthopaedic Knowledge Update 10

    68.

    Zumstein MA, Jost B, Hempel J, Hodler J, Gerber C:


    The clinical and structural long-term results of open repair of massive tears of the rotator cuff. J Bone Joint
    Surg Am 2008;90(11):2423-2431.
    Long-term follow-up of open cuff repairs showed durable clinical results, despite a retear rate of 57%. A wide
    lateral extension of the acromion was identified as a
    previously unknown risk factor for retearing. Level of
    evidence: IV.

    69.

    More K, Davis AD, Afra R, Kaye EK, Schepsis A, Voloshin I: Arthroscopic versus mini-open rotator cuff repair: A comprehensive review and meta-analysis. Am J
    Sports Med 2008;36(9):1824-1828.
    A meta-analysis of case series comparing arthroscopic to
    mini-open repair reported no difference in functional
    outcomes or complication rates. A variety of repair
    methods were reviewed in the selected series. Level of
    evidence: III.

    70.

    Herrera MF, Bauer G, Reynolds F, Wilk RM, Bigliani


    LU, Levine WN: Infection after mini-open rotator cuff
    repair. J Shoulder Elbow Surg 2002;11(6):605-608.

    71.

    Rockwood CA Jr, Lyons FR: Shoulder impingement


    syndrome: Diagnosis, radiographic evaluation, and
    treatment with a modified Neer acromioplasty. J Bone
    Joint Surg Am 1993;75(3):409-424.

    72.

    Liem D, Alci S, Dedy N, Steinbeck J, Marquardt B,


    Mllenhoff G: Clinical and structural results of partial
    supraspinatus tears treated by subacromial decompression without repair. Knee Surg Sports Traumatol Arthrosc 2008;16(10):967-972.
    Forty-six patients with grade I or II (Ellman) partialthickness, articular-sided, cuff tears were treated with
    arthroscopic subacromial decompression and dbridement (grade II only). At 50.6 months, only three patients progressed to a full-thickness tear. Good or excellent results were reported in 87% of patients. Level of
    evidence: IV.

    73.

    Kartus J, Kartus C, Rostgrd-Christensen L, Sernert N,


    Read J, Perko M: Long-term clinical and ultrasound
    evaluation after arthroscopic acromioplasty in patients
    with partial rotator cuff tears. Arthroscopy 2006;22(1):
    44-49.

    74.

    Kamath G, Galatz LM, Keener JD, Teefey S, Middleton


    W, Yamaguchi K: Tendon integrity and functional out-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 24: Shoulder Instability and Rotator Cuff Tears

    come after arthroscopic repair of high-grade partialthickness supraspinatus tears. J Bone Joint Surg Am
    2009;91(5):1055-1062.
    Arthroscopic completion and repair of partial-thickness
    cuff tears resulted in 88% healing rate. Advanced age
    was associated with repair failure. Level of evidence: IV.
    75.

    76.

    Castagna A, Delle Rose G, Conti M, Snyder SJ, Borroni


    M, Garofalo R: Predictive factors of subtle residual
    shoulder symptoms after transtendinous arthroscopic
    cuff repair: A clinical study. Am J Sports Med 2009;
    37(1):103-108.
    Transtendinous repair techniques resulted in residual
    shoulder discomfort at the extremes of motion in 41%
    of patients. Large tendon retraction and/or a relatively
    small exposure footprint area in an older patient without a traumatic etiology were predictive of residual
    symptoms. Level of evidence: IV.
    Grasso A, Milano G, Salvatore M, Falcone G, Deriu L,
    Fabbriciani C: Single-row versus double-row arthroscopic rotator cuff repair: A prospective randomized clinical study. Arthroscopy 2009;25(1):4-12.
    In a prospective study comparing single- versus doublerow arthroscopic cuff repair, the authors found no difference in clinical or functional outcome at 2 years. Age,
    sex, and baseline strength significantly and independently influenced outcome. Level of evidence: I.

    77.

    Kim DH, Elattrache NS, Tibone JE, et al: Biomechanical


    comparison of a single-row versus double-row suture
    anchor technique for rotator cuff repair. Am J Sports
    Med 2006;34(3):407-414.

    78.

    Ma CB, Comerford L, Wilson J, Puttlitz CM: Biomechanical evaluation of arthroscopic rotator cuff repairs:
    Double-row compared with single-row fixation. J Bone
    Joint Surg Am 2006;88(2):403-410.
    Lo IK, Burkhart SS: Double-row arthroscopic rotator
    cuff repair: Re-establishing the footprint of the rotator
    cuff. Arthroscopy 2003;19(9):1035-1042.

    80.

    Burks RT, Crim J, Brown N, Fink B, Greis PE: A prospective randomized clinical trial comparing arthroscopic single- and double-row rotator cuff repair:
    Magnetic resonance imaging and early clinical evaluation. Am J Sports Med 2009;37(4):674-682.
    The authors compared arthroscopic single- and doublerow rotator cuff repairs. No substantial difference was
    found between repair types at a minimum of 12 months.
    The average tear size was 1.8 cm, and most tears
    (82.5%) were small or medium size (1 to 3 cm).

    81.

    Franceschi F, Ruzzini L, Longo UG, et al: Equivalent


    clinical results of arthroscopic single-row and doublerow suture anchor repair for rotator cuff tears: A randomized controlled trial. Am J Sports Med 2007;35(8):
    1254-1260.
    Sixty patients prospectively randomized to single- or
    double-row arthroscopic rotator cuff repair showed no
    difference in outcome clinically or on MRI arthrography
    at 2 years. Level of evidence: I.

    2011 American Academy of Orthopaedic Surgeons

    Sugaya H, Maeda K, Matsuki K, Moriishi J: Repair integrity and functional outcome after arthroscopic
    double-row rotator cuff repair: A prospective outcome
    study. J Bone Joint Surg Am 2007;89(5):953-960.
    On postoperative MRI, the retear rate was 5% for small
    to medium size tears and 40% for large and massive
    tears. The average clinical outcome improved significantly, but large postoperative defects were associated
    with lower functional scores. Level of evidence: IV.

    83.

    Park JY, Lhee SH, Choi JH, Park HK, Yu JW, Seo JB:
    Comparison of the clinical outcomes of single- and
    double-row repairs in rotator cuff tears. Am J Sports
    Med 2008;36(7):1310-1316.
    A cohort study of 78 patients retrospectively compared
    arthroscopic single- and double-row cuff repairs. There
    was no difference in clinical or functional outcome for
    tears smaller than 3 cm. Patients with tears larger than 3
    cm had better clinical results with double-row repairs.
    No postoperative imaging was used. Level of evidence:
    II.

    84.

    Charousset C, Grimberg J, Duranthon LD, Bellaiche L,


    Petrover D: Can a double-row anchorage technique improve tendon healing in arthroscopic rotator cuff repair? A prospective, nonrandomized, comparative study
    of double-row and single-row anchorage techniques
    with computed tomographic arthrography tendon healing assessment. Am J Sports Med 2007;35(8):12471253.
    The authors compared arthroscopic single- and doublerow cuff repairs and found no significant clinical difference between the repair types. Postoperative CT arthrography showed significantly better healing with
    double-row repairs at 6-month follow-up. Level of evidence: II.

    85.

    Park MC, Cadet ER, Levine WN, Bigliani LU, Ahmad


    CS: Tendon-to-bone pressure distributions at a repaired
    rotator cuff footprint using transosseous suture and suture anchor fixation techniques. Am J Sports Med 2005;
    33(8):1154-1159.

    86.

    Park MC, ElAttrache NS, Tibone JE, Ahmad CS, Jun


    BJ, Lee TQ: Part I: Footprint contact characteristics for
    a transosseous-equivalent rotator cuff repair technique
    compared with a double-row repair technique. J Shoulder Elbow Surg 2007;16(4):461-468.
    An arthroscopic transosseous equivalent rotator cuff repair technique showed improved pressurized contact
    area and overall pressure between tendon and footprint
    when compared with a double-row technique.

    87.

    Zheng N, Harris HW, Andrews JR: Failure analysis of


    rotator cuff repair: A comparison of three double-row
    techniques. J Bone Joint Surg Am 2008;90(5):10341042.
    A biomechanical study comparing double-row fixation
    with corkscrew anchors, knotless anchors, and transosseous tunnels showed a higher individual failure rate
    with corkscrew anchors compared to knotless anchor
    and transosseous techniques. Level of evidence: controlled laboratory study.

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    79.

    82.

    313

    Section 3: Upper Extremity

    88.

    Frank JB, ElAttrache NS, Dines JS, Blackburn A, Crues


    J, Tibone JE: Repair site integrity after arthroscopic
    transosseous-equivalent suture-bridge rotator cuff repair. Am J Sports Med 2008;36(8):1496-1503.
    Retrospective analysis of arthroscopic transosseous
    equivalent cuff repair showed that 88% of small and
    medium, and 86% of large and massive tears were
    healed on 12-month postoperative MRIs. Persistent
    tears were not correlated with patient age or the initial
    tear size. Level of evidence: IV.
    Klepps S, Bishop J, Lin J, et al: Prospective evaluation of
    the effect of rotator cuff integrity on the outcome of
    open rotator cuff repairs. Am J Sports Med 2004;32(7):
    1716-1722.

    90.

    Galatz LM, Ball CM, Teefey SA, Middleton WD, Yamaguchi K: The outcome and repair integrity of completely
    arthroscopically repaired large and massive rotator cuff
    tears. J Bone Joint Surg Am 2004;86(2):219-224.

    91.

    Iannotti JP, Codsi MJ, Kwon YW, Derwin K, Ciccone J,


    Brems JJ: Porcine small intestine submucosa augmentation of surgical repair of chronic two-tendon rotator
    cuff tears: A randomized, controlled trial. J Bone Joint
    Surg Am 2006;88(6):1238-1244.

    92.

    Gerber C, Maquieira G, Espinosa N: Latissimus dorsi


    transfer for the treatment of irreparable rotator cuff
    tears. J Bone Joint Surg Am 2006;88(1):113-120.

    93.

    Nov-Josserand L, Costa P, Liotard JP, Safar JF, Walch


    G, Zilber S: Results of latissimus dorsi tendon transfer
    for irreparable cuff tears. Orthop Traumatol Surg Res
    2009;95(2):108-113.

    94.

    Costouros JG, Espinosa N, Schmid MR, Gerber C: Teres minor integrity predicts outcome of latissimus dorsi
    tendon transfer for irreparable rotator cuff tears.
    J Shoulder Elbow Surg 2007;16(6):727-734.
    A retrospective review of 22 patients who underwent
    latissimus dorsi tendon transfer for massive irreparable
    posterior-superior rotator cuff tears demonstrated significant improvement in mean absolute Constant scores,
    age-adjusted Constant scores, and subjective shoulder
    values. Patients with preoperative teres minor fatty infiltration less than or equal to grade 2 demonstrated significantly better postoperative Constant scores, active
    elevation, and external rotation. Level of evidence: IV.

    95.

    Jost B, Puskas GJ, Lustenberger A, Gerber C: Outcome


    of pectoralis major transfer for the treatment of irreparable subscapularis tears. J Bone Joint Surg Am 2003;
    85(10):1944-1951.

    96.

    Resch H, Povacz P, Ritter E, Matschi W: Transfer of the


    pectoralis major muscle for the treatment of irreparable
    rupture of the subscapularis tendon. J Bone Joint Surg
    Am 2000;82(3):372-382.

    97.

    Hawkins RJ, Misamore GW, Hobeika PE: Surgery for


    full-thickness rotator-cuff tears. J Bone Joint Surg Am
    1985;67(9):1349-1355.

    3: Upper Extremity

    89.

    The authors recommend latissimus dorsi tendon transfer


    for irreparable posterosuperior rotator cuff tears with
    loss of active external rotation associated with a deficient teres minor muscle. They caution against latissimus dorsi tendon transfer in the absence of active motion deficiency. Level of evidence: IV.

    314

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 25

    Shoulder and Elbow Disorders in


    the Athlete
    Joseph Bernstein, MD

    Matthew Pepe, MD

    Lee Kaplan, MD

    Shoulder Disorders

    Dr. Bernstein or an immediate family member has received royalties from Clinical Orthopaedics and Related
    Research. Neither Dr. Kaplan nor any immediate family
    member has received anything of value from or owns
    stock in a commercial company or institution related directly or indirectly to the subject of this chapter. Dr.
    Pepe or an immediate family member is a member of a
    Speakers bureau or has made paid presentations on behalf of Tornier.

    2011 American Academy of Orthopaedic Surgeons

    Clinical Evaluation
    The clinical evaluation of a throwing athlete begins
    with careful consideration of the shoulder symptoms.
    Although some throwers may report nonspecific symptoms, such as constant pain or a dead arm, others
    may describe focal complaints that localize the pathology, either in terms of the anatomic structure or the
    phase of throwing that induces the symptoms. A general history, to exclude a cause not associated with
    throwing, must also be obtained.
    The physical examination includes palpation of all
    of the bony and soft-tissue landmarks. Range of motion should be assessed, with particular attention to the
    total arc of motion. It should be remembered that the
    shoulders of throwing athletes may undergo adaptive
    changes that begin during early adolescence. As such,
    throwers may have decreased internal rotation and increased external rotation in the abducted arm. Likewise, the coracohumeral ligament and the anterior
    band of the inferior glenohumeral ligament, which restrain external rotation in the abducted arm, can become lax in the throwing shoulder.2,3 The main osseous
    change is increased retroversion of the proximal humerus, which enables the throwing shoulder to achieve
    additional external rotation while keeping the glenohumeral joint located.4 The examiner must also remember
    that laxity of the medial collateral ligament of the elbow (either symptomatic or asymptomatic) may increase apparent external rotation of the shoulder by
    valgus gapping of the elbow.5 Close attention to scapular dynamic is also important. Although the scapula
    and surrounding muscles may not be painful, poor
    scapular dynamics may predispose the arm to a compensatory injury in the glenohumeral joint.
    Special and eponymous physical examination maneuvers for specific lesions have been developed, but
    the hallmark of preoperative anatomic diagnosis is
    MRI, typically enhanced with an injection of contrast
    material. The limitations of MRI are its inability to

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    The throwing athlete is at increased risk for injury to


    the shoulder because of the large and repetitive forces
    generated during the throwing motion. Injuries may occur from a single supraphysiologic load or from repeated subthreshold loads that cumulatively damage
    the tissue.
    The act of throwing has been classified, with some
    variation, into five stages: windup, early cocking, late
    cocking, acceleration, and deceleration with followthrough. This classification centers on the essential
    physical challenge of each phase (Figure 1). In the late
    cocking phase, the throwing arm is externally rotated
    with the arm abducted; the greater this external rotation, the greater the velocity that can be obtained from
    the internal rotator muscles in the acceleration phase.
    At the completion of the throwing motion, the arm has
    been internally rotated through an arc of approximately 180. This arc is traversed at speeds approaching 7,000 per second, with great forces applied to both
    accelerate and decelerate the arm.1 As such, the arm is
    structurally challenged to move within a wide arc while
    maintaining the location of the humeral head within
    the glenoid fossa.
    The needed range of motion is attained by allowing
    just enough soft-tissue laxity, and the humeral location
    is maintained by the action of both static and dynamic
    stabilizers. Static stability is provided by the capsule
    and ligaments, and dynamic stability is conferred by
    the eccentric contraction of the rotator cuff muscles. If
    the capsule and ligaments are insufficiently lax, the
    forces of throwing applied to these tight tissues may
    damage them. Likewise, if the capsule and ligaments

    are too loose or if the rotator cuff does not hold the humeral head in contact against the glenoid, forceful
    abutment between the articular surfaces may lead to injury. The cuff itself is subject to repetitive microtrauma
    with every throw as it eccentrically contracts to stabilize the humeral head in the glenoid.

    315

    Section 3: Upper Extremity

    Figure 1

    Illustration showing the five main stages of overhead throwing motion. (Adapted with permission from DiGiovine
    NM, Jobe FW, Pink M, Perry J: An electromyographic analysis of the upper extremity in pitching. J Shoulder Elbow
    Surg 1992;1:1525.)

    portray the dynamic relationship between structures


    and its inability to identify specifically the source of
    symptoms (as opposed to simply identifying structures
    that are incidentally abnormal in appearance). An overreliance on MRI and excessive focus on every anatomic
    perturbation may lead to diagnostic excess, overtreatment, and an increase in iatrogenic complications.

    Instability and Laxity

    3: Upper Extremity

    The term shoulder instability typically refers to subluxation or dislocation, with the patient often describing a
    sensation indicating excessive humeral head translation
    on the glenoid.6 This sensation is rarely reported by the
    throwing athlete. Rather, the throwing athlete will present with what has been termed subtle or microinstabilitya form of pathologic laxity that predisposes the
    shoulder to secondary injury; that is, the athlete will report pain with throwing or loss of mechanical effectiveness whose occult cause is instability.7 The thrower may
    also report paresthesias in the arm because of possible
    traction on the nerves about the shoulder girdle caused
    by the glenohumeral instability. A sense of subluxation
    or frank dislocation is atypical.
    The proposed causes of the pathologic laxity include
    repetitive microtrauma to the anterior capsule (as the
    arm is maximally externally rotated) or contracture of
    the posterior capsule, causing secondary damage to the
    anterior structures. Repeated forceful loading of the
    humeral head may create primary laxity of the anterior
    stabilizing soft tissues; conversely, a tight posterior capsule that shifts the humeral head forward may result in
    excessive stresses on the anterior structures. A combination of factors may be involved.
    316

    Orthopaedic Knowledge Update 10

    If instability is considered, the shoulder examination


    should attempt to measure anterior translation and the
    presence of apprehension when the arm is abducted
    and externally rotated. A positive relocation test, defined as relief of the pain or apprehension when a posterior force is applied, can be helpful. Tightness of the
    posterior capsule should be ascertained by measuring
    the arc of rotation with the patient supine (or by other
    means that hold the scapula fixed) and the arm abducted.
    Treatment of pathologic laxity depends on the severity of the laxity and the presence of concomitant abnormalities. Most throwers with evidence of pathologic
    laxity without labral detachment can be treated by a
    program of rehabilitation. Particular emphasis should
    be placed on stretching (to minimize any capsular contractures) and on strengthening the rotator cuff (to increase dynamic stability of the glenohumeral joint).
    Surgery is reserved for patients who have not been successfully treated with nonsurgical care. The precise surgical plan is defined by the physical findings. Any frank
    tissue damage, such as a Bankart lesion, should be repaired. Labral repairs, capsular repair shifts and plication, and rotator interval closures have been recommended, but excellent results are not uniformly
    obtained. If a tight posterior capsule contributes to the
    instability, a release may be indicated.

    Superior Labrum Anterior Posterior Tears


    Superior labrum anterior posterior (SLAP) tears are
    common injuries in the throwing athlete, causing pain
    with throwing and loss of velocity. SLAP tears have
    been categorized into various types,8 but the main dis-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 25: Shoulder and Elbow Disorders in the Athlete

    Figure 2

    Illustrations and arthroscopic images of SLAP lesions. A, Type I lesion characterized by superior labral fraying with
    degeneration. B, Type II lesion characterized by detachment of the superior labrum/biceps anchor from the glenoid. C, Type III lesion with a bucket-handle tear of the superior labrum with an intact biceps anchor. D, Type IV
    lesion with a bucket-handle tear of the superior labrum with extension of the labral tear into the biceps tendon.
    (Illustrations Stephen J. Snyder, MD, Van Nuys, CA.)

    2011 American Academy of Orthopaedic Surgeons

    tightening of the repair causing postoperative stiffness


    and loss of motion.11 Although controversial, biceps tenotomy or tenodesis can be considered in nonthrowing
    athletes.

    Internal Impingement
    Partial, articular-sided, rotator cuff tears are common
    in the throwing athlete. In throwing athletes, these
    tears are believed to be caused by either a tensile or
    compressive failure of the tendon. Tensile failure results
    from repetitive eccentric contractions.12 Compressive
    failure is believed to occur when the cuff is compressed
    in a position of arm abduction and external rotation
    between the greater tuberosity of the humeral head and
    the posterior glenoid. This produces internal impingement of the articular side of the rotator cuff.13 The term
    internal impingement is used to contrast this condition
    with subacromial (external) impingement on the bursal
    surface of the cuff (Figure 3).
    The first-line treatment for patients with a suspected
    cuff lesion from internal impingement is a physical
    therapy program dedicated to restoring normal kinematics to the shoulder and stretching to relieve capsular
    contractures.14 Specific stretches, such as the sleeper
    stretch and the cross-body adduction stretch, can be
    helpful in eliminating posterior capsule tightness. Subacromial injections and nonsteroidal anti-inflammatory
    drugs (NSAIDs) can be used judiciously during the initial treatment period. As shoulder motion improves and
    pain decreases, therapy should focus on strengthening
    the rotator cuff and periscapular musculature. An interval throwing program can be initiated. If improvement
    does not occur, surgery may be warranted; however, ar-

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    tinction is whether the biceps anchor and capsule are


    intact (Figure 2). The most common variant is a tear
    with the biceps anchor detached. These injuries are believed to result from a peelback mechanism, namely,
    when the shoulder is abducted and maximally externally rotated and the distal part of the biceps anchor
    becomes avulsed from the posterior-superior glenoid
    rim.1
    The throwing athlete with a SLAP tear often reports
    decreased throwing velocity and pain in the late cocking phase of the throwing motion. Mechanical symptoms, such as catching or locking, may be reported.
    Many physical examination maneuvers have been proposed for detecting SLAP tears, but these maneuvers
    might be too unreliable for clinical use.9 A SLAP tear is
    best diagnosed visually on imaging studies or arthroscopically. Correlating the patients symptoms with
    radiographic and intraoperative findings is often challenging.
    The initial treatment for a patient with a suspected
    SLAP tear is strengthening and stretching of the shoulder with physical therapy; surgery is indicated if nonsurgical treatments fail. Surgical treatment consists of
    dbriding frayed tissue and stabilizing the biceps anchor and labrum back to the glenoid. Range-of-motion
    exercises for the elbow, wrist, and fingers should be
    started just after surgery; however, the shoulder should
    be immobilized for 2 weeks and external rotation
    should be avoided for 4 weeks. A recent study showed
    that arthroscopic repair of SLAP tears in throwing athletes allowed 70% to 80% of patients to return to a
    preinjury level of performance.10 The most common
    complication seen after a type II SLAP repair is over-

    317

    Section 3: Upper Extremity

    Figure 3

    Arthroscopic view through the posterior portal of a small partial-thickness tear of the articular side of the rotator
    cuff. (Reproduced from Wolff AB, Sethi P, Sutton KM, Covey AS, Magit DP, Medvecky M: Partial-thickness rotator
    cuff tears. J Am Acad Orthop Surg 2006;14:715-725.)

    throscopic dbridement of partial tears has achieved inconsistent results, with some athletes having difficulty
    in returning to sports participation.15 Compression between the greater tuberosity and the posterior glenoid
    in the position of arm abduction and external rotation
    is also seen in asymptomatic throwers.16

    Scapular Dyskinesis

    3: Upper Extremity

    Scapular dysfunction during throwing disrupts normal


    throwing biomechanics and places the athlete at risk
    for injury to the labrum, rotator cuff, and capsule.
    Overuse and accompanying fatigue of the shoulder
    complex causes an imbalance of the periscapular musculature. Such power imbalances lead to protraction of
    the scapula and alterations of the geometric relationship of the glenoid and humeral head. If the scapula
    fails to retract normally, excessive angulation of the humerus occurs relative to the glenoid and excessive stress
    is placed on the anterior capsule of the shoulder and
    posterosuperior labrum.
    Throwers with scapular dyskinesis present with a
    range of symptoms, including anterior shoulder pain,
    posterosuperior scapular pain, and proximolateral
    (subacromial) discomfort; a loss of velocity and pain
    with throwing may also be reported. The affected scapula is usually lower and more protracted than the scapula on the uninjured side, and the inferomedial border
    of the scapula is prominent. Tenderness in the coracoid
    region is a common finding. Treatment of scapular dyskinesis begins with strengthening the core musculature.
    After core stability is corrected and scapular motion is
    normalized, emphasis is placed on strengthening the
    periscapular muscles, especially the serratus anterior
    and lower trapezius. These muscles help hold the scapula in the correct retracted position and can be
    strengthened with low row, inferior glide, and lawn
    mower pull exercises.17 The last phase of rehabilitation,
    after scapular motion has normalized and periscapular
    strength has returned, focuses on rotator cuff strength318

    Orthopaedic Knowledge Update 10

    ening, with exercises that emphasize closed kinetic


    chain strengthening. Successful treatment of scapular
    dyskinesis requires a 2- to 3-month course of therapy.

    Acromioclavicular Joint Injuries


    Although acromioclavicular (AC) joint injuries are
    common in contact sports, the AC joint infrequently
    causes acute pain in the throwing athlete. Over a long
    career, repetitive throwing can produce inflammation
    and microtrauma in the AC joint. Some athletes have a
    hyperemic response in the distal clavicle that results in
    bone resorption and secondary arthritic changes. Reports of pain with overhead motion and reaching
    across the body are common. When taking the patients
    history, information on previous trauma should be elicited because low-grade AC joint separations can induce
    arthritic changes.
    Classic physical examination findings include tenderness to palpation over the AC joint and discomfort during the cross-body test. Radiographic analysis of AC
    joint pathology should include AP, axillary, and Zanca
    views. The Zanca view is taken with 10 to 15 of cephalic tilt, with the patient in an upright position and
    without any support to the injured arm. These views
    may show distal clavicle osteolysis and arthritic
    changes not seen otherwise. An injection with a combination of steroid and local anesthetic may be helpful
    for diagnosis as well as initial treatment.
    As with many conditions in the throwing athlete, the
    treatment of AC joint arthrosis begins with NSAIDs
    and physical therapy, with a program emphasizing
    strengthening and stretching of the shoulder girdle. A
    distal clavicle resection may be performed if improvement does not occur with nonsurgical management. If
    there is any doubt regarding the source of the symptoms, a diagnostic shoulder arthroscopy should be part
    of the surgical procedure. The most common cause of
    failed surgery is inadequate posterior-superior resection
    of bone; however, care should be taken not to resect

    2011 American Academy of Orthopaedic Surgeons

    Chapter 25: Shoulder and Elbow Disorders in the Athlete

    more than 1 cm of clavicle because this can injure the


    coracoclavicular ligaments and produce instability.18
    The athlete can usually return to sports 3 months after
    surgery if motion and strength have been restored.

    Neurovascular Injuries

    2011 American Academy of Orthopaedic Surgeons

    Elbow Disorders
    3: Upper Extremity

    Although neurovascular injuries are rare in throwers,


    such injuries have been described in overhead athletes
    and should be considered in the differential diagnosis
    of the painful shoulder. The theme common to these
    conditions is extrinsic pressure on nerves or adjacent
    blood vessels. For example, the suprascapular nerve
    can be compressed at the suprascapular and spinoglenoid notches and can mimic intrinsic rotator cuff disease. Entrapment at the suprascapular notch will affect
    the supraspinatus and infraspinatus, whereas compression at the spinoglenoid notch will weaken the infraspinatus. Injuries to the suprascapular nerve are well described in volleyball players, but the exact incidence of
    these injuries in baseball players is unknown. The extremes of arm positioning and the forces generated by
    the throwing motion have been postulated to cause
    stretching and compression of the suprascapular nerve,
    causing a type II SLAP tear and the development of
    paralabral cysts. Overhead athletes with suprascapular
    nerve injuries present with poorly localized pain in the
    posterolateral shoulder, weakness, and pain that may
    radiate down the arm. In the later stages of the injury,
    examination of the shoulder may show atrophy of the
    supraspinatus and/or infraspinatus. On examination,
    significant weakness is usually revealed when testing
    external rotation, with a presentation that may be very
    similar to rotator cuff tendinitis. Magnetic resonance
    arthrography is useful in identifying labral cysts or a
    hypertrophied scapular ligament, in quantifying the degree of atrophy of the muscles, and in assessing the integrity of the rotator cuff tendons. Electromyography
    can be helpful in making the diagnosis and in providing
    information regarding the severity and location of the
    compression.
    Treatment for a suprascapular nerve injury depends
    on the underlying etiology. For patients without an anatomic cause for the compression, activity modification
    is the best initial treatment, along with NSAIDs and
    strengthening exercises for the rotator cuff, deltoid, and
    scapula. Most patients respond positively to this treatment protocol. Athletes with evidence of early muscle
    atrophy, anatomic compression, or those in whom nonsurgical management fails are candidates for surgery. If
    the nerve compression is located at the suprascapular
    notch, open or arthroscopic release of the transverse
    scapular ligament using a superior approach may be
    needed. Paralabral cysts can be treated with arthroscopic repair of the labrum, with anchors and indirect decompression of the cyst. Spinoglenoid cysts usually respond to arthroscopic treatment, although
    successful open treatment has been reported.19
    Quadrilateral space syndrome is a compression neuropathy of the axillary nerve within the four-sided area
    bounded by the teres minor superiorly, the teres major

    inferiorly, the long head of the triceps medially, and the


    proximal humerus laterally. As is the case with many
    other conditions affecting the throwing athlete, the
    compression of the structures within the quadrilateral
    space appears to be greatest in the late cocking phase of
    throwing. Symptoms of quadrilateral space syndrome
    are initially vague. Athletes may report mild discomfort
    and weakness with throwing activities. There may be
    associated night pain and lateral arm paresthesias.
    Physical findings may include weakness with abduction, loss of sensation in the axillary nerve distribution,
    and atrophy of the deltoid muscle. Tenderness over the
    quadrilateral space has been suggested as a reliable
    physical examination finding in the throwing athlete.20
    Arteriography is the study of choice for diagnosing
    quadrilateral space syndrome; however, for maximal
    accuracy the dye must be injected with the arm at the
    side and in the late cocking phase position of abduction
    and external rotation. The diagnosis is made when the
    artery is occluded in the abduction-external rotation
    position and relieved when the arm is brought down to
    the side. Nonsurgical management, consisting of rest,
    NSAIDs, and physical therapy focused on stretching
    and strengthening the posterior shoulder, is the preferred initial treatment option. If success is not
    achieved after 6 months of nonsurgical treatment, decompression has been shown to be a beneficial option.
    Thoracic outlet syndrome is a rare (and controversial) cause of neurovascular disorders in throwing athletes. In thoracic outlet syndrome, anomalous bands of
    the pectoralis minor,21 an anomalous first rib, or extremes of arm positioning (for example, the late cocking phase of throwing) are believed to compress the
    neurovascular structures as they exit the thoracic cavity. Symptoms caused by the ischemia include arm
    heaviness, fatigue, cold intolerance, paresthesias, and
    coolness and numbness in the fingers. During the physical examination, the radial pulse should be checked
    with the arm at the side and then with the shoulder in
    the abducted, externally rotated position (the Wright
    test). Surgical options for thoracic outlet syndrome that
    is recalcitrant to rest and therapy include first rib resection, release of anomalous bands of fascia, scalenectomy, and pectoralis minor tenotomy.

    Elbow Instability
    During the late cocking and acceleration phases of
    throwing, the elbow is rapidly extended more than 90
    and is exposed to high valgus stresses. These forces can
    lead to attenuation, partial tears, or even complete rupture of the medial ligament complex. Because throwing
    creates tension on the medial side specifically, the lateral ligament complex is not typically injured in the
    throwing athlete.
    Valgus instability usually manifests as pain occurring
    in the medial epicondyle region during the late cocking/
    early acceleration phase of throwing. Ulnar nerve

    Orthopaedic Knowledge Update 10

    319

    Section 3: Upper Extremity

    3: Upper Extremity

    symptoms can be induced by traction (secondary to instability) or from direct mechanical irritation of the
    nerve by the ligament. Arthrosis of the elbow joint occurs as a secondary adaptation to the stress, with osteophyte formation along the posteromedial olecranon
    and calcification in the ligament. Posteromedial impingement will typically cause pain in a more posterior
    location at or near the terminal extension.
    A thorough history and physical examination is the
    key to diagnosing ulnar collateral ligament injuries in a
    throwing athlete. It is important to elicit information
    about previous symptoms or injuries. Throwers may report having experienced an acute pop or sharp medial elbow pain. Some throwers have an insidious onset
    of pain without a specific inciting event; throwing velocity, command, and control are affected. Mechanical
    symptoms may signal the presence of loose bodies. In
    younger pitchers, it is important to obtain information
    on pitch counts and the types of pitches thrown because elevated pitch counts and curveballs and sliders
    have been associated with pain.22 More recent studies
    have shown that the type of pitch has substantially less
    effect on shoulder and elbow loads than the absolute
    number of pitches thrown and that throwing a fastball
    causes higher elbow loads than throwing a curveball.23
    Discussions with coaches and athletic trainers also can
    be beneficial because correct pitching mechanics lower
    valgus elbow loads and increase pitching efficiency.24
    The physical examination of the thrower with medial elbow pain involves evaluating the entire extremity.
    It is important to exclude pathology in the shoulder
    and scapula because problems there can produce referred elbow pain or induce a secondary injury at the
    elbow (by abnormal mechanics). Particular attention
    should be paid to examining the shoulder for a posterior capsular contracture as a cause of medial elbow
    pain. A substantial percentage of throwers with an ulnar collateral ligament insufficiency have a glenohumeral internal rotation deficit when compared with
    asymptomatic pitchers.25 The cervical spine also should
    be examined in any thrower with neurologic symptoms
    because cervical nerve root pathology can mimic ulnar
    neuropathy at the elbow. The range of motion of the
    affected elbow in flexion and extension and in pronation and supination should be measured with a goniometer and compared with the contralateral side. It is
    common for even asymptomatic pitchers to have a flexion contracture of the elbow. Measurements taken before and after pitching show a significant decrease in elbow extension both immediately and 24 hours after
    throwing.26
    Valgus stress testing is performed at both 0 and 30
    to evaluate the medial collateral ligament. Asymptomatic throwers typically have a degree of developmental laxity of the medial restraints of the injured elbow
    when compared with the contralateral side.27 A dynamic valgus stress test is believed to be sensitive and
    specific for ulnar collateral ligament tears. In this test, a
    constant valgus load is applied to the maximally flexed
    elbow as it is brought rapidly into extension. A positive
    finding occurs when medial pain is reproduced between
    320

    Orthopaedic Knowledge Update 10

    the arcs of 120 and 70.28 Tenderness in valgus extension overload occurs along the posteromedial olecranon. Pain is reproduced with valgus and forced extension of the elbow. Flexor pronator tendinitis may also
    manifest as medial-sided elbow pain. Tenderness is
    noted at or just distal to the medial epicondyle, and
    pain is reproduced with resisted wrist flexion and forearm pronation. The ulnar nerve is palpated for tenderness and instability. Tinel and cubital tunnel compression tests can be used to check for ulnar nerve
    irritability, which can occur in isolation or concomitant
    with ulnar collateral insufficiency.
    Standard AP, lateral, and oblique radiographs are
    routinely obtained and may show calcification within
    the ligament as well as posterior compartment osteophytes. MRI is a useful tool in evaluating the soft tissues of the elbow, including the collateral ligaments, articular surface, and ulnar nerve. Noncontrast MRI can
    identify full-thickness tears of the ulnar collateral ligament, hypertrophy, or tears of the flexor pronator origin. Consideration must be given, however, to the very
    high rate of abnormal findings in the asymptomatic
    high-level thrower.29,30 In a study that evaluated the elbows of professional pitchers with plain radiographs, a
    significant number of radiographic abnormalities were
    reported; however, the pathologic findings did not correlate with impairment.30 The pathologic findings did
    correlate with activity (the number of innings pitched
    professionally). Using contrast material adds to the sensitivity of the MRI study, particularly for partialthickness tears; however, the instillation of this fluid
    may cause discomfort that may interfere with athletic
    performance for several days. Dynamic ultrasound has
    been used to evaluate the medial collateral ligament but
    produces a high rate of abnormal findings in the
    asymptomatic major league pitcher.31,32 Ultrasound also
    has been shown to have high accuracy in diagnosing
    medial epicondylitis.33 The accuracy of ultrasound may
    be dependent on the skill of the examiner.
    Nonsurgical treatment is the preferred first step in
    treating medial-sided elbow pain. Rest, coupled with
    stretching and strengthening exercises, should be prescribed. Corticosteroid injections may offer short-term
    relief in the patient with refractory medial elbow pain
    but have not been shown to be better than placebo.
    Platelet-rich plasma injections may avoid the possible
    adverse side effects of corticosteroid injections, but they
    too may rely on a placebo effect.34 The authors of one
    study reported that nonsurgical treatment of an ulnar
    collateral ligament injury in a pitcher has a success rate
    of 42%,35 with success defined as a return to the same
    or a higher level of competition. No factors from either
    the patients history or physical examination could predict a successful outcome.
    Direct repair of the ulnar collateral ligament is possible if rupture occurs at the proximal or distal end and
    if the remaining ligament tissue is adequate. This scenario is more typical in younger, adolescent athletes
    who have not experienced much wear and tear. A preoperative MRI or ultrasound will define the location of
    the tear and the quality of the remaining tissue and

    2011 American Academy of Orthopaedic Surgeons

    Chapter 25: Shoulder and Elbow Disorders in the Athlete

    Figure 4

    Illustrations showing ulnar collateral ligament repair


    techniques. A, Jobe technique showing the figure-of-8
    graft pattern. B, Docking reconstruction with sutures
    tensioning the graft. C, Hybrid reconstruction with
    interference screw on the ulna and docking technique
    on the epicondyle. (Panel C adapted with permission
    from Conway JE: The DANE TJ procedure for elbow
    medial ulnar collateral ligament insufficency. Tech
    Shoulder Elbow Surg 2006;7:36-43. Panels A and B
    adapted with permission from Safran MR: Injury to
    the ulnar collateral ligament: Diagnosis and treatment. Sports Med Arthrosc 2003;11:15-24.)

    plan the treatment, though final treatment decisions are


    made intraoperatively, based on visualization of the ligament. The repair is best performed using suture anchors with braided nonabsorbable suture. In one study,
    nearly all the athletes achieved a good to excellent result and returned to the same level of competition.36
    Various techniques have been described for reconstruction, including the traditional Jobe technique, the docking procedure, and interference screw fixation37-39 (Figure 4). When performed by an experienced surgeon,
    ligament reconstruction of the anterior band of the ulnar collateral ligament (without ulnar nerve transposition) offers athletes a good chance for successful return
    to their preinjury level of competition.37

    Medial Epicondylitis

    2011 American Academy of Orthopaedic Surgeons

    Figure 5

    A, Valgus extension overload of the posterior


    compartment resulting in traction spurs on the
    medial aspect of the ulnar notch (arrow). B, Posteromedial osteophytes are present within the
    olecranon fossa. (Reproduced from Miller CD,
    Savoie FH III: Valgus extension injuries of the
    elbow in the throwing athlete. J Am Acad Orthop Surg 1994;2:261-269.)

    3: Upper Extremity

    Medial epicondylitis is a syndrome characterized by


    medial elbow pain and is associated with degeneration
    of the flexor pronator origin. It may also be associated
    with ulnar collateral ligament insufficiency or ulnar
    nerve symptoms. Physical examination findings include
    tenderness over the anterior aspect of the medial epicondyle and pain that is reproduced with resisted pronation and wrist flexion. It is important to rule out
    concomitant medial instability in the throwing athlete.
    Although nonsurgical management has a very high success rate,40 the condition may take several months for
    overall resolution. Surgical treatment involves excising
    the area of tendinopathy. The ulnar nerve may be transposed if there is also cubital tunnel compression.

    Valgus Extension Overload


    Posteromedial impingement of the olecranon against
    the medial wall of the olecranon fossa is believed to result from valgus loads placed on the elbow in the early
    acceleration phase of throwing (Figure 5). This stress

    Orthopaedic Knowledge Update 10

    321

    Section 3: Upper Extremity

    causes reactive osteophyte formation along the posteromedial wall of the olecranon, a spur that causes impingement in extension. Pain is typically located posteromedially and is reported in the deceleration phase of
    throwing. The pain may be mild at first, but progression over the course of the game is common.41 An axial
    view of the olecranon with the elbow flexed to 110,
    MRI, or CT will define the osteophyte and identify any
    loose bodies if present. Nonsurgical treatment, which is
    always attempted first, typically has a poor prognosis if
    a posteromedial osteophyte is present.
    Surgical treatment of isolated posteromedial impingement involves excision of the posterior and medial
    olecranon osteophytes, either arthroscopically or
    through a miniopen approach. Care must be taken not
    to remove more than 3 mm of the normal olecranon
    because greater resection will cause a substantial increase in the strain in the anterior band of the medial
    collateral ligament.42 In patients with signs and symptoms of valgus instability in addition to impingement,
    resection of the posteromedial osteophyte alone is not
    indicated. Because the olecranon osteophytes were
    likely caused by elbow instability,43 the athlete will continue to have instability pain postoperatively if the primary cause of the instability is not treated. In such
    cases, the ulnar collateral ligament should be reconstructed and the osteophytes should be removed.

    6.

    Braun S, Kokmeyer D, Millett PJ: Shoulder injuries in


    the throwing athlete. J Bone Joint Surg Am 2009;91(4):
    966-978.
    A current concepts review of pathologic conditions affecting the shoulder of the throwing athlete is presented
    along with associated treatment options. The authors
    emphasize the importance of physical therapy and rehabilitation as the initial treatment for most throwingrelated conditions. Level of evidence: V.

    7.

    Ryu RK, Dunbar WH, Kuhn JE, McFarland EG, Chronopoulos E, Kim TK: Comprehensive evaluation and
    treatment of the shoulder in the throwing athlete. Arthroscopy 2002;18(9, suppl 2):70-89.

    8.

    Snyder SJ, Karzel RP, Del Pizzo W, Ferkel RD, Friedman MJ: SLAP lesions of the shoulder. Arthroscopy
    1990;6(4):274-279.

    9.

    Calvert E, Chambers GK, Regan W, Hawkins RH,


    Leith JM: Special physical examination tests for superior labrum anterior posterior shoulder tears are clinically limited and invalid: A diagnostic systematic review.
    J Clin Epidemiol 2009;62(5):558-563.
    A review of the current literature with epidemiologic
    methodology was performed. The authors concluded
    that physical examination maneuvers to detect SLAP lesions are not valid or reliable. Level of evidence: I.

    10.

    Ide J, Maeda S, Takagi K: Sports activity after arthroscopic superior labral repair using suture anchors in
    overhead-throwing athletes. Am J Sports Med 2005;
    33(4):507-514.

    11.

    Brockmeier SF, Voos JE, Williams RJ III, Altchek DW,


    Cordasco FA, Allen AA; Hospital for Special Surgery
    Sports Medicine and Shoulder Service: Outcomes after
    arthroscopic repair of type-II SLAP lesions. J Bone Joint
    Surg Am 2009;91(7):1595-1603.
    The authors discuss the results of type II SLAP lesions
    treated with arthroscopic suture anchor fixation. Thirtyfour of 47 patients were throwing athletes. With a minimum 2-year follow-up, 25 of the athletes (74%) returned to sports. The major complication with this
    procedure was postoperative stiffness, which occurred
    in four patients. Level of evidence: IV.

    12.

    Nakagawa S, Yoneda M, Hayashida K, Wakitani S,


    Okamura K: Greater tuberosity notch: An important indicator of articular-side partial rotator cuff tears in the
    shoulders of throwing athletes. Am J Sports Med 2001;
    29(6):762-770.

    13.

    Heyworth BE, Williams RJ III: Internal impingement of


    the shoulder. Am J Sports Med 2009;37(5):1024-1037.
    A comprehensive review on internal impingement is presented. The authors discuss the clinical presentation and
    physical examination and imaging findings seen with
    this condition and review treatment options. A treatment algorithm for internal impingement is included.
    Level of evidence: V.

    14.

    Matava MJ, Purcell DB, Rudzki JR: Partial-thickness

    3: Upper Extremity

    Annotated References
    1.

    Burkhart SS, Morgan CD, Kibler WB: The disabled


    throwing shoulder: Spectrum of pathology. Part I:
    Pathoanatomy and biomechanics. Arthroscopy 2003;
    19(4):404-420.

    2.

    Kuhn JE, Bey MJ, Huston LJ, Blasier RB, Soslowsky LJ:
    Ligamentous restraints to external rotation of the humerus in the late-cocking phase of throwing: A cadaveric biomechanical investigation. Am J Sports Med
    2000;28(2):200-205.

    3.

    Fitzpatrick MJ, Tibone JE, Grossman M, McGarry MH,


    Lee TQ: Development of cadaveric models of a throwers shoulder. J Shoulder Elbow Surg 2005;14(1, suppl
    S)49S-57S.

    4.

    5.

    Crockett HC, Gross LB, Wilk KE, et al: Osseous adaptation and range of motion at the glenohumeral joint in
    professional baseball pitchers. Am J Sports Med 2002;
    30(1):20-26.
    Mihata T, Safran MR, McGarry MH, Abe M, Lee TQ:
    Elbow valgus laxity may result in an overestimation of
    apparent shoulder external rotation during physical examination. Am J Sports Med 2008;36(5):978-982.
    The authors perform a controlled laboratory study to
    determine if an increase in elbow valgus laxity affects
    assessment of shoulder external rotation measured during physical examination at 90 of elbow flexion.

    322

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 25: Shoulder and Elbow Disorders in the Athlete

    and adolescent baseball pitchers. Am J Sports Med


    2009;37(8):1484-1491.

    rotator cuff tears. Am J Sports Med 2005;33(9):14051417.


    15.

    Payne LZ, Altchek DW, Craig EV, Warren RF: Arthroscopic treatment of partial rotator cuff tears in
    young athletes: A preliminary report. Am J Sports Med
    1997;25(3):299-305.

    16.

    Halbrecht JL, Tirman P, Atkin D: Internal impingement


    of the shoulder: Comparison of findings between the
    throwing and nonthrowing shoulders of college baseball
    players. Arthroscopy 1999;15(3):253-258.

    17.

    Kibler WB, McMullen J: Scapular dyskinesis and its relation to shoulder pain. J Am Acad Orthop Surg 2003;
    11(2):142-151.

    18.

    Zvijac JE, Popkin CA, Botto-van Bemden A: Salvage


    procedure for chronic acromioclavicular dislocation
    subsequent to overzealous distal clavicle resection. Orthopedics 2008;31(12):pii.
    The authors describe a technique to treat AC instability
    after excessive distal clavicle resection. Level of evidence: IV.

    19.

    Ringel SP, Treihaft M, Carry M, Fisher R, Jacobs P: Suprascapular neuropathy in pitchers. Am J Sports Med
    1990;18(1):80-86.

    20.

    McAdams TR, Dillingham MF: Surgical decompression


    of the quadrilateral space in overhead athletes. Am J
    Sports Med 2008;36(3):528-532.
    This study reports on quadrilateral space syndrome in
    four overhead throwing athletes who required surgical
    decompression. The cause was fibrous bands in three
    patients and venous dilatation in one. All athletes returned to full activity by 3 months. Level of evidence:
    IV.
    Simovitch RW, Bal GK, Basamania CJ: Thoracic outlet
    syndrome in a competitive baseball player secondary to
    the anomalous insertion of an atrophic pectoralis minor
    muscle: A case report. Am J Sports Med 2006;34(6):
    1016-1019.

    22.

    Lyman S, Fleisig GS, Andrews JR, Osinski ED: Effect of


    pitch type, pitch count, and pitching mechanics on risk
    of elbow and shoulder pain in youth baseball pitchers.
    Am J Sports Med 2002;30(4):463-468.

    23.

    Dun S, Loftice J, Fleisig GS, Kingsley D, Andrews JR: A


    biomechanical comparison of youth baseball pitches: Is
    the curveball potentially harmful? Am J Sports Med
    2008;36(4):686-692.
    The authors studied the kinetics of the fastball, curveball, and change-up baseball pitches in youth pitchers
    and determined that the curveball may not be more
    harmful than the fastball. Recent epidemiologic research
    indicates that amount of pitching is a stronger risk factor for injury than type of pitches thrown.

    24.

    Davis JT, Limpisvasti O, Fluhme D, et al: The effect of


    pitching biomechanics on the upper extremity in youth

    2011 American Academy of Orthopaedic Surgeons

    25.

    Dines JS, Frank JB, Akerman M, Yocum LA: Glenohumeral internal rotation deficits in baseball players with
    ulnar collateral ligament insufficiency. Am J Sports Med
    2009;37(3):566-570.
    The authors studied throwers with ulnar collateral ligament insufficiency and determined that pathologic glenohumeral internal rotation deficit may be associated
    with elbow valgus instability. Level of evidence: III.

    26.

    Reinold MM, Wilk KE, Macrina LC, et al: Changes in


    shoulder and elbow passive range of motion after pitching in professional baseball players. Am J Sports Med
    2008;36(3):523-527.
    In a controlled laboratory study, the authors noted a
    substantial decrease in passive range of motion immediately after baseball pitching that is present 24 hours after throwing. These results may suggest a newly defined
    mechanism to adaptations in range of motion resulting
    from acute musculoskeletal and potential osseous and
    capsular adaptations.

    27.

    Ellenbecker TS, Mattalino AJ, Elam EA, Caplinger RA:


    Medial elbow joint laxity in professional baseball pitchers: A bilateral comparison using stress radiography.
    Am J Sports Med 1998;26(3):420-424.

    28.

    ODriscoll SW, Lawton RL, Lawton RL, Smith AM:


    The moving valgus stress test for medial collateral ligament tears of the elbow. Am J Sports Med 2005;33(2):
    231-239.

    29.

    Kooima CL, Anderson K, Craig JV, Teeter DM, van


    Holsbeeck M: Evidence of subclinical medial collateral
    ligament injury and posteromedial impingement in professional baseball players. Am J Sports Med 2004;32(7):
    1602-1606.

    30.

    Wright RW, Steger-May K, Klein SE: Radiographic findings in the shoulder and elbow of Major League Baseball pitchers. Am J Sports Med 2007;35(11):1839-1843.
    The authors found that degenerative changes in the
    dominant shoulder and elbow of professional pitchers
    develop over time because of chronic repetitive stresses
    across joints. Level of evidence: IV.

    31.

    De Smet AA, Winter TC, Best TM, Bernhardt DT: Dynamic sonography with valgus stress to assess elbow ulnar collateral ligament injury in baseball pitchers. Skeletal Radiol 2002;31(11):671-676.

    32.

    Nazarian LN, McShane JM, Ciccotti MG, OKane PL,


    Harwood MI: Dynamic US of the anterior band of the
    ulnar collateral ligament of the elbow in asymptomatic
    major league baseball pitchers. Radiology 2003;227(1):
    149-154.

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    21.

    The authors performed a descriptive laboratory study


    and determined that proper pitching mechanics may
    help prevent pain and injuries to the shoulder and elbow
    in youth pitchers.

    323

    Section 3: Upper Extremity

    33.

    Park GY, Lee MY: Diagnostic value of ultrasonography


    for clinical medial epicondylitis. Arch Phys Med Rehabil
    2008;89(4):738-742.
    In a prospective, single-blind study, the authors attempted
    to determine the value of ultrasonography as a diagnostic
    tool for detecting clinical medial epicondylitis.

    34.

    Mishra A, Pavelko T: Treatment of chronic elbow tendinosis with buffered platelet-rich plasma. Am J Sports
    Med 2006;34(11):1774-1778.

    35.

    Rettig AC, Sherrill C, Snead DS, Mendler JC, Mieling P:


    Nonoperative treatment of ulnar collateral ligament injuries in throwing athletes. Am J Sports Med 2001;
    29(1):15-17.

    36.

    Savoie FH III, Trenhaile SW, Roberts J, Field LD, Ramsey JR: Primary repair of ulnar collateral ligament injuries of the elbow in young athletes: A case series of injuries to the proximal and distal ends of the ligament.
    Am J Sports Med 2008;36(6):1066-1072.
    The authors concluded that primary repair of proximal
    and distal injuries of the medial ulnar collateral ligament is an acceptable treatment option in young athletes. Level of evidence: IV.
    Thompson WH, Jobe FW, Yocum LA, Pink MM: Ulnar
    collateral ligament reconstruction in athletes: Musclesplitting approach without transposition of the ulnar
    nerve. J Shoulder Elbow Surg 2001;10(2):152-157.

    Dodson CC, Thomas A, Dines JS, Nho SJ, Williams RJ


    III, Altchek DW: Medial ulnar collateral ligament reconstruction of the elbow in throwing athletes. Am J
    Sports Med 2006;34(12):1926-1932.

    39.

    Dines JS, ElAttrache NS, Conway JE, Smith W, Ahmad


    CS: Clinical outcomes of the DANE TJ technique to
    treat ulnar collateral ligament insufficiency of the elbow.
    Am J Sports Med 2007;35(12):2039-2044.
    The authors studied 22 athletes over a 3-year period
    and determined that the use of the DANE TJ technique
    for ulnar collateral ligament reconstruction led to favorable results. Level of evidence: IV.

    40.

    Gabel GT, Morrey BF: Operative treatment of medical


    epicondylitis: Influence of concomitant ulnar neuropathy at the elbow. J Bone Joint Surg Am 1995;77(7):
    1065-1069.

    41.

    Wilson FD, Andrews JR, Blackburn TA, McCluskey G:


    Valgus extension overload in the pitching elbow. Am J
    Sports Med 1983;11(2):83-88.

    42.

    Kamineni S, ElAttrache NS, Odriscoll SW, et al: Medial


    collateral ligament strain with partial posteromedial
    olecranon resection: A biomechanical study. J Bone
    Joint Surg Am 2004;86(11):2424-2430.

    43.

    Ahmad CS, Park MC, Elattrache NS: Elbow medial ulnar collateral ligament insufficiency alters posteromedial olecranon contact. Am J Sports Med 2004;32(7):
    1607-1612.

    3: Upper Extremity

    37.

    38.

    324

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 26

    Elbow and Forearm Trauma


    David L. Glaser, MD

    April D. Armstrong, MD

    Radial Head Fractures


    Fractures of the radial head are among the most common elbow fractures, occurring in approximately 20%
    of all elbow fractures. The typical mechanism of injury
    is a fall on an outstretched hand with the forearm in
    pronation.

    Classification
    Several classification systems have been used to describe radial head fractures but the observer reliability
    of these systems has been questioned.1 There have been
    several variations of the original Mason system, which
    classified radial head fractures into three categories:
    type I, a nondisplaced fracture; type II, a displaced partial articular fracture with or without comminution;
    and type III, a comminuted radial head fracture involving the whole head (Figure 1). This system was modified to quantify the extent of the radial head involvement and to include radial neck fractures.2 Type I was
    defined as a fracture of the radial head or neck with
    less than 2 mm of displacement, type II as a fracture of
    the radial head or neck displaced 2 mm or more and involving 30% or more of the articular surface, type III
    as a comminuted fracture of the radial head or neck,
    and type IV as an elbow dislocation with any fracture
    of the radial head. The Mason classification was later
    modified to include clinical examination and intraoperative findings so that it could help guide treatment decisions.3

    Patient Examination and Imaging

    Dr. Glaser or an immediate family member is a member


    of a speakers bureau or has made paid presentations
    on behalf of Mitek. Neither Dr. Armstrong nor any immediate family member has received anything of value
    from or owns stock in a commercial company or institution related directly or indirectly to the subject of this
    chapter.

    2011 American Academy of Orthopaedic Surgeons

    Treatment
    Nondisplaced fractures of the radial head may cause elevation of the anterior and posterior fat pads (the sail
    sign) by an intra-articular hemarthrosis. These fractures
    can be treated nonsurgically with a brief period of immobilization in a sling, followed by early motion. Good
    results have been reported in 85% to 95% of patients
    with these injuries.5,6
    For displaced fractures, the decision for surgical fixation and the type of surgical treatment remains controversial. Surgical approaches vary based on the specific pathology of the fracture. For isolated radial head
    fractures in which a single lateral approach is planned,
    the patient is positioned supine with an arm board or
    the affected arm is placed over the body. An extensile
    posterior skin incision, which will allow access to the
    medial elbow if needed, is also possible from the supine
    position. The Kocher approach is preferred if the LCL
    is known to be disrupted, whereas the more anterior
    extensor digitorum communis-splitting approach is
    used if the LCL is intact; this approach avoids injury to
    the lateral ulnar collateral ligament.
    Excision of capitellum or radial head fragments
    should be avoided if the fragments comprise more than
    approximately 25% to 33% of the capitellar surface
    area or 25% of the surface area of the radial head.6,7
    Historically, radial head resection has been considered
    in patients with isolated, displaced, and comminuted
    radial head fractures without associated ligamentous
    injury. Excision alone should generally be considered
    an option only in low-demand, sedentary patients. Radial head replacement in the absence of demonstrable
    instability or associated injuries is controversial. Biome-

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Lateral elbow pain and tenderness or limitation in elbow or forearm motion should alert the examiner to
    the possibility of a radial head fracture. Although tenderness over the radial head is expected, tenderness at
    other sites suggests the presence of an associated injury.4 Point tenderness over the lateral epicondyle may
    indicate a lateral collateral ligament (LCL) injury. Ten-

    derness over the sublime tubercle or medial epicondyle


    or ecchymosis on the medial aspect of the elbow may
    indicate a medial collateral ligament (MCL) injury. Pain
    and tenderness at the distal radioulnar joint or in the
    forearm should raise suspicion of an interosseous ligament disruption leading to axial forearm instability,
    termed an Essex-Lopresti lesion.3
    AP and lateral radiographs of the elbow are typically
    sufficient to diagnose a radial head injury. The radiocapitellar view is obtained by positioning the patient
    for a lateral view but angling the tube 45 toward the
    shoulder. CT is commonly used to better define details
    of the fracture. Joint aspiration with an injection of a
    local anesthetic helps assess mechanical blocks to motion.

    325

    Section 3: Upper Extremity

    Figure 1

    Mason classification of radial head fractures. A, Type I are minimally or nondisplaced fractures. B, Type II fractures
    have more than 2 mm of displacement. C, Type III fractures are severely comminuted. (Reproduced with permission
    from the Mayo Foundation for Medical Education and Research, Rochester, MN, 1983.)

    Figure 2

    Safe zone for the application of hardware on the radial head. (Reproduced from Hotchkiss RN: Displaced fractures
    of the radial head: Internal fixation or excision? J Am Acad Orthop Surg 1997;5:8.)

    3: Upper Extremity

    chanical studies following radial head resection have


    shown altered kinematics and stability, which may contribute to the increased rate of radiographic degeneration.8 The biomechanical implications of radial head resection suggest that restoration of radiocapitellar
    contact with a radial head replacement is advisable.
    In those fractures amenable to repair, stable fixation
    of the articular surface and restoration of the headneck relationship can be achieved using a variety of devices. In fractures in which a portion of the head is still
    connected to the neck, the intact head can be used as a
    scaffold for securing the fractured fragments using either small standard screws (1.5 to 3.0 mm), fully
    threaded Kirschner wires, or headless screws. For more
    complex fracture patterns or those involving the radial
    neck, mini-implant plates are useful.9
    326

    Orthopaedic Knowledge Update 10

    The safe zone has been identified as the posterolateral aspect of the radial head that does not articulate
    with the sigmoid notch of the ulna during forearm rotation3 (Figure 2). With the forearm in neutral rotation,
    the safe zone is the portion of the radial head that presents laterally in the wound. Alternatively, this zone can
    be found within the 90 angle bound by the radial styloid and the Lister tubercle distally.
    For displaced radial head fractures with more than
    three fracture fragments, radial head replacement may
    be the preferred technique.6 Appropriately sized radial
    head replacement implants will restore the length of the
    radius and radiocapitellar contact. Good clinical results
    have been reported with metallic radial head implants
    for comminuted radial head fractures.10-13 Long-term
    effects on the capitellar articular cartilage and compli-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 26: Elbow and Forearm Trauma

    cations such as implant loosening and failure require


    further study.
    Various implants are available for radial head replacement. However, clinical evidence supporting a particular design, such as bipolar versus monopolar, cemented versus uncemented, and anatomic versus
    asymmetric head shape, is not yet available.
    Attention to the technical aspects of radial head replacement will ensure the best possible outcomes. The
    resected radial head serves as the optimal template for
    sizing the prosthetic implant. After the implant has
    been inserted, the elbow should be moved through a
    range of motion while the surgeon observes the radiocapitellar contact for congruency and tracking and
    scrutinizes the height and diameter of the implant. Elbow alignment and implant sizing also can be assessed
    for parallelism by using fluoroscopy to examine the
    medial ulnotrochlear joint space.

    Distal Humerus Fractures

    Classification
    Fractures of the distal humerus can be classified according to the Orthopaedic Trauma Association/AO
    comprehensive classification of fractures of long bones:
    type A (nonarticular), type B (partial articular), and
    type C (complete articular).14 These categories are further subdivided based on the position of the fracture
    line and the degree of comminution.

    Treatment

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Nonsurgical management of distal humerus fractures is


    rarely recommended. Although nonsurgical treatment
    may be appropriate for nondisplaced fractures, surgical
    fixation allows immediate motion and is generally preferred. In low-demand patients with preexisting neurologic impairment or if surgery is contraindicated
    because of medical comorbidities, nonsurgical management may be the only treatment option.
    The elbow joint can be exposed through several different surgical approaches. A longitudinal posterior approach can permit the elevation of broad skin flaps and
    provide extensile exposure of both the medial and lateral sides of the elbow. For isolated condylar fractures,
    a medial or a lateral approach can be considered. An
    ulnar nerve transposition should be considered in all
    cases. Several options exist for approaching the fracture
    itself, including an olecranon osteotomy, a tricepssparing approach, and a triceps-splitting approach. The
    Bryan-Morrey approach involves subperiosteal reflection of the triceps insertion from medial to lateral in
    continuity with the forearm fascia and anconeus muscle.15 The triceps-reflecting anconeus pedicle approach
    described by ODriscoll16 may also be used. When
    treating complex articular fractures, a chevron-shaped
    osteotomy with the apex pointing distally facilitates anatomic repositioning, enhances stability, and provides a
    broader interface of cancellous bone. The osteotomy
    should be located at the depth of the semilunar notch,

    where there is the least amount of articular cartilage.


    Osteotomy should be avoided if total elbow arthroplasty is being considered.
    An anatomic study showed that the percentage of articular surface visible after triceps-splitting, tricepssparing, and olecranon osteotomy were 35%, 46%,
    and 57%, respectively.17 If an osteotomy is performed it
    can be fixed by either compression plating, tension
    band wiring, or with an intramedullary compression
    screw. Predrilling helps achieve an anatomic reduction
    when an intramedullary screw will be used. Variations
    of the olecranon osteotomy have been reported. Recently, the anconeus flap transolecranon approach,
    which combines a proximally based anconeus flap with
    an apex distal chevron osteotomy of the olecranon, has
    been described.18 This procedure involves incising the
    Kocher interval (between the extensor carpi ulnaris and
    anconeus muscles) and elevating the anconeus muscle
    in a proximal direction off the ulna. The anconeus remains attached to the proximal olecranon and triceps,
    which preserves its neurovascular supply. This process
    maintains the dynamic stabilizing effect of the anconeus muscle and also provides a vascularized bed
    over the osteotomy, which is hypothesized to reduce the
    incidence of nonunion. A recent study of olecranon osteotomies in 67 patients reported no nonunions and an
    8% rate of hardware removal.19
    Surgical treatment of intra-articular distal humerus
    fractures that follows the principles of stable internal
    fixation with two-column plating, anatomic restoration
    of the articular surface, and early mobilization yields
    satisfactory functional and radiographic outcomes.20,21
    Methods of internal fixation include parallel, orthogonal, triple, and fixed-angle plating.22-26 The findings of a
    2009 study support the literature regarding the high
    success rate of parallel plating, although many techniques lead to successful healing if properly applied.27
    Although there is controversy regarding optimal
    plate positioning, it is generally agreed that, if applied
    appropriately with adequate plates, both parallel and
    orthogonal placement can provide necessary stability.
    In addition to screws that are placed through the plate,
    interfragmentary screws of various sizes and threaded
    Kirschner wires (if needed) cut at the edge of the fracture fragments can be used to achieve stable fixation. A
    compression plate, 3.5-mm pelvic reconstruction plates,
    and precontoured plates are sufficiently rigid to provide
    stable fixation. In contrast, one third semitubular plates
    have insufficient strength and are susceptible to breakage in this location; therefore, they are not adequate for
    fixation of distal humerus fractures.
    Primary total elbow arthroplasty for treating comminuted distal humerus fractures has become a viable
    option for elderly, low-demand patients.28-32 In a series
    of 43 fractures treated with primary total elbow arthroplasty, patients achieved a mean range of motion from
    24 to 131 at 7-year follow-up.28 Thirty-two of 49 patients had no further surgery and had no complications.
    Five revision arthroplasties were required. In an extensive review of 92 elbows treated with total elbow arthroplasty as a salvage procedure for distal humeral
    327

    Section 3: Upper Extremity

    Figure 3

    Regan-Morrey classification of coronoid fractures. A, Type I fractures are described as avulsion fractures of the
    tip of the coronoid, and usually do not require surgical treatment. B, Type II fractures involve 50% or less of the
    height of the coronoid, and frequently do not require treatment. C, Type III fractures involve more than 50% of
    the height of the coronoid. (Reproduced with permission from Regan WD, Morrey BF: Coronoid process and
    Monteggia fractures, in Morrey BF, ed: The Elbow and Its Disorders, ed 3. Philadelphia, PA, WB Saunders, 2000,
    pp 396-408.)

    nonunion, improvements were reported in most patients.30 No pain or mild pain was reported in 74% of
    patients and 85% had satisfactory subjective results.
    However, the reoperation rate was 35%. Implant survival was 96% at 2 years, 82% at 5 years, and 65% at
    10 and 15 years. Another study of total elbow arthroplasty reported good results with a 29% single complication rate.31
    In a retrospective review of 24 patients older than 65
    years treated with total elbow arthroplasty or open reduction and internal fixation for type C2 or C3 distal
    humerus fractures, the authors concluded that total elbow arthroplasty was supported in this patient population, particularly in those with osteoporosis and rheumatoid arthritis.32 However, the study size was small
    and follow-up was only 2 years. In a prospective study
    evaluating fracture fixation versus total elbow arthroplasty in elderly patients, the authors reported no difference in functional outcomes at 2-year follow-up using the Disabilities of the Arm, Shoulder and Hand
    scoring system.33 The authors stated that arthroplasty is
    the preferred method of treatment if stable fixation
    cannot be achieved.

    Complications
    3: Upper Extremity

    Complications following fixation of distal humerus


    fractures are surprisingly common, ranging from 25%
    to 48%.25,28-32 Complications include heterotopic ossification, olecranon nonunion, infection, ulnar neuropathy, nonunion, and fixation failure.

    Coronoid Fractures

    Classification
    The classic method for classifying coronoid fractures is
    based on the height of the coronoid fragment (Figure 3).
    Type I represents a fracture of the coronoid tip that is
    328

    Orthopaedic Knowledge Update 10

    believed to be related to a shearing mechanism. This injury was originally described as a brachialis avulsion
    fracture, but the insertion of the brachialis is more distal
    to the coronoid tip. Typically, the fragment remains attached to the anterior capsule.34 Type II fractures involve
    50% or less of the coronoid height, and type III involve
    more than 50% of the coronoid height and can include
    the attachment of the MCL. Based on biomechanical
    studies, it has been proposed that, in an otherwise stable
    elbow, coronoid fractures of 50% or more of the coronoid height should be fixed.35-37 In a retrospective review
    of 103 coronoid fractures, patients with associated injuries, particularly radial head fractures, scored lower on
    the Mayo elbow performance score, had less elbow extension, more pain, and less pronation/supination than
    those without associated injuries.38

    Biomechanics and Treatment


    In an elbow that is unstable because of a fracturedislocation, the coronoid process plays an important
    role in elbow stability. CT scans of elbows with a terrible triad injury showed that the average height for the
    coronoid fragment was 35% of the total height of the
    coronoid.39 Coronoid fractures related to terrible triad
    injuries tend to have a transverse fracture pattern.40 It is
    typically recommended that all coronoid fractures be
    fixed when the elbow is unstable, especially type II and
    III injuries. Results of testing in biomechanical cadaver
    models have suggested that the terrible triad injury patterns could be rendered stable with fixation or replacement of the radial head and LCL repair, without fixation of the small (type I) coronoid fragments.37,41 It also
    has been suggested that MCL repair may be more important than type I coronoid fracture fixation.41 However, there are no randomized clinical studies addressing these issues. Therefore, it is more routinely
    advocated that type I fractures be fixed because they
    represent an anterior capsular injury, which can have
    an impact on elbow stability. A recent biomechanical

    2011 American Academy of Orthopaedic Surgeons

    Chapter 26: Elbow and Forearm Trauma

    study highlighted the fact that open reduction and


    internal fixation of type II coronoid fractures is particularly important in a tenuous collateral ligament repair. 42 Isolated repair and overtightening of a collateral
    ligament can off balance the elbow if the opposing
    collateral ligament is torn, particularly with a type II
    coronoid fracture.
    The coronoid fracture may be fixed with suture
    through drill holes in the ulna, or larger fragments may
    be treated with screw fixation. Biomechanically, it has
    been shown that a screw inserted from posterior to anterior yielded greater strength and fixation stiffness
    compared with anterior to posterior placement.43 Precontoured plates are also commercially available for
    coronoid fixation. Small series of arthroscopically assisted open reduction and internal fixation of coronoid
    fractures have reported good results.44,45

    Capitellum and Trochlea Fractures

    Classification
    Coronal fractures of the distal humerus are rare, accounting for fewer than 1% of distal humeral fractures.
    Early classification systems for capitellar and trochlear
    fractures have not been useful for guiding treatment.46
    More recently, a new classification system has been
    proposed that also helps to direct treatment.47 Capitellar and trochlear fractures are divided into three types.
    Type I fractures primarily involve the capitellum, with
    or without the lateral trochlear ridge. Type II fractures
    involve both the capitellum and trochlea as one piece,
    and type III fractures involve both the capitellum and
    trochlea as separate pieces. These groups are further
    subdivided into class A (without) and B (with) posterior condylar comminution (Figure 4). Patients with
    isolated noncomminuted fractures have better results
    and fewer complications than those with more complex
    fractures.47,48 However, on average, most patients will
    achieve functional range of motion; functional results
    appear durable over time.47,48

    Surgical Treatment

    2011 American Academy of Orthopaedic Surgeons

    Results and Complications


    Although surgical treatment results are generally favorable with capitellar and trochlear fractures, there are
    notable complication and reoperation rates associated
    with these fractures. Reported reoperation rates are
    43% to 48%.46,47 Reasons for reoperation include
    prominent hardware, nonunion, and contracture release. Osteonecrosis is not commonly reported.

    Olecranon Fractures
    Fractures of the olecranon occur in approximately 10%
    of all elbow fractures as either an isolated injury or part
    of a more complex fracture pattern.49 These fractures
    result from either a direct blow to the bone or indirectly as an avulsion from forces generated by the triceps muscle.

    Classification
    The Mayo classification of olecranon fractures is based
    on three variables: displacement, stability, and comminution.50 Type I fractures are nondisplaced; type II fractures are displaced, but the ulnohumeral joint is stable;
    and type III fractures are displaced and unstable. Each
    fracture type is subdivided into noncomminuted (A)
    and comminuted (B) fractures.

    Treatment
    Several treatment options for internal fixation of olecranon fractures have been described, including tensionband wiring, plate fixation, intramedullary screw fixation, and triceps advancement after fragment excision.
    The method of internal fixation is based primarily on
    the fracture type.
    Nondisplaced fractures of the olecranon (Mayo type
    IA and IB), although exceedingly rare, can be treated
    nonsurgically. These fractures are defined by displacement less than 2 mm, and no change in position with
    gentle flexion to 90 or extension of the elbow against
    gravity. Type IA and IB fractures are immobilized in a
    long arm cast for 3 to 4 weeks followed by protected
    range-of-motion exercises. Flexion past 90 should be
    avoided until radiographic bone healing is complete at
    approximately 6 to 8 weeks. In elderly patients, range
    of motion may be initiated earlier than 3 weeks if tolerated by the patient, with the goal of preventing stiffness. A follow-up radiograph should be obtained
    within 5 to 7 days after cast application to ensure that
    fracture displacement has not occurred. Immobilization
    in full extension is not recommended because stiffness

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Capitellar and trochlear fractures may be approached


    through a posterior midline skin incision, a bicolumn
    approach with separate medial and lateral incisions, or
    even an olecranon osteotomy.47 For type I fractures, a
    lateral interval approach (Kaplan and/or Kocher approach) with screw fixation may be used (Figure 5).
    Type II fractures also require visualization of the medial
    aspect of the trochlea, which can be achieved through a
    flexor pronator-splitting approach, olecranon osteotomy, or sectioning of the LCL. The optimal approach
    for visualizing the trochlea requires further study. Typically, screws are used for fixation. Type III fractures
    will often require an olecranon osteotomy for adequate
    exposure. It may be possible to visualize the fracture
    from the lateral approach if the LCL is disrupted. A variety of fixation methods have been described, including lag screws, headless compression screws, bioab-

    sorbable screws, threaded Kirschner wires, and plate


    fixation (particularly if there is posterior comminution). For the subtype B fractures with posterior comminution, plate fixation with or without bone graft is
    advocated. There has been some mention of using a
    distal humerus hemiarthroplasty with an anatomically
    shaped component for these more comminuted articular fractures.29

    329

    3: Upper Extremity

    Section 3: Upper Extremity

    Figure 4

    Classification of capitellar and/or trochlear fractures. (Reproduced with permission from Dubberley JH, Faber KJ,
    MacDermid JC, Patterson SD, King GJW: Outcome after open reduction and internal fixation of capitellar and
    trochlear fractures. J Bone Joint Surg Am 2006;88:46-54.)

    is more likely. Fractures that require full extension for


    reduction should be surgically treated.
    Displaced olecranon fractures (Mayo types IIA, IIB,
    IIIA, and IIIB) require surgical treatment. Several types
    of internal fixation are available, including tensionband wiring, plate fixation, intramedullary screw fixation, and triceps advancement after fragment excision.
    The goal of internal fixation is to restore the joint sur330

    Orthopaedic Knowledge Update 10

    faces without changing the shape of the greater sigmoid


    notch using fixation that is sufficiently stable to permit
    early motion. Transverse fractures without comminution (Mayo type IIA) are amenable to tension-band wiring or plating, depending on the relationship to the
    midpoint of the greater sigmoid notch. The tension
    band construct can be fashioned using either Kirschner
    wires or an intramedullary screw.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 26: Elbow and Forearm Trauma

    In fractures with comminution (Mayo type IIB and


    IIIB) or following a fracture-dislocation (Mayo type
    IIIA or IIIB), optimal fixation can be achieved with
    plate fixation. Treatment with the tension-band technique may not provide a sufficiently stable construct,
    which can lead to displacement.

    Complications
    Hardware irritation requiring removal is one of the
    most common complications after internal fixation of
    olecranon fractures. Complaints related to prominent
    hardware are common. Although a mild loss of motion
    (of approximately 10 to 15 primarily in extension) is
    common, it is rarely a significant problem. Nonunion
    of olecranon fractures has been reported in up to 1% of
    patients.

    Diaphyseal Forearm Fractures


    Plate osteosynthesis is considered the standard treatment for diaphyseal radius and ulna forearm fractures.
    Patient-based functional outcomes show that plate fixation restores the normal anatomy of the bones and
    normal motion; however, a moderate reduction (30%)
    in forearm, wrist, and grip strength has been reported.51 Recently, an interlocking intramedullary nail
    system has been described for treating radial and ulnar
    fractures, and has achieved a high rate of osseous consolidation for simple (noncomminuted) diaphyseal fractures.52 Patients with poor soft-tissue integrity have
    been suggested as candidates for treatment with this
    technique. Reported disadvantages of this approach are
    the need for a brace and longer periods of immobilization.

    Elbow Dislocation

    2011 American Academy of Orthopaedic Surgeons

    Lateral approaches for capitellar fracture fixation.


    (Reproduced from Ruchelsman DE, Tejwani NC,
    Kwon YW, Egol KE: Coronal plane partial articular fractures of the distal humerus: Current concepts in management. J Am Acad Orthop Surg
    2008;16:716-728.)

    crossing the elbow joint that provides a compressive


    force to the joint (the common flexor and extensor
    muscle groups).

    Simple Dislocations
    Most dislocations occur in a posterior or posterolateral
    direction, although anterior, medial, lateral, and divergent patterns have been reported. Biomechanical testing
    has demonstrated that a combination of valgus force,
    axial load, supination, and external rotation can result
    in a posterolateral dislocation.55 Other biomechanical
    models have shown posterior dislocation following
    varus rather than valgus loading.56
    Although a variety of mechanisms may result in elbow dislocation, the primary lesion appears to be injury to the LCL, with a spectrum of injury to other ligamentous and osseous structures following a circular
    path laterally to medially (Figure 6). The LCL ligament
    is composed of the lateral ulnar collateral ligament, radial collateral ligament, accessory collateral ligament,
    and annular ligament. Although it is generally agreed
    that the lateral ulnar collateral ligament appears to be
    the primary restraint to posterolateral rotatory instability,57 some investigators believe that the radial collateral
    ligament and accessory collateral ligament also contribute significantly to lateral elbow stability.58,59
    Controversy exists regarding the involvement of the
    MCL in elbow dislocations. The MCL is composed of
    an anterior oblique, posterior oblique, and transverse
    ligament. The anterior oblique band resists valgus
    stress throughout the elbow range of motion. Although
    some biomechanical models have demonstrated that
    posterior dislocation is possible with an intact anterior
    band,55 other studies have suggested that the anterior
    oblique band is disrupted following posterior dislocation.60,61 The variability of pathoanatomy associated
    with elbow instability highlights the importance of
    carefully assessing and recognizing all potential sources
    of instability.

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    The elbow is the second most commonly dislocated


    large joint, following the shoulder.53 The management
    of the unstable elbow has evolved considerably over recent years as knowledge of the anatomic stabilizers of
    the elbow and the pathoanatomy of instability has increased. The goals of treating an unstable elbow are to
    restore functional stability and motion. Achieving these
    goals requires managing soft-tissue injuries (in simple
    dislocations) or addressing these injuries in conjunction
    with fracture management (in complex instability).
    Simple dislocations, which account for approximately
    50% to 60% of elbow dislocations, often can be managed with closed reduction and treatment, whereas
    complex injury patterns often require surgical treatment.54
    Elbow stability is provided by both static and dynamic constraints. The three primary static constraints
    are the ulnohumeral bony articulation, the anterior
    bundle of the MCL, and the LCL complex. The secondary static constraints include the capsule and the radial
    head. The dynamic constraints refer to any muscle

    Figure 5

    331

    Section 3: Upper Extremity

    on the capitellum is common, and is analogous to a


    Hill-Sachs lesion in the shoulder. The stability of the
    joint is not affected by this impaction fracture.

    Complex Dislocation

    Figure 6

    Illustration showing the spectrum of elbow instability. Stage 1: lateral ulnar collateral ligament
    disruption. Stage 2: anterior and posterior capsular disruption. Stage 3: MCL disruption (partial
    or complete). (Reproduced with permission from
    ODriscoll SW, Morrey BF, Korinek S, An KH:
    Elbow subluxation and dislocation: A spectrum
    of instability. Clin Orthop Relat Res 1992;280:
    186-197.)

    3: Upper Extremity

    The treatment algorithm for simple elbow dislocations has shifted toward early mobilization to prevent
    flexion contracture of the elbow62 (Figure 7). The bony
    constraint of the elbow is already highly congruous and
    the compressive forces of the dynamic stabilizers protect the soft-tissue injury. Following reduction of an elbow dislocation, it is typically immobilized for 5 to 7
    days at 90, with the forearm positioned to allow for
    concentric reduction of the ulnohumeral articulation.
    At follow-up, the splint is removed and active range of
    motion is commenced through the stable flexion and
    extension arc (stable forearm position);63 an extension
    block brace is commonly used for 3 to 4 weeks. The extension block is progressively decreased so that by 6 to
    8 weeks the patient achieves full stable extension. Forearm active pronation and supination at 90 of elbow
    flexion is started early to prevent rotational contracture. A drop sign refers to a static widening of the ulnohumeral joint on the lateral radiograph.64 Ulnohumeral incongruence must be corrected by
    changing the forearm position, splinting, or surgery to
    repair soft-tissue injury or remove entrapped osteochondral or soft-tissue structures. If the LCL complex
    is disrupted and the MCL is intact, the elbow may be
    more stable with the forearm in pronation.65 If the LCL
    is intact and the MCL is ruptured, the elbow may be
    more stable with the forearm in supination.66 If both
    ligaments are disrupted, the elbow may be placed in
    neutral rotation to protect both the medial and lateral
    ligamentous structures. A posterior impaction fracture
    332

    Orthopaedic Knowledge Update 10

    The terrible triad injury to the elbow refers to an elbow dislocation with an associated fracture, typically a
    fracture of the radial head and coronoid process (Figure 8). Disruption of the LCL is a critical component of
    the terrible triad lesion, and is almost uniformly observed in a fracture-dislocation of the elbow.67 The ligament often avulses from its isometric origin on the lateral aspect of the capitellum (Figure 9), along with a
    component of the extensor origin lesion from the lateral epicondyle. Cadaver testing has shown that fracture repair of the radial head and coronoid alone does
    not restore stability, and that optimal stability and kinematics require isometric and appropriately tensioned
    repair of the LCL.68
    The MCL, especially the anterior band, is well established as a primary restraint to valgus instability of the
    elbow. Complex instability often can result in MCL injury, either as an intrasubstance lesion or as an avulsion
    of the origin along with a sleeve of the common flexor
    origin. Although the MCL is critical to normal valgus
    stability, routine repair or reconstruction following
    complex instability may not be necessary because of the
    role of the radial head as a secondary stabilizer, especially in the setting of an intact or repaired coronoid
    process.69
    The potential for elbow instability increases with the
    increasing height of the fragment.70 In a cadaver model,
    a 30% loss of coronoid height in association with removal of the radial head in a ligamentously intact elbow resulted in elbow instability.71 Because isolated
    loss of 50% or more of the coronoid height also results
    in elbow instability, it is critical to repair coronoid fractures, especially type II and III fractures. Although
    small fragments (type I) may not directly impart significant instability, they are often a hallmark of an anterior capsular injury, which can have an impact on stability and repair.34
    Historically, treatment results of terrible triad injuries have been suboptimal and have been associated
    with a high complication rate, recurrent instability, arthrosis, and stiffness.72 The use of a systematic algorithmic approach to this injury pattern, which appreciates
    both the bony and soft-tissue injuries, has improved
    clinical results.69,73-75
    A standard approach to treating terrible triad injuries is to sequentially repair injured structures from
    deep to superficial (Figure 10). A midline posterior incision is advocated to allow access to both the medial
    and lateral joint spaces; or a bicolumn approach can be
    used with separate medial and lateral approaches. The
    coronoid is initially fixed through a space created by
    the fractured radial head or through a medial approach. There is often a rent in the flexor pronator
    mass that allows access to the coronoid. The coronoid
    is fixed with sutures or screws depending on the size of

    2011 American Academy of Orthopaedic Surgeons

    Chapter 26: Elbow and Forearm Trauma

    Algorithm for treatment of simple elbow dislocations. (Reproduced from Armstrong AD: Acute, recurrent, and
    chronic elbow instability, in Galatz LM, ed: Orthopaedic Knowledge Update: Shoulder and Elbow 3. Rosemont, IL,
    American Academy of Orthopaedic Surgeons, 2008, pp 461-476.)

    Figure 8

    Lateral radiograph of a fracture-dislocation of


    the elbow. The small arrows point to the anteriorly displaced coronoid fractures, which may
    be confused for radial head fragments (large
    arrow). (Courtesy of Bradford Parsons, MD,
    New York, NY.)

    2011 American Academy of Orthopaedic Surgeons

    Figure 9

    3: Upper Extremity

    Figure 7

    The LCL (small arrow) typically avulses from its


    isometric origin (large arrow pointing to cautery
    mark on lateral capitellum) and often can be
    repaired isometrically in the acute injury. (Courtesy of Bradford Parsons, MD, New York, NY.)

    Orthopaedic Knowledge Update 10

    333

    3: Upper Extremity

    Section 3: Upper Extremity

    Figure 10

    Algorithm showing the standard protocol for treating a terrible triad injury. (Reproduced from Armstrong AD:
    Acute, recurrent, and chronic elbow instability, in Galatz LM, ed: Orthopaedic Knowledge Update: Shoulder and
    Elbow 3. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2008, pp 461-476.)

    the fracture. Next, the radial head is either fixed or replaced. Internal fixation of the radial head will improve
    joint stability, but only if it can be fixed with a construct that is as stable as the native radial head. Radial
    head replacement should be anatomic, restoring normal
    length and size.
    334

    Orthopaedic Knowledge Update 10

    Recent biomechanical studies have shown the importance of the radial head as a secondary valgus stabilizer;
    however, full valgus stability of the elbow will not be
    achieved unless the MCL is repaired or reconstructed.76
    The radial head is also an important constraint to varus
    and external rotatory forces about the elbow, but less

    2011 American Academy of Orthopaedic Surgeons

    Chapter 26: Elbow and Forearm Trauma

    important than the LCL. Biomechanically, varus and


    external rotator instability of the elbow is worsened
    with radial head excision with a deficient LCL complex.68 Radial head replacement improves the varus and
    external rotator stability of the elbow, but stability is
    not fully restored until the LCL is repaired. Biomechanical studies also have shown the combined importance
    of the radial head and the coronoid fracture in a terrible
    triad injury. The radial head alone could not stabilize
    the elbow joint when 50% to 70% of the coronoid was
    resected, despite an intact MCL and LCL.41,70,71
    Following repair of the bony injuries, the soft-tissue
    injuries are treated. LCL rupture is universal to these
    injuries and must be repaired to the anatomic axis of
    rotation of the elbow at the center of the capitellar curvature. Avulsion of the common extensor origin from
    the lateral epicondyle, leaving it devoid of any soft tissue, is a common occurrence. Lateral soft-tissue repair
    also should include the common extensor muscles. In
    most instances, the joint is rendered stable by this
    point; however, if the elbow is still unstable, consideration should be given to repair of the medial structure
    and ultimately to the use of an external fixator if the elbow cannot be stabilized. Early consideration of hinged
    external fixation has been advocated.77 Postoperative
    rehabilitation should follow the same protocol as previously described for simple elbow dislocations. The primary goal of surgery is to achieve a stable elbow, which
    will allow early range of motion.

    Distal Biceps Tendon Injuries

    2011 American Academy of Orthopaedic Surgeons

    Illustration of the biceps tendon insertions.


    (Reproduced with permission from Athwal GS,
    Steinmann SP, Rispoli DM: The distal biceps
    tendon: Footprint and relevant clinical anatomy. J Hand Surg Am 2007;32:1225-1229.)

    incision techniques. Surgical treatment is typically advocated for patients who are more active or those who
    often perform twisting motions of the forearm. Nonsurgical treatment of distal biceps tendon injuries results in a modest reduction in supination strength and
    minimal reduction in elbow flexion strength.83 Classically, the two-incision Boyd-Anderson approach was
    used for distal biceps reconstruction. The singleincision anterior approach evolved in an attempt to decrease the incidence of radioulnar synostosis; however,
    heterotopic ossification also has been reported with the
    single-incision anterior approach.84 Excellent clinical
    results have been reported with both approaches.
    A variety of fixation methods have been reported in
    the literature, including bone tunnels, suture anchors,
    interference screws, or button.85-87 Biomechanically the
    Endobutton (Smith & Nephew, Memphis, TN) may
    have a higher initial load-to-failure strength;87,88 however, in contrast, it has also been shown to have comparable strength to suture anchor fixation.89 Overall,
    surgical fixation techniques have shown similar clinical
    results.84,90-92 Small case series for late reconstruction of
    chronic distal biceps injuries with either Achilles tendon allograft or autologous hamstring graft have
    shown promising results for improving supination
    strength.93,94

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Recent studies focusing on the treatment of distal biceps rupture have described the normal anatomy of the
    tendon along with different fixation techniques and
    surgical approaches. The biceps tendon inserts on the
    ulnar aspect of the bicipital tuberosity,78,79 which has
    surgical implications for anatomic repair of the tendon.
    A patient with limited supination may not be a good
    candidate for a single-incision approach because anatomic repair would be difficult.79 There are two distinct
    insertion points of the tendonthe anteromedial fibers
    (short head) insert more inferiorly, whereas the posterolateral fibers (long head) insert more proximally80 (Figure 11). This gives the tendon a twisted appearance at
    its insertion. The short head of the biceps tendon is the
    origin of the lacertus fibrosus, which is key to proper
    anatomic alignment at surgery.81
    Although the diagnosis of distal biceps tendon rupture is largely clinical, MRI can be helpful in establishing the diagnosis. Because of the anatomic positioning
    of the biceps tendon, visualizing a rupture and the tendon itself with standard positioning can be difficult.
    Recently, a modified positioning technique involving a
    flexed elbow, abducted shoulder, and supinated forearm (termed FABS) has been popularized. This technique significantly enhances the visualization of the biceps tendon with MRI.82
    The two current surgical approaches for distal biceps repair are the two-incision and anterior single-

    Figure 11

    335

    Section 3: Upper Extremity

    The authors report on the long-term outcome of surgically treated Mason type II radial head fractures. They
    concluded that surgical treatment of stable, isolated, displaced partial articular (Mason type II) fractures of the
    radial head show no appreciable advantage over the
    long-term results of nonsurgical treatment of these fractures as described in prior reports. The appeal of surgical treatment is diminished by potential complications.

    Annotated References
    1.

    Sheps DM, Kiefer KR, Boorman RS, et al: The interobserver reliability of classification systems for radial head
    fractures: The Hotchkiss modification of the Mason
    classification and the AO classification systems. Can J
    Surg 2009;52(4):277-282.

    3: Upper Extremity

    The interobserver reliability of two commonly used classification systems, the Hotchkiss modification of the
    Mason classification and the AO classification system,
    were evaluated. The authors concluded that, according
    to the criteria of Landis and Koch, there was moderate
    interobserver reliability for the Hotchkiss modification
    of the Mason classification, and fair interobserver reliability for the AO classification. Collapsing the Hotchkiss classification improved the reliability to substantial,
    and collapsing the AO system improved reliability to the
    lower end of moderate.
    2.

    Broberg MA, Morrey BF: Results of treatment of


    fracture-dislocations of the elbow. Clin Orthop Relat
    Res 1987;216:109-119.

    3.

    Hotchkiss RN: Displaced fractures of the radial head:


    Internal fixation or excision? J Am Acad Orthop Surg
    1997;5(1):1-10.

    4.

    van Riet RP, Morrey BF: Documentation of associated


    injuries occurring with radial head fracture. Clin Orthop Relat Res 2008;466(1):130-134.
    This article reviews the authors experience with 333 radial head fractures with the purpose of describing the
    spectrum of associated injuries that commonly occur in
    conjunction with a radial head fracture. A system based
    on the Mason fracture classification was proposed to
    document the presence of additional articular and ligamentous injuries.

    Smets S, Govaers K, Jansen N, Van Riet R, Schaap M,


    Van Glabbeek F: The floating radial head prosthesis for
    comminuted radial head fractures: A multicentric study.
    Acta Orthop Belg 2000;66(4):353-358.

    11.

    Doornberg JN, Linzel DS, Zurakowski D, Ring D: Reference points for radial head prosthesis size. J Hand
    Surg Am 2006;31(1):53-57.

    12.

    van Riet RP, van Glabbeek F, de Weerdt W, Oemar J,


    Bortier H: Validation of the lesser sigmoid notch of the
    ulna as a reference point for accurate placement of a
    prosthesis for the head of the radius: A cadaver study.
    J Bone Joint Surg Br 2007;89(3):413-416.
    A review of the Antwerp University Hospitals experience with radial head fractures from 1997 to 2002
    showed that 88 of 333 radial head fractures (26%) had
    associated injuries. Based on this clinical experience, an
    accurate and comprehensive description of associated
    injuries was developed. The proposed system offered a
    reproducible (98%) extension of the current Mason
    fracture classification system to document the presence
    of additional articular and ligamentous injuries.

    13.

    Pike JM, Athwal GS, Faber KJ, King GJ: Radial head
    fractures: An update. J Hand Surg Am 2009;34(3):557565.
    The authors summarize diagnosis and treatment options
    for treatment of radial head fractures.

    5.

    Caputo AE, Burton KJ, Cohen MS, King GJ: Articular


    cartilage injuries of the capitellum interposed in radial
    head fractures: A report of ten cases. J Shoulder Elbow
    Surg 2006;15(6):716-720.

    14.

    Muller M, Nazanan S, Koch P, et al: Fracture and dislocation compendium: Orthopaedic trauma association
    committee for coding and classification. J Orthop
    Trauma 2001;10(suppl 1):311-324.

    6.

    Ring D, Quintero J, Jupiter JB: Open reduction and internal fixation of fractures of the radial head. J Bone
    Joint Surg Am 2002;84(10):1811-1815.

    15.

    Bryan RS, Morrey BF: Extensive posterior exposure of


    the elbow: A triceps-sparing approach. Clin Orthop
    Relat Res 1982;166(166):188-192.

    7.

    Bain GI, Ashwood N, Baird R, Unni R, Oka Y: Management of Mason type-III radial head fractures with a
    titanium prosthesis, ligament repair, and early mobilization: Surgical technique. J Bone Joint Surg Am 2005;
    87(pt 1, suppl 1)136-147.

    16.

    ODriscoll SW: The triceps-reflecting anconeus pedicle


    (TRAP) approach for distal humeral fractures and nonunions. Orthop Clin North Am 2000;31(1):91-101.

    17.

    Wilkinson JM, Stanley D: Posterior surgical approaches


    to the elbow: A comparative anatomic study. J Shoulder
    Elbow Surg 2001;10(4):380-382.

    18.

    Athwal GS, Rispoli DM, Steinmann SP: The anconeus


    flap transolecranon approach to the distal humerus.
    J Orthop Trauma 2006;20(4):282-285.

    19.

    Coles CP, Barei DP, Nork SE, Taitsman LA, Hanel DP,
    Bradford Henley M: The olecranon osteotomy: A sixyear experience in the treatment of intraarticular frac-

    8.

    9.

    336

    10.

    Beingessner DM, Dunning CE, Gordon KD, Johnson


    JA, King GJ: The effect of radial head fracture size on
    elbow kinematics and stability. J Orthop Res 2005;23:
    210-217.
    Lindenhovius AL, Felsch Q, Ring D, Kloen P: The longterm outcome of open reduction and internal fixation of
    stable displaced isolated partial articular fractures of the
    radial head. J Trauma 2009;67(1):143-146.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 26: Elbow and Forearm Trauma

    tures of the distal humerus. J Orthop Trauma 2006;


    20(3):164-171.
    20.

    Doornberg JN, van Duijn PJ, Linzel D, et al: Surgical


    treatment of intra-articular fractures of the distal part of
    the humerus: Functional outcome after twelve to thirty
    years. J Bone Joint Surg Am 2007;89(7):1524-1532.

    Gofton WT, Macdermid JC, Patterson SD, Faber KJ,


    King GJ: Functional outcome of AO type C distal humeral fractures. J Hand Surg Am 2003;28(2):294-308.

    26.

    Greiner S, Haas NP, Bail HJ: Outcome after open reduction and angular stable internal fixation for supraintercondylar fractures of the distal humerus: Preliminary results with the LCP distal humerus system. Arch
    Orthop Trauma Surg 2008;128(7):723-729.
    This study evaluated the surgical reposition, fracture
    healing, pain, function, and patient satisfaction after
    open reduction with an angular stable fixation. Anatomically preshaped, angular stable implants facilitate
    surgical reduction and stabilization of the fracture and
    may allow early postoperative rehabilitation. Clinical
    and radiological results are promising, with good range
    of motion and flexion and extension force.

    27.

    Athwal GS, Hoxie SC, Rispoli DM, Steinmann SP: Precontoured parallel plate fixation of AO/OTA type C distal humerus fractures. J Orthop Trauma 2009;23(8):
    575-580.
    This study reports on the clinical effectiveness of precontoured parallel plating for the management of Orthopaedic Trauma Association type C distal humerus
    fractures and provides support for prior reports of the
    successful use of parallel plating techniques. The complication rate of 53% in procedures performed by experienced surgeons highlights the complexity of these fractures. Preoperative patient counseling is paramount.

    28.

    Mller LP, Kamineni S, Rommens PM, Morrey BF: Primary total elbow replacement for fractures of the distal
    humerus. Oper Orthop Traumatol 2005;17(2):119-142.

    29.

    Athwal GS, Goetz TJ, Pollock JW, Faber KJ: Prosthetic


    replacement for distal humerus fractures. Orthop Clin
    North Am 2008;39(2):201-212, vi.
    This article focuses on the evaluation and management
    of distal humerus fractures with prosthetic replacements.

    30.

    Cil A, Veillette CJ, Sanchez-Sotelo J, Morrey BF: Linked


    elbow replacement: A salvage procedure for distal humeral nonunion. J Bone Joint Surg Am 2008;90(9):
    1939-1950.
    This article reports the long-term experience with linked
    semiconstrained total elbow arthroplasty as a salvage
    procedure for patients with distal humeral nonunion not
    amenable to internal fixation. The authors concluded
    that linked semiconstrained total elbow arthroplasty is a
    salvage procedure that can provide pain relief and restore motion and function in patients with a distal humeral nonunion that is not amenable to internal fixation.

    31.

    Kamineni S, Morrey BF: Distal humeral fractures


    treated with noncustom total elbow replacement.
    J Bone Joint Surg Am 2004;86(5):940-947.

    32.

    Frankle MA, Herscovici D Jr, DiPasquale TG, Vasey


    MB, Sanders RW: A comparison of open reduction and
    internal fixation and primary total elbow arthroplasty

    This investigation addressed the long-term clinical and


    radiographic results of surgical treatment of intraarticular distal humeral fractures (AO type C) as assessed with use of standardized outcome measures. The
    authors concluded that long-term results of open reduction and internal fixation of AO type C fractures of the
    distal part of the humerus are similar to those reported
    in the short term, suggesting that the results are durable.
    Functional ratings and perceived disability were predicated more on pain than on functional impairment and
    did not correlate with radiographic signs of arthrosis.
    21.

    Pollock JW, Faber KJ, Athwal GS: Distal humerus fractures. Orthop Clin North Am 2008;39(2):187-200, vi.
    This review article focused on the management of intraarticular fractures of the distal humerus. The surgical
    management of these cases using careful preoperative
    planning, adequate exposure, and stable fixation was
    emphasized.

    22.

    Sanchez-Sotelo J, Torchia ME, ODriscoll SW: Complex


    distal humeral fractures: Internal fixation with a
    principle-based parallel-plate technique. J Bone Joint
    Surg Am 2007;89(5):961-969.
    The goal of this study was to determine the outcome of
    treating complex distal humerus fractures with a
    principle-based technique that maximizes fixation in the
    articular fragments and stability at the supracondylar
    level. The study demonstrated that stable fixation and a
    high rate of union of complex distal humeral fractures
    can be achieved when a principle-based surgical technique that maximizes fixation in the distal segments and
    stability at the supracondylar level is used. The early
    stability achieved with this technique permits intensive
    rehabilitation to restore elbow motion.

    23.

    24.

    Ek ET, Goldwasser M, Bonomo AL: Functional outcome of complex intercondylar fractures of the distal
    humerus treated through a triceps-sparing approach.
    J Shoulder Elbow Surg 2008;17(3):441-446.
    This study aimed to review the functional outcome of
    complex intra-articular fractures of the distal humerus
    (AO/ASIF type C) managed with open reduction and internal fixation through a posterior triceps-sparing approach. All patients achieved good clinical scores as determined by the Mayo Clinic Performance Index.
    Quality of life assessment (SF-36) revealed no significant
    difference compared to the general population. The authors concluded that the posterior triceps-sparing approach provides adequate exposure to the fracture site
    and allows early rehabilitation.
    Huang TL, Chiu FY, Chuang TY, Chen TH: The results
    of open reduction and internal fixation in elderly patients with severe fractures of the distal humerus: A critical analysis of the results. J Trauma 2005;58(1):62-69.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    25.

    337

    Section 3: Upper Extremity

    onoid process of the ulna. J Bone Joint Surg Br 2009;


    91(5):632-635.
    A retrospective review 103 coronoid fractures is presented. Coronoid fracture with associated injuries have
    a higher rate of complications and poorer results.

    in the treatment of intraarticular distal humerus fractures in women older than age 65. J Orthop Trauma
    2003;17(7):473-480.

    3: Upper Extremity

    33.

    34.

    Ablove RH, Moy OJ, Howard C, Peimer CA, SDoia S:


    Ulnar coronoid process anatomy: Possible implications
    for elbow instability. Clin Orthop Relat Res 2006;449:
    259-261.

    35.

    Closkey RF, Goode JR, Kirschenbaum D, Cody RP: The


    role of the coronoid process in elbow stability: A biomechanical analysis of axial loading. J Bone Joint Surg Am
    2000;82(12):1749-1753.

    36.

    Hull JR, Owen JR, Fern SE, Wayne JS, Boardman ND


    III: Role of the coronoid process in varus osteoarticular
    stability of the elbow. J Shoulder Elbow Surg 2005;
    14(4):441-446.

    37.

    Beingessner DM, Dunning CE, Stacpoole RA, Johnson


    JA, King GJ: The effect of coronoid fractures on elbow
    kinematics and stability. Clin Biomech (Bristol, Avon)
    2007;22(2):183-190.
    The authors report on a biomechanical study determining the effect of coronoid fractures on elbow kinematics
    and stability. Elbow kinematics are altered with increasing fracture size. Repair of type II and III coronoid fractures and LCL repair is recommended.

    38.

    338

    McKee MD, Veillette CJ, Hall JA, et al: A multicenter,


    prospective, randomized, controlled trial of open
    reduction-internal fixation versus total elbow arthroplasty for displaced intra-articular distal humeral fractures in elderly patients. J Shoulder Elbow Surg 2009;
    18(1):3-12.
    This paper reports the results of a prospective randomized controlled trial to compare functional outcomes,
    complications, and reoperation rates in elderly patients
    with displaced intra-articular, distal humeral fractures
    treated with open reduction and internal fixation
    (ORIF) or primary semiconstrained total elbow arthroplasty (TEA). Patients who underwent TEA had substantially better Mayo Elbow Performance Scores at 3
    months (83 versus 65, P = .01), 6 months (86 versus 68,
    P = .003), 12 months (88 versus 72, P = .007), and 2
    years (86 versus 73, P = .015) compared with the ORIF
    group. Patients who underwent TEA had significantly
    better Disabilities of the Arm, Shoulder and Hand(DASH) scores at 6 weeks (43 versus 77, P = .02) and 6
    months (31 versus 50, P = .01) but not at 12 months (32
    versus 47, P = .1) or 2 years (34 versus 38, P = .6). The
    mean flexion-extension arc was 107 (range, 42 -145)
    in the TEA group and 95 (range, 30-140) in the
    ORIF group (P = .19). Reoperation rates for TEA (3 of
    25, 12%) and ORIF (4 of 15, 27%) were not statistically different (P = .2). They concluded that TEA is a
    preferred alternative for ORIF in elderly patients with
    complex distal humeral fractures that are not amenable
    to stable fixation. Elderly patients have an increased
    baseline DASH score and appear to accommodate objective limitations in function with time.

    Adams JE, Hoskin TL, Morrey BF, Steinmann SP: Management and outcome of 103 acute fractures of the cor-

    Orthopaedic Knowledge Update 10

    39.

    Doornberg JN, van Duijn J, Ring D: Coronoid fracture


    height in terrible-triad injuries. J Hand Surg Am 2006;
    31(5):794-797.

    40.

    Doornberg JN, Ring D: Coronoid fracture patterns.


    J Hand Surg Am 2006;31(1):45-52.

    41.

    Beingessner DM, Stacpoole RA, Dunning CE, Johnson


    JA, King GJ: The effect of suture fixation of type I coronoid fractures on the kinematics and stability of the elbow with and without medial collateral ligament repair.
    J Shoulder Elbow Surg 2007;16(2):213-217.
    The authors of this biomechanical study examined the
    effect of type I coronoid fracture and ligament repair on
    elbow kinematics. MCL repair may be more important
    than fixation of type I coronoid fractures.

    42.

    Pollock JW, Pichora J, Brownhill J, et al: The influence


    of type II coronoid fractures, collateral ligament injuries, and surgical repair on the kinematics and stability
    of the elbow: An in vitro biomechanical study. J Shoulder Elbow Surg 2009;18(3):408-417.
    This biomechanical study examined elbow kinematics
    with type II coronoid fractures and ligament repair. Repair of type II coronoid fractures and ligament repair
    should be performed when possible to restore normal
    kinematics and care should be taken to prevent overtensioning of the ligament repair.

    43.

    Moon JG, Zobitz ME, An KN, ODriscoll SW: Optimal


    screw orientation for fixation of coronoid fractures.
    J Orthop Trauma 2009;23(4):277-280.
    Posteroanterior screw placement was biomechanically
    superior to anteroposterior screw placement in fixing
    coronoid fractures.

    44.

    Hausman MR, Klug RA, Qureshi S, Goldstein R, Parsons BO: Arthroscopically assisted coronoid fracture
    fixation: A preliminary report. Clin Orthop Relat Res
    2008;466(12):3147-3152.
    Four patients were treated with arthroscopically assisted
    reduction of a coronoid fracture. The patients had no
    recurrent instability and all had a functional arc of motion.

    45.

    Adams JE, Merten SM, Steinmann SP: Arthroscopicassisted treatment of coronoid fractures. Arthroscopy
    2007;23(10):1060-1065.
    In seven coronoid fractures treated arthroscopically, all
    achieved functional, pain-free motion.

    46.

    Ring D, Jupiter JB, Gulotta L: Articular fractures of the


    distal part of the humerus. J Bone Joint Surg Am 2003;
    85(2):232-238.

    47.

    Dubberley JH, Faber KJ, Macdermid JC, Patterson SD,

    2011 American Academy of Orthopaedic Surgeons

    Chapter 26: Elbow and Forearm Trauma

    experimental study of the osseous constraint. J Shoulder


    Elbow Surg 2003;12(3):287-292.

    King GJ: Outcome after open reduction and internal


    fixation of capitellar and trochlear fractures. J Bone
    Joint Surg Am 2006;88(1):46-54.
    48.

    49.

    Guitton TG, Doornberg JN, Raaymakers EL, Ring D,


    Kloen P: Fractures of the capitellum and trochlea.
    J Bone Joint Surg Am 2009;91(2):390-397.
    In 27 patients treated for capitellar/trochlea fractures
    who were followed for 1 year or longer, those with more
    complex fractures had worse results and a higher complication rate; however, results were durable over time.
    Veillette CJ, Steinmann SP: Olecranon fractures. Orthop
    Clin North Am 2008;39(2):229-236, vii.
    The treatment of olecranon fractures is summarized,
    with an emphasis on anatomic reduction and stable fixation using one of the many techniques available to surgeons.

    50.

    Morrey BF: Current concepts in the treatment of fractures of the radial head, the olecranon, and the coronoid. Instr Course Lect 1995;44:175-185.

    51.

    Droll KP, Perna P, Potter J, Harniman E, Schemitsch


    EH, McKee MD: Outcomes following plate fixation of
    fractures of both bones of the forearm in adults. J Bone
    Joint Surg Am 2007;89(12):2619-2624.
    In 30 patients treated with open reduction and internal
    fixation of a both-bone forearm fracture, anatomy and
    motion were restored; however, a moderate reduction in
    upper extremity strength was reported.

    52.

    53.

    Safran MR, Baillargeon D: Soft-tissue stabilizers of the


    elbow. J Shoulder Elbow Surg 2005;14(1, suppl S):
    179S-185S.
    de Haan J, Schep NW, Tuinebreijer WE, Patka P, den
    Hartog D: Simple elbow dislocations: A systematic review of the literature. Arch Orthop Trauma Surg 2010;
    130(2):241-249.
    The authors present a systematic review of the literature, with an overview of the management and outcome
    of simple elbow dislocations.

    55.

    ODriscoll SW, Morrey BF, Korinek S, An KN: Elbow


    subluxation and dislocation: A spectrum of instability.
    Clin Orthop Relat Res 1992;280:186-197.

    56.

    Deutch SR, Jensen SL, Olsen BS, Sneppen O: Elbow


    joint stability in relation to forced external rotation: An

    2011 American Academy of Orthopaedic Surgeons

    ODriscoll SW, Bell DF, Morrey BF: Posterolateral rotatory instability of the elbow. J Bone Joint Surg Am
    1991;73(3):440-446.

    58.

    McAdams TR, Masters GW, Srivastava S: The effect of


    arthroscopic sectioning of the lateral ligament complex
    of the elbow on posterolateral rotatory stability.
    J Shoulder Elbow Surg 2005;14(3):298-301.

    59.

    Dunning CE, Zarzour ZD, Patterson SD, Johnson JA,


    King GJ: Ligamentous stabilizers against posterolateral
    rotatory instability of the elbow. J Bone Joint Surg Am
    2001;83(12):1823-1828.

    60.

    Deutch SR, Jensen SL, Tyrdal S, Olsen BS, Sneppen O:


    Elbow joint stability following experimental osteoligamentous injury and reconstruction. J Shoulder Elbow
    Surg 2003;12(5):466-471.

    61.

    Josefsson PO, Gentz CF, Johnell O, Wendeberg B: Surgical versus non-surgical treatment of ligamentous injuries following dislocation of the elbow joint: A prospective randomized study. J Bone Joint Surg Am 1987;
    69(4):605-608.

    62.

    Maripuri SN, Debnath UK, Rao P, Mohanty K: Simple


    elbow dislocation among adults: A comparative study
    of two different methods of treatment. Injury 2007;
    38(11):1254-1258.
    Simple elbow dislocations treated with cast versus sling
    immobilization are compared. The authors advocate
    early mobilization of the elbow following a simple elbow dislocation.

    63.

    Duckworth AD, Kulijdian A, McKee MD, Ring D: Residual subluxation of the elbow after dislocation or
    fracture-dislocation: Treatment with active elbow exercises and avoidance of varus stress. J Shoulder Elbow
    Surg 2008;17(2):276-280.
    The authors describe their clinical experience with the
    drop sign and support that slight residual subluxation
    can reduce with active mobilization.

    64.

    Coonrad RW, Roush TF, Major NM, Basamania CJ:


    The drop sign, a radiographic warning sign of elbow instability. J Shoulder Elbow Surg 2005;14(3):312-317.

    65.

    Armstrong AD, Dunning CE, Faber KJ, Duck TR, Johnson JA, King GJ: Rehabilitation of the medial collateral
    ligament-deficient elbow: An in vitro biomechanical
    study. J Hand Surg Am 2000;25(6):1051-1057.

    66.

    Dunning CE, Zarzour ZD, Patterson SD, Johnson JA,


    King GJ: Muscle forces and pronation stabilize the lateral ligament deficient elbow. Clin Orthop Relat Res
    2001;388(388):118-124.

    67.

    McKee MD, Schemitsch EH, Sala MJ, Odriscoll SW:


    The pathoanatomy of lateral ligamentous disruption in

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    54.

    Lee YH, Lee SK, Chung MS, Baek GH, Gong HS, Kim
    KH: Interlocking contoured intramedullary nail fixation
    for selected diaphyseal fractures of the forearm in
    adults. J Bone Joint Surg Am 2008;90(9):1891-1898.
    Interlocking contoured intramedullary nail fixation of
    the radius and ulna was used to treat 27 patients with
    forearm fractures. A high rate of osseous consolidation
    was reported but a longer period of immobilization was
    required. The authors reported 81% excellent and 11%
    good results. This fixation technique should be considered in patients with soft-tissue defects.

    57.

    339

    Section 3: Upper Extremity

    triad injury. J Bone Joint Surg Am 2008;90(suppl 4):


    75-84.
    The authors describe an approach to terrible triad injuries involving the earlier consideration of external fixation.

    complex elbow instability. J Shoulder Elbow Surg 2003;


    12(4):391-396.
    68.

    69.

    70.

    Forthman C, Henket M, Ring DC: Elbow dislocation


    with intra-articular fracture: The results of operative
    treatment without repair of the medial collateral ligament. J Hand Surg Am 2007;32(8):1200-1209.
    In 34 complex elbow dislocations with coronoid and radial head fractures, the patients were treated with lateral
    ligament repair, without MCL repair. Thirty-two of 34
    elbows remained stable and averaged 120 of ulnohumeral motion. The authors concluded that MCL
    repair is not required. Level of evidence: IV.
    Fern SE, Owen JR, Ordyna NJ, Wayne JS, Boardman
    ND III: Complex varus elbow instability: A terrible
    triad model. J Shoulder Elbow Surg 2009;18(2):269274.
    Using a cadaver terrible triad model, the authors demonstrated that repair of a radial head and LCL injury,
    when associated with at least 50% coronoid bone loss,
    fails to restore varus stability of the elbow.

    71.

    Schneeberger AG, Sadowski MM, Jacob HA: Coronoid


    process and radial head as posterolateral rotatory stabilizers of the elbow. J Bone Joint Surg Am 2004;86(5):
    975-982.

    72.

    Ring D, Jupiter JB, Zilberfarb J: Posterior dislocation of


    the elbow with fractures of the radial head and coronoid . J Bone Joint Surg Am 2002;84:547-551.

    73.

    Pugh DM, Wild LM, Schemitsch EH, King GJ, McKee


    MD: Standard surgical protocol to treat elbow dislocations with radial head and coronoid fractures. J Bone
    Joint Surg Am 2004;86:1122-1130.

    74.

    McKee MD, Pugh DM, Wild LM, Schemitsch EH, King


    GJ: Standard surgical protocol to treat elbow dislocations with radial head and coronoid fractures: Surgical
    technique. J Bone Joint Surg Am 2005;87(pt 1, suppl 1):
    22-32.

    75.

    Winter M, Chuinard C, Cikes A, Pelegri C, Bronsard N,


    de Peretti F: Surgical management of elbow dislocation
    associated with non-reparable fractures of the radial
    head. Chir Main 2009;28(3):158-167.
    Thirteen patients treated with a standard surgical approach for a terrible triad injury had reliable and reproducible results.

    3: Upper Extremity

    340

    Jensen SL, Olsen BS, Tyrdal S, Sjbjerg JO, Sneppen O:


    Elbow joint laxity after experimental radial head excision and lateral collateral ligament rupture: Efficacy of
    prosthetic replacement and ligament repair. J Shoulder
    Elbow Surg 2005;14(1):78-84.

    76.

    Beingessner DM, Dunning CE, Gordon KD, Johnson


    JA, King GJ: The effect of radial head excision and arthroplasty on elbow kinematics and stability. J Bone
    Joint Surg Am 2004;86:1730-1739.

    77.

    Zeiders GJ, Patel MK: Management of unstable elbows


    following complex fracture-dislocations: The terrible

    Orthopaedic Knowledge Update 10

    78.

    Mazzocca AD, Cohen M, Berkson E, et al: The anatomy of the bicipital tuberosity and distal biceps tendon.
    J Shoulder Elbow Surg 2007;16(1):122-127.
    This anatomic study provides dimensions and describes
    the angular relationship of the radial head and styloid.

    79.

    Hutchinson HL, Gloystein D, Gillespie M: Distal biceps


    tendon insertion: An anatomic study. J Shoulder Elbow
    Surg 2008;17:342-346.
    This anatomic study quantifies the angular relationships
    of the distal biceps tendon.

    80.

    Kulshreshtha R, Singh R, Sinha J, Hall S: Anatomy of


    the distal biceps brachii tendon and its clinical relevance. Clin Orthop Relat Res 2007;456:117-120.
    The authors offer descriptive analysis of the distal biceps tendon anatomic insertion.

    81.

    Athwal GS, Steinmann SP, Rispoli DM: The distal biceps tendon: Footprint and relevant clinical anatomy.
    J Hand Surg Am 2007;32(8):1225-1229.
    This anatomic study showed that the short head of the
    distal biceps tendon has a consistent relationship to the
    lacertus fibrosus, which has implications for orienting
    the tendon during surgical repair.

    82.

    Chew ML, Giuffr BM: Disorders of the distal biceps


    brachii tendon. Radiographics 2005;25(5):1227-1237.

    83.

    Freeman CR, McCormick KR, Mahoney D, Baratz M,


    Lubahn JD: Nonoperative treatment of distal biceps
    tendon ruptures compared with a historical control
    group. J Bone Joint Surg Am 2009;91(10):2329-2334.
    Eighteen patients with 20 unrepaired distal biceps tendon ruptures were retrospectively assessed. The medial
    supination and elbow flexion strengths for the injured
    arm and contralateral arm were 63% and 93%, respectively. Nonsurgical treatment yielded modest reduction
    in supination strength.

    84.

    El-Hawary R, Macdermid JC, Faber KJ, Patterson SD,


    King GJ: Distal biceps tendon repair: Comparison of
    surgical techniques. J Hand Surg Am 2003;28(3):496502.

    85.

    Lemos SE, Ebramzedeh E, Kvitne RS: A new technique:


    In vitro suture anchor fixation has superior yield
    strength to bone tunnel fixation for distal biceps tendon
    repair. Am J Sports Med 2004;32(2):406-410.

    86.

    Krushinski EM, Brown JA, Murthi AM: Distal biceps


    tendon rupture: Biomechanical analysis of repair
    strength of the Bio-Tenodesis screw versus suture anchors. J Shoulder Elbow Surg 2007;16(2):218-223.
    The authors compared the strength and stiffness of distal biceps repairs using biotenodesis screw or suture an-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 26: Elbow and Forearm Trauma

    The authors reported that distal biceps repair using the


    Endobutton technique yielded good results in 26 patients.

    chor techniques in cadavers. The biotenodesis screw


    technique showed more initial pullout strength compared with suture anchors.
    87.

    Mazzocca AD, Burton KJ, Romeo AA, Santangelo S,


    Adams DA, Arciero RA: Biomechanical evaluation of 4
    techniques of distal biceps brachii tendon repair. Am J
    Sports Med 2007;35(2):252-258.

    91.

    John CK, Field LD, Weiss KS, Savoie FH III: Singleincision repair of acute distal biceps ruptures by use of
    suture anchors. J Shoulder Elbow Surg 2007;16(1):
    78-83.
    The authors of this study showed that the one-incision
    approach and fixation with suture anchors is a safe and
    effective method for distal biceps repair.

    92.

    Hartman MW, Merten SM, Steinmann SP: Mini-open


    2-incision technique for repair of distal biceps tendon
    ruptures. J Shoulder Elbow Surg 2007;16(5):616-620.
    Distal biceps tendon repair using the two-incision technique achieved good results in 33 patients.

    93.

    Patterson RW, Sharma J, Lawton JN, Evans PJ: Distal


    biceps tendon reconstruction with tendoachilles allograft: A modification of the endobutton technique utilizing an ACL reconstruction system. J Hand Surg Am
    2009;34(3):545-552.
    This article describes reconstruction of distal biceps injuries with tendo Achilles allograft, with the Endobutton technique for fixation.

    94.

    Wiley WB, Noble JS, Dulaney TD, Bell RH, Noble DD:
    Late reconstruction of chronic distal biceps tendon ruptures with a semitendinosus autograft technique.
    J Shoulder Elbow Surg 2006;15(4):440-444.

    In a biomechanical comparison of four techniques of


    distal biceps tendon repair, the Endobutton technique
    had the highest load to failure.
    88.

    Kettler M, Tingart MJ, Lunger J, Kuhn V: Reattachment of the distal tendon of biceps: Factors affecting the
    failure strength of the repair. J Bone Joint Surg Br 2008;
    90(1):103-106.
    The Endobutton-based method had the highest load-tofailure in a biomechanical comparison of distal biceps
    tendon repair techniques.

    89.

    Spang JT, Weinhold PS, Karas SG: A biomechanical


    comparison of EndoButton versus suture anchor repair
    of distal biceps tendon injuries. J Shoulder Elbow Surg
    2006;15(4):509-514.

    90.

    Peeters T, Ching-Soon NG, Jansen N, Sneyers C, Declercq G, Verstreken F: Functional outcome after repair
    of distal biceps tendon ruptures using the endobutton
    technique. J Shoulder Elbow Surg 2009;18(2):283-287.

    3: Upper Extremity

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    341

    Chapter 27

    Elbow Instability and


    Reconstruction
    Bradford O. Parsons, MD

    Matthew L. Ramsey, MD

    Arthritis

    Osteoarthritis
    Osteoarthritis of the elbow joint can occur primarily or
    secondary to trauma. Primary osteoarthritis usually occurs in middle-aged men who often have performed
    manual labor. In the early stages, nonsurgical management with nonsteroidal anti-inflammatory drugs, activity modification, and corticosteroid injections can be
    helpful. Arthroscopic dbridement and synovectomy,
    and dbridement or interpositional arthroplasty are
    generally recommended for younger, active patients
    who do not respond to nonsurgical management. For
    older and more sedentary patients, total elbow arthroplasty is considered the procedure of choice.
    A 2008 study reported on arthroscopic osteophyte
    resection and capsulectomy in 41 patients with primary
    osteoarthritis.1 At follow-up of more than 2 years, the
    authors identified significant improvements in flexion
    and extension, supination, and functional scores. Many
    patients (81%) reported good to excellent results with
    a significant decrease in pain; complications were rare.
    In a study with seven patients, the outcomes of treating osteochondral lesions in the elbow with autologous
    osteochondral transplantation were reported.2 The
    grafts were harvested from the lateral femoral condyle.
    Significant improvements occurred in pain and functional scores. Graft viability was confirmed in all patients with postoperative MRI.

    2011 American Academy of Orthopaedic Surgeons

    Inflammatory Arthritis
    The Larsen classification is generally used for the stratification of elbow joint involvement in rheumatoid arthritis (Figure 1). Surgical arthroscopy remains an important modality for treatment, especially when the
    inflammatory component is significant and the bony
    structures are relatively well preserved.
    In a study reviewing the use of either open or arthroscopic synovectomy in 58 rheumatoid elbows, no
    significant differences between the techniques were
    identified in elbows with a preoperative arc of flexion
    of less than 90.5 In patients with an elbow arc of motion greater than 90, arthroscopic synovectomy provided better function than the open approach.
    In patients with inflammatory changes with symptoms and dysfunction refractory to nonsurgical measures, semiconstrained total elbow arthroplasty remains
    a reliable method of treatment. A 2009 study compared
    complication rates between patients with and without
    rheumatoid arthritis who were treated with total elbow
    arthroplasty.6 Data from 3,617 patients were analyzed;
    888 patients were identified as having rheumatoid arthritis and the remainder were classified as nonrheumatic patients. Complication rates were low in both
    groups; however, there were more medical complications and longer hospital stays in the nonrheumatic
    group. The authors concluded that complications after
    total elbow arthroplasty were rare and nearly equivalent in rheumatoid and nonrheumatoid patients.
    In 49 patients age 40 years or younger treated with
    total elbow arthroplasty (6 bilateral procedures), 30
    patients had inflammatory arthritis and 19 had post-

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Dr. Parsons or an immediate family member serves as a


    paid consultant to or is an employee of Zimmer and has
    received research or institutional support from Zimmer.
    Dr. Ramsey or an immediate family member serves as a
    board member, owner, officer, or committee member of
    the Philadelphia Orthopaedic Society and Bucks Surgical
    Specialty Hospital; has received royalties from Zimmer
    Ascension; is a member of a speakers bureau or has
    made paid presentations on behalf of DePuy/Mitek;
    serves as a paid consultant to or is an employee of Zimmer Ascension; has received research or institutional
    support from Ortho-McNeil Janssen Scientific Affairs and
    Biomet; and has stock or stock options held in Johnson
    & Johnson, Norvartis, and Teva.

    A recent study reported on 11 patients younger than


    50 years who were treated with arthroscopic ulnohumeral arthroplasty for degenerative arthritis of the
    elbow after failed nonsurgical treatment.3 An allarthroscopic technique was used. It was concluded that
    the procedure resulted in significant short-term pain relief, restoration of motion, and improved function.
    In a recent radiographic study of arthritic elbows using CT scanning, a higher incidence of ulnohumeral osteophytes (95%) was identified compared with radiocapitellar joint osteophytes (59%).4 The study authors
    challenged the notion that osteoarthritis originates in
    the radiohumeral joint.

    343

    Section 3: Upper Extremity

    Figure 1

    Figure 2

    Larsen classification system for the rheumatoid elbow. A, Stage I: normal architecture and osteoporosis. Synovitis is
    present. B, Stage II: joint-space narrowing and intact joint architecture. Synovitis is present. C, Stage III: alteration
    of joint architecture. D, Stage IV, gross joint destruction and minimal synovitis. (Reproduced from Athwal GS, Faber
    KJ, King GJW: Elbow reconstruction, in Fischgrund JS, ed: Orthopaedic Knowledge Update 9. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2008, pp 333-342.)

    A progressive static splint is used to manage elbow stiffness. (Reproduced from Bruno RJ, Lee
    ML, Strauch RJ, Rosenwasser MP: Posttraumatic
    elbow stiffness: Evaluation and management. J
    Am Acad Orthop Surg 2002;10(2):106-116.)

    traumatic arthritis.7 During the recorded follow-up


    (minimum of 5 years), 12 of the elbows required a second surgical procedure. The rate of revision was higher
    for patients with posttraumatic arthritis.

    Stiffness

    3: Upper Extremity

    Loss of motion after injury or elbow surgery can lead


    to significant functional disability. Although the exact
    cause of the development of elbow contracture remains
    unclear, several factors have been theorized to contribute to this disorder, including the high degree of congruity of the elbow joint, its propensity for developing
    heterotopic bone, cocontraction of the periarticular
    muscle groups, and irritability of the ulnar nerve.
    Treatment of posttraumatic or postoperative elbow
    stiffness can be unreliable. As a result, prevention with
    range-of-motion exercises and other modalities, including static progressive splinting, is critical in managing
    these patients (Figure 2). Any injury that does not require surgical treatment (for example, nondisplaced radial head fractures) should be treated with an early
    range-of-motion program. Injuries that require surgical
    treatment should be fixed in a stable manner so that the
    344

    Orthopaedic Knowledge Update 10

    rehabilitation process can begin a few days following


    the surgical procedure.
    If nonsurgical management fails to restore mobility,
    arthroscopic or open contracture release can restore
    motion in patients with dysfunction. Arthroscopic release is generally reserved for patients with mild contractures, whereas open releases are performed in patients with severe stiffness, a significant amount of
    heterotopic bone, or those with ankylosis. Manipulation under anesthesia is commonly performed in the
    knee for treating stiffness following total knee arthroplasty. In 51 patients treated with manipulation under
    anesthesia for contracture release of a stiff elbow an average of 40 days after surgery, the mean postmanipulation arc of motion increased to 78 from 40 preoperatively.8 The authors concluded that manipulation under
    anesthesia is a safe and valuable adjunct in the treatment of elbow stiffness.
    Continuous passive motion (CPM) after elbow contracture release has been used to maintain motion in
    the early postoperative period. CPM after open contracture release in two matched cohorts of 16 patients
    was evaluated in a 2009 study. The preoperative arc of
    motion (flexion and extension) averaged 38 in the
    CPM group and 42 in the group with no CPM.9 The
    improvement and the final arc of motion between both
    groups were comparable, differing by 5. The authors
    concluded that there was no demonstrable benefit of
    postoperative CPM after open contracture release.

    Elbow Instability
    The elbow joint is stabilized by a combination of static
    and dynamic constraints. The static stabilizers are divided between a set of primary and secondary stabilizers. The primary stabilizers of the elbow include the ulnohumeral articulation (coronoid process), the medial
    collateral ligament (MCL), and the lateral collateral ligament (LCL) complex. The secondary stabilizers include the radiocapitellar articulation and the common
    flexor and extensor origins. The anterior capsule also

    2011 American Academy of Orthopaedic Surgeons

    Chapter 27: Elbow Instability and Reconstruction

    Figure 3

    Axial view of fracture of the tip of the coronoid


    process seen in conjunction with recurrent instability patterns of the elbow. (Reproduced from
    ODriscoll SW, Jupiter JB, Cohen MS, Ring D,
    McKee MD: Difficult elbow fractures: Pearls
    and pitfalls. Instr Course Lect 2003;52:113-134.)

    contributes to the stability of the elbow as an anterior


    restraint, especially in terminal extension. Further stability is conferred by the action of the muscles spanning
    the elbow, including the brachialis, triceps, and anconeus, which impart compressive forces across the
    joint. Traumatic injury to any single primary stabilizer
    may lead to elbow instability, with most injuries involving a spectrum of pathology.
    In addition to acute instability, a variety of recurrent
    instability patterns of the elbow have been described,
    including posterolateral rotatory instability, varus posteromedial rotatory instability, and valgus instability.
    Chronic dislocation or failed management of complex
    instability may also occur, although more rarely.

    Recurrent Instability

    Posterolateral Rotatory Instability


    The most common etiology of symptomatic recurrent
    instability occurs following injury to the LCL, specifically the lateral ulnar collateral ligament (LUCL) complex, resulting in posterolateral rotatory instability.10
    This condition describes a sequence of instability that
    occurs with supination, axial loading, valgus stress, and
    extension of the elbow, resulting in subluxation of the

    2011 American Academy of Orthopaedic Surgeons

    Illustration of the pivot-shift test. See text for


    description of the test. (Reproduced with permission from Morrey BF: The Elbow and Its Disorders. Philadelphia, PA, WB Saunders, 2000.)

    radial head posterior to the capitellum, and rotation of


    the semilunar notch away from the trochlea. Most
    commonly, posterolateral rotatory instability occurs
    following traumatic injury (elbow dislocation), which
    can result in an attenuated LUCL complex. Other etiologies also have been described, including iatrogenic injury during lateral elbow procedures, such as lateral
    epicondylitis release, or from progressive ligament attenuation secondary to chronic cubitus varus malunion.
    Most patients with posterolateral rotatory instability
    report pain and occasional catching or clunking
    sensations, often when pushing off from the arm of a
    chair. The lateral pivot-shift test has been shown to be a
    provocative test that can identify posterolateral rotatory instability, although it can be difficult to perform
    in an awake patient because of apprehension and
    guarding (Figure 4). This test is often more reliable in
    an anesthetized patient. The test is performed with the
    arm flexed over the head of a supine patient. The forearm is supinated, elbow extended, and a valgus load is
    placed across the elbow. In this position the elbow is
    subluxated. As the elbow is slowly flexed, maintaining
    a supinated forearm and valgus load, the radial head
    will reduce, often with a clunk (in an anesthetized patient), confirming LCL insufficiency. When performed
    under fluoroscopy, the radial head can be visualized
    posterior to the capitellum on lateral imaging when the
    elbow is extended. Additionally, the ulnohumeral joint
    can appear widened; both the radiocapitellar and ulnohumeral joint congruencies are restored to normal
    with elbow flexion.
    More recently, other diagnostic tests have been described, including the tabletop relocation test,11 chair
    push-up test, and floor push-up test.12 All of these tests
    mimic the subluxating force associated with posterolateral rotatory instability, involving active extension of
    the elbow with the forearm supinated and the hand on
    a platform (either the floor, table, or armchair). In all

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Recurrent instability of the elbow is rare and often subtle, with most patients describing pain as the primary
    symptom. A history of recurrent dislocation is extremely rare. As such, a high index of suspicion is required to diagnose this condition because static imaging studies may appear normal and physical
    examination findings may be limited by pain and
    guarding. Three pathologic entities of recurrent instability have been described: posterolateral rotatory instability, varus posteromedial rotatory instability, and
    valgus instability. A new classification of fractures of
    the coronoid process has furthered the understanding
    of the role of this structure in these instability patterns
    (Figure 3).

    Figure 4

    345

    Section 3: Upper Extremity

    Figure 5

    Illustration of the location of the isometric point


    of the origin of the LUCL on the lateral aspect
    of the capitellum. Docking hole placement requires the hole to be centered slightly posterior
    and proximal to the isometric point to keep the
    ligament graft tensioned in extension. (Reproduced from Armstrong AD: Acute, recurrent,
    and chronic elbow instability, in Galatz LM, ed:
    Orthopaedic Knowledge Update: Shoulder and
    Elbow 3. Rosemont, IL, American Academy of
    Orthopaedic Surgeons, 2008, pp 461-476.)

    3: Upper Extremity

    tests, a positive finding is indicated by patient apprehension or a report of pain with elbow extension. Similar to a relocation test for anterior shoulder instability,
    in the tabletop relocation test the examiner places their
    thumb over the radial head and posterolateral gutter of
    the elbow to prevent instability; this minimizes the patients symptoms. These tests are reliable and reproducible in an awake patient.
    Standard imaging studies are often of little value in
    evaluating posterolateral rotatory instability. Static radiographs are often normal. Although MRI can identify
    acute avulsion of the origin of the LUCL from the lateral humerus, as seen in acute instability, in recurrent
    instability the LUCL is often attenuated, and MRI may
    not be helpful. Fluoroscopic evaluation during a pivot
    shift test or other provocative test may demonstrate
    subluxation of the radial head posterior to the capitellum.
    The management of symptomatic, recurrent posterolateral rotatory instability most often involves reconstruction of the LUCL complex, using either autograft
    or allograft. Repair of the LUCL in patients with recurrent elbow instability yields inferior results to reconstruction with tendon graft, often because of attenuation of the native ligament tissue.13 However, repair has
    been successfully performed for acute instability, both
    with open, or more recently, arthroscopic techniques.14
    A variety of reconstruction techniques have been described, with the original technique using tendon graft
    placed through a tunnel in the supinator crest of the
    346

    Orthopaedic Knowledge Update 10

    ulna and then weaved in a figure-of-8 fashion through


    a Y tunnel configuration in the humerus, with the
    graft tied to itself over the lateral column.10 Conversely,
    the graft may be docked on the humeral side with sutures exiting the Y tunnels and tied over the column,
    or a single-strand graft can be docked on both the ulnar
    and humeral side with interference screws or sutures
    through bone tunnels.15 Reconstruction techniques using lateral triceps tissue also have been described.16,17
    Regardless of the technique, the critical aspect of repair and reconstruction remains the reestablishment of
    the isometric origin of the LUCL on the lateral aspect
    of the capitellum. The isometric point is the exact center of rotation of the joint, which is located in the center of the lateral face of the hemisphere of the capitellum (Figure 5). An important technical aspect of tunnel
    placement is to establish the humeral tunnel so that the
    distal corner of the tunnel is at the isometric point, not
    the center of the tunnel, ensuring appropriate tension.
    The graft is secured with the arm in neutral rotation
    and 45 of flexion. Postoperatively, patients are protected from varus stress across the elbow and shoulder
    abduction is avoided; early range-of-motion therapy is
    started.
    Intermediate results of the surgical management of
    posterolateral rotatory instability have recently been
    described in 45 patients, with 12 repairs and 33 reconstructions with tendon graft.13 Eighty-six percent of patients were subjectively satisfied, with better results observed in patients with a posttraumatic etiology and
    those treated with elbow reconstruction. Patients with
    primary reports of instability had better outcomes than
    those who reported pain.
    Varus Posteromedial Rotatory Instability
    More recent attention has focused on fractures involving the anteromedial facet of the coronoid, resulting in
    a complex pattern of instability termed varus posteromedial rotatory instability. This type of instability develops as a result of injury to the anteromedial facet of
    the coronoid and rupture of the LCL complex. In this
    setting, a varus force fractures the anteromedial facet of
    the coronoid with rupture of the LCL, leading to subluxation of the ulnohumeral joint into the defect created by the anteromedial coronoid fracture.18-21 As a result, fracture to the anteromedial facet can be subtle
    but can lead to significant ulnohumeral instability. An
    important aspect of anteromedial facet injuries in relationship to elbow stability is the involvement of the
    sublime tubercle, which is the insertion point of the anterior bundle of the MCL.
    The mechanism of injury is different from the valgus
    stress to an axially loaded and supinated forearm that
    is involved in posterolateral rotatory instability. In posteromedial rotatory instability, the radial head does not
    impact the capitellum, as occurs in most fracturedislocations of the elbow; therefore, the radial head is
    often spared. Repair of posteromedial rotatory instability requires both a medial and lateral approach that
    fixes the coronoid fragment and repairs the LCL com-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 27: Elbow Instability and Reconstruction

    Figure 6

    Three-dimensional CT scan of an anteromedial


    coronoid fracture. The arrow indicates the fracture fragment. (Reproduced from Steinmann SP:
    Coronoid process fracture. J Am Acad Orthop
    Surg 2008;16(9):519-529.)

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    plex. In a biomechanical study, it has been shown that


    it may be possible for small subtype I anteromedial coronoid fractures to be managed with isolated repair of
    the LCL if the MCL is intact.22
    To identify posteromedial rotatory instability, a high
    index of suspicion is required because elbow radiographs may appear relatively normal on AP and lateral
    views. Some radiographic clues may include a double
    density of the coronoid subchondral plate on lateral
    images, or a narrowing of the anteromedial ulnohumeral joint space on AP images. Varus stress radiographs may highlight LCL insufficiency and show
    trochlear-coronoid contact. CT scans can help identify
    the anteromedial coronoid fracture and confirm the diagnosis (Figure 6).
    Although the diagnosis may be difficult, it is critical
    because nonsurgical treatment often results in persistent incongruity of the elbow, altered kinematics, and
    early arthrosis of the ulnohumeral joint.20,22 Surgical
    treatment is necessary to restore the coronoid architecture, often using an anteromedial buttress plate via a
    medial approach, followed by LCL isometric repair. At
    an average follow-up of 26 months, 18 patients with
    anteromedial facet fractures of the coronoid were evaluated.21 Six patients had varus subluxation of the elbow; four had not had fixation of the anteromedial
    facet and two had loss of fixation. Arthrosis developed
    in all six of these patients; results were fair to poor. The
    12 patients with secure fixation of the anteromedial
    facet fracture had good to excellent elbow function.
    Early range of motion is started after surgical repair.21 Anatomic repair and healing of the coronoid and
    LCL has yielded favorable results.20

    Valgus Instability
    Disruption of the MCL, specifically the anterior band
    of the MCL, can result in recurrent valgus instability of
    the elbow. MCL injuries may occur secondary to
    trauma (such as a dislocation) or as the result of repetitive stress (most commonly observed in throwing athletes). As opposed to lateral-sided instability, medial instability was historically believed to be well tolerated in
    most patients because little valgus load is placed across
    the elbow during the activities of daily living. Secondary stabilizers such as the radial head often minimize
    the severity of instability so that frank recurrent dislocation is rare. As such, findings of valgus instability
    may be subtle, and often can be confused with medial
    epicondylitis or an inflamed cubital tunnel.
    Most patients who report symptomatic valgus instability are overhead athletes, predominantly baseball
    players. The elbow is subjected to a high valgus load
    during the acceleration phase of throwing, placing tremendous stress on the anterior band of the MCL.
    Throwers may report experiencing a pop associated
    with a sudden drop in velocity following acute rupture
    of the anterior band of the MCL. However, some patients cannot identify any cardinal event and primarily
    report pain during throwing motion, or a loss of velocity or accuracy. Adding to the diagnostic difficulty,
    many throwers with anterior band MCL insufficiency
    also report posteromedial elbow pain resulting from
    posteromedial impingement of the olecranon during the
    deceleration phase of throwing, termed valgus extension overload.
    The physical examination centers on provocative
    testing of the MCL. Tenderness is often elicited over the
    MCL origin. Integrity of the flexor pronator mass is assessed, as is the ulnar nerve and cubital tunnel. Posteromedial tenderness over the olecranon may indicate valgus extension overload. A variety of provocative
    maneuvers have been described to identify MCL injury,
    including the valgus stress test, milking maneuver, and
    moving valgus stress test. Valgus stress testing is performed with the elbow in 30 flexion, unlocking the
    olecranon from the fossa. The milking maneuver is performed with the elbow in 90 flexion. With the examiner holding the patients ipsilateral thumb, a valgus
    stress is placed on the elbow with the forearm supinated. Pain at the MCL origin is considered a positive
    finding. More recently, a variant of the milking maneuver, the moving valgus stress test, was reported to be
    100% sensitive and 75% specific for MCL injury when
    compared with arthroscopic or open visualization of
    the ligament.23 In this maneuver, the arm is positioned
    in the same manner used in the milking maneuver, but
    the elbow is taken through a range of motion while a
    maximal valgus stress is applied across the joint. Reproducible pain in the medial elbow between 70 and
    120 is considered a positive test.
    Similar to posterolateral and posteromedial rotatory
    instability, static radiographs of patients with valgus instability are often normal. A posteromedial osteophyte
    of the olecranon in patients with valgus extension overload may be apparent on radiographs but is often sub347

    Section 3: Upper Extremity

    3: Upper Extremity

    tle. Valgus stress radiographs may show medial ulnohumeral joint widening, especially in posttraumatic
    valgus instability. MRI can be helpful in identifying
    acute ruptures of the anterior band of the MCL,
    chronic thickening associated with repetitive injury,
    and injury to the flexor-pronator origin.
    Patients with symptomatic valgus instability are initially managed nonsurgically, with therapy aimed at
    strengthening the flexor-pronator muscles, along with
    rest from throwing for a minimum of 6 weeks. Patients
    can resume throwing if symptoms abate, with careful
    attention placed on throwing mechanics. Nonsurgical
    treatment has been used with success in some throwing
    athletes, with 13 of 31 athletes (42%) returning to their
    preinjury level of sports activity at an average of 24
    weeks following rehabilitation and rest.24
    If nonsurgical treatment is unsuccessful, patients can
    be candidates for MCL reconstruction with tendon
    graft. Primary repair, as is the case in posterolateral rotatory instability, is often inferior to reconstruction in
    recurrent valgus instability, except in rare cases of early
    identification of acute avulsion injuries.25 Similar to
    LUCL reconstruction, a variety of reconstruction techniques for the anterior band of the MCL have been described, including figure-of-8 graft passage through the
    ulnar and humeral tunnels, docking techniques, and the
    use of fixation devices such as Endobuttons (Smith &
    Nephew, Memphis, TN) or interference screws with
    single- or double-strand tendon grafts.
    Recently, a biomechanical study evaluated four conventional reconstruction methods: figure-of-8 fixation,
    humeral docking, interference screw fixation, and
    single-strand Endobutton reconstruction. The humeral
    docking and Endobutton techniques were stronger than
    the figure-of-8 and interference screw fixation methods,
    although none were as strong as the native ligament.26
    Conversely, another biomechanical analysis found that
    interference screw fixation of the ulnar side, associated
    with humeral docking, yields graft fixation strength
    equal to 95% of that provided by the native MCL under valgus loading.27
    Conventional approaches use a flexor-pronator split
    rather than the original technique with reflection of the
    flexor mass off the epicondyle in an effort to preserve
    the role of the flexor group as a dynamic stabilizer of
    the medial elbow. Management of the ulnar nerve is
    dictated by the presence of preoperative ulnar nerve
    symptoms; routine transposition has been abandoned
    because of the potential for ulnar nerve irritation. Although not truly isometric, the anterior band of the
    MCL is nearly isometric, with the origin at the center
    of rotation of the medial aspect of the trochlea; humeral fixation should be placed at this site.26
    Results following reconstruction have been excellent, with most series reporting more than 90% of patients returning to preinjury levels of throwing and
    sports participation.28-30 Few clinical data are available
    to demonstrate the superiority of one technique over
    another.
    348

    Orthopaedic Knowledge Update 10

    Chronic Instability
    Chronic instability of the elbow is rare. Management of
    a chronic simple dislocation or the more common complex dislocation is challenging, with results inferior to
    those obtained following appropriate closed treatment
    or surgical management of an acute dislocation. Failed
    prior surgical stabilization, especially following complex instability, is the most common etiology of chronic
    instability and requires careful assessment of the osseous and ligamentous structures critical for elbow stability. In addition to the inherent ligamentous and osseous
    pathophysiology, articular derangement is often present, as are fibrous adhesions of the joint that fill the
    widened joint space of a chronically dislocated elbow.
    Heterotopic ossification, which may encase the neurovascular structures around the elbow, adds complexity
    to treating the disorder. The periarticular muscles, especially the triceps, are often contracted, potentially requiring lengthening or release. Most studies show that
    closed reduction of a chronically dislocated elbow is
    unlikely to achieve successful restoration of stability or
    function, especially after 3 to 4 weeks of being dislocated.31
    Surgical management is aimed at concentric reduction of the joint, with removal of any fibrous tissue or
    adhesions preventing reduction, ligament reconstruction, and triceps lengthening (when necessary). Chronic
    complex dislocations require restoration of the osseous
    constraints, especially the coronoid process. Unfortunately, coronoid insufficiency is frequently present after
    neglected or failed prior surgical stabilization of terrible
    triad injuries, and carries a guarded prognosis, especially when bone loss exceeds 50%. Reconstruction of
    coronoid bone loss is very challenging.32
    Hinged external fixation is often required when
    managing the chronically dislocated elbow, and has
    been used with success in limited series.33,34 When
    greater then 50% of the articular surface is damaged,
    interposition arthroplasty or prosthetic replacement is
    considered, depending on the patients physiologic age
    and activity level. Regardless of the reconstructive technique, patients should be aware of the potential goals
    of treatment, which are restoration of concentric reduction and a functional range of motion. Persistent pain
    and limitation of motion, especially in extension, often
    occur following successful management of this complex
    disorder.

    Annotated References
    1.

    Adams JE, Wolff LH III, Merten SM, Steinmann SP: Osteoarthritis of the elbow: Results of arthroscopic osteophyte resection and capsulectomy. J Shoulder Elbow
    Surg 2008;17(1):126-131.
    In this series the authors present the retrospective results
    of 41 patients who underwent arthroscopic osteophyte
    removal and capsulectomy. At minimum 2-year followup, total flexion improved from 117.3 to 131.6 and
    extension improved from 21.4 to 8.4. Overall the au-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 27: Elbow Instability and Reconstruction

    average follow-up of 91 months, 22% of elbows had


    undergone additional surgery, and 93% (51) were
    graded as good-excellent according to Mayo Elbow Performance Scores. The revision rate is higher in patients
    with a posttraumatic etiology.

    thors cited 81% good to excellent results according to


    Mayo Elbow Performance Scores.
    2.

    3.

    4.

    Ansah P, Vogt S, Ueblacker P, Martinek V, Woertler K,


    Imhoff AB: Osteochondral transplantation to treat osteochondral lesions in the elbow. J Bone Joint Surg Am
    2007;89(10):2188-2194.
    This series reviews the results of seven patients with osteochondral lesions of the elbow (five capitellar, one
    trochlea, and one radial head) who were managed with
    autologous lateral femoral condyle cylindrical osteochondral plugs. At an average follow-up of 59 months,
    Broberg-Morrey and pain scores were significantly improved and all grafts were viable and congruent on MRI
    scans.
    Krishnan SG, Harkins DC, Pennington SD, Harrison
    DK, Burkhead WZ: Arthroscopic ulnohumeral arthroplasty for degenerative arthritis of the elbow in patients
    under fifty years of age. J Shoulder Elbow Surg 2007;
    16(4):443-448.
    In their series of 11 patients younger than 50 years with
    symptomatic elbow osteoarthritis managed by arthroscopic ulnohumeral arthroplasty, the authors demonstrated an average improvement in arc of motion of
    73 and improved pain scores at minimum follow-up of
    2 years.
    Lim YW, van Riet RP, Mittal R, Bain GI: Pattern of osteophyte distribution in primary osteoarthritis of the elbow. J Shoulder Elbow Surg 2008;17(6):963-966.
    In a consecutive series of 22 patients with osteoarthritis
    of the elbow, 95% of patients demonstrated ulnohumeral osteophytes on three-dimensional CT scans.
    Conversely, radiohumeral osteophytes were observed in
    only 59% of patients.
    Tanaka N, Sakahashi H, Hirose K, Ishima T, Ishii S: Arthroscopic and open synovectomy of the elbow in rheumatoid arthritis. J Bone Joint Surg Am 2006;88(3):521525.

    6.

    Cook C, Hawkins R, Aldridge JM III, Tolan S, Krupp


    R, Bolognesi M: Comparison of perioperative complications in patients with and without rheumatoid arthritis
    who receive total elbow replacement. J Shoulder Elbow
    Surg 2009;18(1):21-26.
    Using data analyzed from the Nationwide Inpatient
    Sample database, the authors found that in 3,617 total
    elbow arthroplasties, overall complication rates were
    low and nearly equivalent between patients with rheumatoid arthritis (888 patients) compared to other diagnoses. Length of stay was longer in patients without
    rheumatoid arthritis.

    7.

    Celli A, Morrey BF: Total elbow arthroplasty in patients


    forty years of age or less. J Bone Joint Surg Am 2009;
    91(6):1414-1418.
    The authors retrospectively reviewed the results of 49
    patients (55 elbows) younger than 40 years with elbow
    arthritis managed with total elbow arthroplasty. Thirty
    patients had a diagnosis of inflammatory arthritis, and
    the remaining 19 patients, posttraumatic arthritis. At an

    2011 American Academy of Orthopaedic Surgeons

    Araghi A, Celli A, Adams R, Morrey B: The outcome of


    examination (manipulation) under anesthesia on the
    stiff elbow after surgical contracture release. J Shoulder
    Elbow Surg 2010;19(2):202-208.
    In a series of 44 patients with stiff postsurgical elbows,
    an examination (with manipulation) of the elbow under
    anesthesia at a mean postoperative date of 40 days
    yielded an improvement in arc of motion from 33 to
    73. Three patients had worsening of ulnar paresthesias,
    with one requiring ulnar nerve transposition.

    9.

    Lindenhovius AL, van de Luijtgaarden K, Ring D, Jupiter J: Open elbow contracture release: Postoperative
    management with and without continuous passive motion. J Hand Surg Am 2009;34(5):858-865.
    In a retrospective matched series of patients undergoing
    open contracture release of stiff elbows, outcomes were
    compared between 16 patients who underwent postoperative CPM compared with 16 control subjects. At final follow-up of 6 months, no difference was observed
    in flexion or extension motion between groups.

    10.

    ODriscoll SW, Bell DF, Morrey BF: Posterolateral rotatory instability of the elbow. J Bone Joint Surg Am
    1991;73(3):440-446.

    11.

    Arvind CH, Hargreaves DG: Tabletop relocation test: A


    new clinical test for posterolateral rotatory instability of
    the elbow. J Shoulder Elbow Surg 2006;15(6):707-708.

    12.

    Regan W, Lapner PC: Prospective evaluation of two diagnostic apprehension signs for posterolateral instability
    of the elbow. J Shoulder Elbow Surg 2006;15(3):344346.

    13.

    Sanchez-Sotelo J, Morrey BF, ODriscoll SW: Ligamentous repair and reconstruction for posterolateral rotatory instability of the elbow. J Bone Joint Surg Br 2005;
    87(1):54-61.

    14.

    Savoie FH III, Field LD, Gurley DJ: Arthroscopic and


    open radial ulnohumeral ligament reconstruction for
    posterolateral rotatory instability of the elbow. Hand
    Clin 2009;25(3):323-329.
    The authors report on a series of 54 patients with posterolateral rotatory instability of the elbow managed
    with open repair or reconstruction (30 patients) or arthroscopic repair (24 patients). The authors report improvement in Andrews-Carson scores of 145 to 180 at
    an average follow-up of 41 months. Acute repairs (10)
    demonstrated the best outcome, and no difference was
    observed between open and arthroscopic repairs. Level
    of evidence: IV.

    15.

    King GJ, Dunning CE, Zarzour ZD, Patterson SD,


    Johnson JA: Single-strand reconstruction of the lateral
    ulnar collateral ligament restores varus and posterolat-

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    5.

    8.

    349

    Section 3: Upper Extremity

    The authors report on a study of 11 collegiate athletes


    with acute rupture of the anterior band of the MCL. After MCL repair, 9 of 11 patients returned to college athletics. Level of evidence: IV.

    eral rotatory stability of the elbow. J Shoulder Elbow


    Surg 2002;11(1):60-64.
    16.

    3: Upper Extremity

    17.

    350

    DeLaMora SN, Hausman M: Lateral ulnar collateral


    ligament reconstruction using the lateral triceps fascia.
    Orthopedics 2002;25(9):909-912.
    Olsen BS, Sjbjerg JO: The treatment of recurrent posterolateral instability of the elbow. J Bone Joint Surg Br
    2003;85(3):342-346.

    18.

    ODriscoll SW, Jupiter JB, Cohen MS, Ring D, McKee


    MD: Difficult elbow fractures: Pearls and pitfalls. Instr
    Course Lect 2003;52:113-134.

    19.

    Sanchez-Sotelo J, ODriscoll SW, Morrey BF: Medial


    oblique compression fracture of the coronoid process of
    the ulna. J Shoulder Elbow Surg 2005;14(1):60-64.

    20.

    Ring D, Doornberg JN: Fracture of the anteromedial


    facet of the coronoid process: Surgical technique. J Bone
    Joint Surg Am 2007;89(suppl 2, pt 2):267-283.
    The authors evaluated 18 patients with anteromedial
    facet coronoid fracture and varus posteromedial rotatory instability. Early ulnohumeral arthrosis developed
    and a fair or poor outcome was reported in six patients
    with coronoid fracture malalignment. The remaining 12
    patients with anatomic coronoid healing had good or
    excellent elbow function. Level of evidence: III.

    21.

    Doornberg JN, Ring DC: Fracture of the anteromedial


    facet of the coronoid process. J Bone Joint Surg Am
    2006;88(10):2216-2224.

    22.

    Pollock JW, Brownhill J, Ferreira L, McDonald CP,


    Johnson J, King G: The effect of anteromedial facet
    fractures of the coronoid and lateral collateral ligament
    injury on elbow stability and kinematics. J Bone Joint
    Surg Am 2009;91(6):1448-1458.
    Using an in vitro cadaver model, the authors assessed
    the impact of the size of an anteromedial facet coronoid
    fracture on elbow stability and kinematics. Elbows with
    subtype I and repaired LCL demonstrated kinematics
    similar to an intact elbow. Subtype II and III fractures
    were unstable with varus and valgus stress.

    23.

    ODriscoll SW, Lawton RL, Smith AM: The moving


    valgus stress test for medial collateral ligament tears of
    the elbow. Am J Sports Med 2005;33(2):231-239.

    24.

    Rettig AC, Sherrill C, Snead DS, Mendler JC, Mieling P:


    Nonoperative treatment of ulnar collateral ligament injuries in throwing athletes. Am J Sports Med 2001;
    29(1):15-17.

    25.

    Richard MJ, Aldridge JM III, Wiesler ER, Ruch DS:


    Traumatic valgus instability of the elbow: Pathoanatomy and results of direct repair. J Bone Joint Surg Am
    2008;90(11):2416-2422.

    Orthopaedic Knowledge Update 10

    26.

    Armstrong AD, Ferreira LM, Dunning CE, Johnson JA,


    King GJ: The medial collateral ligament of the elbow is
    not isometric: An in vitro biomechanical study. Am J
    Sports Med 2004;32(1):85-90.

    27.

    Ahmad CS, Lee TQ, ElAttrache NS: Biomechanical


    evaluation of a new ulnar collateral ligament reconstruction technique with interference screw fixation. Am
    J Sports Med 2003;31(3):332-337.

    28.

    Thompson WH, Jobe FW, Yocum LA, Pink MM: Ulnar


    collateral ligament reconstruction in athletes: Musclesplitting approach without transposition of the ulnar
    nerve. J Shoulder Elbow Surg 2001;10(2):152-157.

    29.

    Dodson CC, Thomas A, Dines JS, Nho SJ, Williams RJ


    III, Altchek DW: Medial ulnar collateral ligament reconstruction of the elbow in throwing athletes. Am J
    Sports Med 2006;34(12):1926-1932.

    30.

    Dines JS, ElAttrache NS, Conway JE, Smith W, Ahmad


    CS: Clinical outcomes of the DANE TJ technique to
    treat ulnar collateral ligament insufficiency of the elbow.
    Am J Sports Med 2007;35(12):2039-2044.
    Following DANE TJ reconstruction of the ulnar collateral ligament of the elbow, 19 of 22 patients had excellent Conway scores at a mean follow-up of 36 months.
    Level of evidence: IV.

    31.

    Lyons RP, Armstrong A: Chronically unreduced elbow


    dislocations. Hand Clin 2008;24(1):91-103.
    The authors present a review of current options for
    treating a chronically dislocated elbow.

    32.

    Papandrea RF, Morrey BF, ODriscoll SW: Reconstruction for persistent instability of the elbow after coronoid
    fracture-dislocation. J Shoulder Elbow Surg 2007;16(1):
    68-77.
    At a minimum 2-year follow-up, 13 of 21 patients
    (62%) treated for chronic instability with associated
    coronoid fracture had successful objective outcomes.
    Eight patients had persistent elbow instability; 16 patients required hinged external fixation as part of their
    treatment. Level of evidence: IV.

    33.

    Jupiter JB, Ring D: Treatment of unreduced elbow dislocations with hinged external fixation. J Bone Joint
    Surg Am 2002;84(9):1630-1635.

    34.

    Ring D, Hannouche D, Jupiter JB: Surgical treatment of


    persistent dislocation or subluxation of the ulnohumeral
    joint after fracture-dislocation of the elbow. J Hand
    Surg Am 2004;29(3):470-480.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 28

    Hand and Wrist Trauma


    Virak Tan, MD

    Leonid I. Katolik, MD

    Fractures and Dislocations of the Hand


    Fractures and dislocations of the hand are common injuries occurring across the age spectrum. These injuries
    may be classified as irreducible, reducible-stable, and
    reducible-unstable. Reducible-stable injuries are typically best managed with immobilization. Irreducible or
    unstable injuries are best treated surgically. When possible, treatment should allow for early functional rehabilitation and should avoid periods of lengthy immobilization.

    Phalangeal Fractures

    Dr. Tan or an immediate family member has received


    royalties from Wright Medical Technology; serves as a
    paid consultant to or is an employee of Wright Medical
    Technology; and has stock or stock options held in
    Wright Medical Technology. Neither Dr. Katolik nor any
    immediate family member has received anything of
    value from or owns stock in a commercial company or
    institution related directly or indirectly to the subject or
    this chapter.

    2011 American Academy of Orthopaedic Surgeons

    Distal Interphalangeal Joint Injuries


    There is no consensus on the treatment of intraarticular injuries of the distal interphalangeal joint.
    Comminuted fractures can be treated with a short period of immobilization, followed by early active motion, which often reestablishes secondary congruity.
    Surgical reduction and stabilization, while yielding an
    aesthetically pleasing radiograph, often results in significant stiffness. Bony mallet injuries should almost universally be treated with immobilization. For large fragments, simple pin fixation or dorsal blocking pin
    fixation can be considered;4 however, splinting alone
    will also yield a satisfactory clinical outcome.

    Proximal Interphalangeal Joint Injuries

    3: Upper Extremity

    Distal phalanx fractures are common, are frequently


    associated with a nail bed injury, and can remain painful or sensitive long after fracture healing has occurred.
    Most of these fractures can be treated with splinting or
    compressive wrapping. Unstable transverse fractures or
    those associated with displaced injuries to the sterile
    matrix can be treated with supplemental longitudinal
    Kirschner wire (K-wire) fixation. If the nail bed is injured, consideration should be given to using fine absorbable sutures for the repair, with splinting of the
    fold with either the native nail plate or foil.
    The treatment of extra-articular fractures of the
    proximal and middle phalanges is predicated on restoring the bony anatomy, maintaining reduction until
    bony union, and achieving functional rehabilitation.
    Fracture stability depends more on the injury mechanism than on the fracture pattern. Injuries that are easily
    reducible and stable following reduction may be treated
    with immobilization and rehabilitation beginning 3 to
    4 weeks after injury. Traction splinting is an effective
    means of maintaining fracture reduction while allowing
    for early motion.1 High-energy injuries with marked
    angulation (> 10), malrotation ( 50% overlap of adjacent digit), shortening, comminution, and associated

    soft-tissue injuries are typically managed surgically.


    Multiple ipsilateral injuries are also typically treated
    surgically.
    The surgical treatment of extra-articular fractures of
    the proximal and middle phalanges must take into account the overlying soft tissues. Failure to do so may
    result in injury to the flexor or extensor apparatus and
    a stiff, dysfunctional finger. With open surgical approaches, meticulous soft-tissue handling and the use of
    soft-tissue sleeve approaches2 may minimize surgical
    trauma and the formation of postoperative adhesions.
    Further advancements in microplate design, plate materials, surface anodization, and the advent of microlocking technology may extend the safe application for
    open treatment of fractures while minimizing complications. The choice of fixation is largely dependent on the
    surgeons preference. A recent prospective randomized
    study found no difference in outcomes for surgically
    treated phalangeal fractures when K-wire and lag screw
    fixation were compared.3

    The proximal interphalangeal (PIP) joint is central to


    functional digital motion; injury to this joint can be
    challenging to treat and rehabilitate. Closed, simple dislocations are reduced under digital block anesthesia
    and tested for stability following reduction. If the joint
    requires less than 40 of flexion to maintain stability, a
    dorsal block splint is applied, and early active flexion is
    started. Long-term thickening of the PIP joint and residual stiffness are common sequelae.
    Hyperextension and axial loading injuries of the PIP
    joint often result in dorsal dislocation with varying degrees of fracture to the volar surface of the middle pha-

    Orthopaedic Knowledge Update 10

    351

    Section 3: Upper Extremity

    langeal base. Fractures comprising less than 30% of the


    joint surface can typically be stablized with dorsal
    block splinting alone. Fractures occupying 30% to
    50% of the joint have tenuous stability. If closed treatment is selected for these injuries, careful follow-up is
    essential to recognize recurrent instability. Fractures requiring more than 40 of PIP joint flexion to maintain
    stability or those involving more than 50% of the joint
    surface should be treated surgically.
    The ideal surgical procedure for unstable PIP joint
    fracture-dislocations has not been determined.5 Static
    dorsal block pinning is favored in some instances because it is simple and avoids a larger surgical exposure.
    It can be effective in acute settings when joint involvement is less than 40% and a dorsal block splint provides a poor fit. The joint must be concentrically reduced before pin application.
    Open reduction and internal fixation of the volar lip
    is effective if the fragment is large. Unfortunately, most
    PIP joint dislocations result in comminution of the
    volar lip. Dynamic external fixation is another option.
    When properly applied, it allows concentric joint motion and distraction throughout range of motion. Although fracture reduction may not be perfect, the applied traction stabilizes articular and metaphyseal
    comminution, allowing sufficient joint remodeling so
    that stable proximal phalangeal condylar containment
    is maintained.
    Volar plate arthroplasty advances the fibrocartilaginous volar plate into the defect left after resecting the
    comminuted and irreparable volar lip. Some surgeons
    have found this procedure to be durable, with high patient satisfaction in long-term follow-up.6 Success appears to be more favorable in acute (present 6 weeks)
    versus chronic injuries (present > 6 weeks).
    Hemihamate arthroplasty is an alternative to volar
    plate arthroplasty. It is based on reestablishing the anatomic concavity of the volar lip and is indicated for
    comminuted fractures involving 50% or more of the
    volar lip; these fractures are not amenable to fixation.
    Although technically difficult, hemihamate arthroplasty
    is useful in restoring a functional range of motion and
    long-term stability for severely injured joints. Acute injuries have a better rate of success than chronic cases.7

    Metacarpophalangeal Joint Injuries


    3: Upper Extremity

    Although many metacarpophalangeal (MCP) joint injuries are irreducible, dorsal dislocations of the MCP
    joint warrant an attempt at closed reduction. Irreducible dislocations generally result from the interposition
    of the volar plate in the joint and buttonholing of the
    metacarpal head between the flexor tendons and the radial lumbrical.
    Open reduction can be safely performed through a
    dorsal or volar approach. With the volar approach,
    great care must be taken to protect the digital nerves,
    which may be severely tented over the metacarpal head.
    The A1 pulley may be released to allow retraction of
    the flexor tendons. The volar plate is then incised longitudinally, allowing for reduction.
    352

    Orthopaedic Knowledge Update 10

    Injuries to the radial or ulnar collateral ligaments of


    the MCP joint are common, particularly involving the
    thumb. Immobilization is adequate to treat partial tears
    or nondisplaced avulsion fractures. Distinguishing partial from complete tears can be clinically difficult.
    Asymmetric laxity is an unreliable diagnostic finding
    given inherent side-to-side differences. The absence of a
    firm end point with stress testing or the presence of
    static subluxation should be used to predict the presence of a complete tear. Surgical repair may be performed using a variety of surgical techniques, including
    suture anchors, with no significant differences in outcomes reported between techniques.8
    Traditionally, acute injuries have been treated with
    primary repair and chronic injuries with tendon graft
    reconstruction. However, with the advent of microbone
    anchors, it appears that primary repair of some ligament injuries in a chronic setting may be satisfactorily
    performed.

    Metacarpal Fractures
    Metacarpal neck fractures may be treated nonsurgically
    with excellent functional outcomes for angulations of
    40 to 50 in the small finger, 30 in the ring finger, 20
    in the middle finger, and 10 in the index finger. Deformities exceeding these limits should be reduced. If open
    reduction is necessary, pinning across the fracture
    should be considered.
    Metacarpal shaft fractures may be grouped into
    three general categories: transverse, oblique, or comminuted. Transverse fractures are unstable but easily reducible. Some dorsal angulation is acceptable, but generally, dorsal angulation exceeding 30 for the small
    finger, 20 for the ring finger, and any dorsal angulation for the index and middle fingers should be treated
    surgically.
    Oblique fractures introduce the potential for shortening and rotational malalignment, which is poorly tolerated. Five degrees of malrotation can produce 1.5 cm
    of digital overlap. The presence of malrotation is a key
    indicator for surgical management. Comminuted fractures lack inherent stability and should be treated surgically.
    Surgical treatment is indicated in the presence of
    multiple fractures because of the loss of supporting architecture in the adjacent digits. It is also indicated for
    oblique fractures (especially those with multiple comminuted fractures) and in open fractures (especially
    those associated with significant soft-tissue injuries).
    Fractures should be surgically treated in polytrauma
    patients who cannot tolerate cast immobilization.
    A variety of percutaneous, interosseous, internal,
    and external fixation devices and techniques are available for metacarpal fracture fixation. Each option offers the surgeon relative advantages with respect to
    construct strength, ease of application, and cost. These
    factors should be evaluated by the surgeon when selecting the appropriate treatment. All options can afford
    excellent outcomes when properly applied.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 28: Hand and Wrist Trauma

    Carpometacarpal Joint Injuries


    Injuries to the carpometacarpal (CMC) joints are relatively uncommon. The metacarpals are very congruously seated onto the distal carpal row with stout volar,
    dorsal, and intermetacarpal ligament attachments. The
    CMC joints of the small and ring fingers act as a mobile hinge allowing flexion, extension, and rotation toward the thumb; this mobility predisposes those joints
    to injury more so than any of the other CMC joints. Although pure dislocation is possible, these injuries more
    commonly occur as fracture-dislocations with variable
    degrees of fracture through the hamate, metacarpal
    bases, or both. Closed reduction and percutaneous pining of the metacarpal base to its neighbor or to the carpus is frequently sufficient. If a large portion of the
    hamate has been avulsed, open reduction and screw or
    plate fixation may be performed.
    A Bennett fracture is an intra-articular fracture of the
    thumb metacarpal base involving avulsion of the thumb
    from the volar oblique ligament of the thumb CMC
    joint. Nonsurgical treatment is possible for the small
    number of these injuries that present with a congruent
    joint and minimal fracture step-off. In most instances,
    the adductor pollicis and the abductor pollicis longus
    act together to pull the metacarpal radially, proximally,
    and into supination, thereby causing subluxation of the
    joint. These injuries should be reduced with traction,
    extension, and pronation toward the small finger. Once
    reduced, the position can be held with K-wires to the index metacarpal or into the carpus. The volar oblique
    fragment does not necessarily need to be captured by
    the wires. If the fracture cannot be reduced by closed
    means, an open approach may afford better visualization. Although congruous reduction without articular
    step-off is the goal, no absolute agreement exists among
    surgeons regarding the acceptable limits of reduction
    and long-term functional implications.9
    A Rolando fracture is a pilon-type injury to the
    thumb CMC joint following axial loading. This splits
    the thumb into diaphyseal, radial, and ulnar articular
    fragments. Occasionally, the joint surface is fragmented. Rolando fractures should generally be treated
    closed with joint unloading by means of a miniexternal fixator and supplemental K-wire stabilization
    of larger fragments. As with Bennett fractures, joint
    congruity does not necessarily correlate with functional
    outcome.10

    Carpal Fractures and Nonunion


    Acute Fractures
    Fractures of a carpal bone are usually caused by a fall
    onto an outstretched hand or by a motor vehicle crash.
    Other causes include injuries caused by contact sports
    or a sudden impact to the palm, as can occur in baseball players or golfers. Carpal bone fractures account
    for 18% of hand fractures, with the bones of the proximal carpal row being the most frequently fractured.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Fractures and Dislocations of the Wrist

    These injuries may be difficult to see on plain radiographs and may require advanced imaging techniques
    (CT or MRI) to confirm the diagnosis.
    The location of the carpal bone fracture depends on
    the hand and wrist position at impact and the forces
    applied. The scaphoid is the most frequently fractured
    carpal bone, followed by the triquetrum and lunate.
    Scaphoid fractures account for up to 80% of all carpal
    fractures. Approximately 345,000 scaphoid fractures
    occur annually in the United States and most occur in
    younger individuals (15 to 60 years of age).11 Because
    the scaphoid is largely covered by cartilage and receives
    most of its blood supply in a retrograde manner, fractures of this bone are more prone to complications than
    fractures of the other carpal bones.
    In general, scaphoid fractures that are nondisplaced
    or minimally displaced (< 1 mm) can be treated by immobilization and have a union rate of approximately
    90%. There is no clear consensus on the type of immobilization needed, such as long arm versus short arm or
    thumb-spica versus nonspica immobilization. Over the
    past decade, there has been a trend toward surgical fixation of nondisplaced or minimally displaced waist
    fractures; however, a systematic literature review did
    not demonstrate better union rates, grip strength, wrist
    motion, patient satisfaction, or shorter return-to-work
    times after surgical fixation.12 One recent study showed
    that an evaluation of long-term outcomes indicated
    that surgical treatment seems to cause more complications and is associated with a higher risk of scaphotrapezial osteoarthritis based on radiographic findings.13
    Surgery is indicated for scaphoid fractures that are
    displaced, comminuted, located at the proximal pole,
    have an intrascaphoid angle greater than 35, or those
    associated with an ipsilateral distal fracture or perilunate dislocation. A cannulated, headless screw placed
    in the central axis appears to provide the most stability
    and avoids prominence. Open reduction can either be
    done through the volar or dorsal approach. The volar
    approach is preferred for distal pole and waist fractures, whereas the proximal pole is best accessed from
    the dorsal side. The blood supply is at risk with the
    dorsal approach. Indirect or arthroscopically assisted
    reduction has facilitated percutaneous screw fixation of
    displaced fractures.
    Most triquetral and lunate fractures are avulsion injuries of the dorsal capsule and are the bony equivalent
    of a wrist sprain. These fractures can be treated with immobilization for 4 to 6 weeks. Kienbck disease should
    be ruled out if a fracture line is seen in the coronal plane
    through the body of the lunate. Fractures of the hamate
    generally occur through the hook from a direct blow to
    the palm. Nondisplaced fractures can be treated with immobilization. Internal fixation or fragment excision can
    be considered for displaced hamate hook fractures.
    Symptomatic partial union or nonunion of the hook of
    the hamate is treated by excision. Grip strength has not
    been shown to be adversely affected by excision of the
    hook of the hamate in most clinical series; however, decreased strength with wrist extension and ulnar deviation has been suggested in a biomechanical study.14
    353

    Section 3: Upper Extremity

    Figure 1

    T1-weighted MRI scan with gadolinium intravenous contrast shows no enhancement of the
    proximal pole of the scaphoid, indicating osteonecrosis in a patient with a scaphoid nonunion. (Courtesy of Virak Tan, MD, Newark, NJ.)

    3: Upper Extremity

    Nonunion
    Risk factors for scaphoid nonunion include proximal
    pole fractures, delayed diagnosis and treatment, patient
    noncompliance, and comminution or displacement at
    the fracture site. MRI with intravenous contrast is used
    to assess the vascularity of the proximal pole (such as
    in cases of osteonecrosis) and the extent of arthritis
    (Figure 1). CT is helpful in determining scaphoid morphology, including any humpback deformity. The treatment of scaphoid nonunion is based on the location of
    the fracture, the presence of osteonecrosis, the amount
    of deformity/collapse, and the extent of arthrosis. Percutaneous screw fixation has been successful in treating
    selected nonunions without displacement, collapse, or
    osteonecrosis. In the presence of humpback deformity,
    structural autologous bone graft from the volar side
    and rigid fixation is necessary for healing. If there is osteonecrosis of the proximal pole, vascularized bone
    grafting should be considered. In long-standing, symptomatic nonunions with significant secondary wrist arthrosis (such as a scaphoid nonunion advanced collapse
    wrist), motion-sparing salvage procedures, such as
    proximal row carpectomy or four-corner fusion, are
    most appropriate.

    Carpal Instability
    In an uninjured wrist, the bones of the proximal carpal
    row act together as an intercalated segment to coordinate movements between the distal radius and ulna and
    the distal carpal row. It is believed that the scaphoid
    functions as a stabilizer of the midcarpal joint, acting
    as a bridge between the proximal and distal carpal
    rows. In the proximal row, the lunate is attached to the
    scaphoid through the U-shaped scapholunate interosseous ligament and to the triquetrum through the
    354

    Orthopaedic Knowledge Update 10

    Figure 2

    Radiographs of a scapholunate dissociation injury.


    A, PA view shows widening of the scapholunate
    interval and a signet ring of the scaphoid. B,
    Lateral view shows dorsal intercalated segment
    instability with a scapholunate angle of 90.
    (Courtesy of Virak Tan, MD, Newark, NJ.)

    C-shaped lunotriquetral interosseous ligament. The opposing forces acting through these interosseous ligaments hold the lunate in a balanced position. As the
    hand is radially deviated, the scaphoid flexes, causing
    the lunate and triquetrum to follow into flexion. With
    ulnar deviation, the reverse occurs and the proximal
    row goes into extension.
    Scapholunate Dissociation
    Injury to the scapholunate interosseous ligament is the
    most common form of wrist instability and can be dynamic or static. Disruption of the scapholunate interosseous ligament removes the scaphoid flexion moment from the lunate, allowing it to assume an
    extended position under the influence of the triquetrum. The scaphoid, in turn, falls into further flexion and supination, creating incongruity at the radioscaphoid facet. This condition is termed dorsal
    intercalated segment instability. It is generally believed
    that if the condition is left untreated, it will progress to
    carpal collapse and an arthritic (scapholunate advanced
    collapse) wrist.
    Most patients with scapholunate dissociation will report wrist pain or weakness with loading. Some patients will report a painful click or snapping sensation
    with motion. Examination will often reveal mild swelling in the scapholunate interval, which may be confused with a ganglion. The scaphoid shift test will often
    increase pain and may produce a clunk.
    Radiographs of a suspected scapholunate interosseous ligament injury should include PA views in neutral,
    along with clenched fist, ulnar deviation, and lateral
    views (Figure 2). Comparing radiographs of the injured
    and uninjured side may be helpful. Bone scintigraphy
    and plain film arthrography have largely been replaced

    2011 American Academy of Orthopaedic Surgeons

    Chapter 28: Hand and Wrist Trauma

    Table 1

    Treatment of Scapholunate Dissociation Based on the Garcia-Elias Classification of Stages


    Stage

    Description

    Treatment

    Partial scapholunate (or stretch) injury

    Arthroscopic dbridement
    K-wire stabilization

    Complete scapholunate ligament tear with repairable dorsal


    ligament

    Direct dorsal ligament repair ( dorsal


    capsulodesis)
    Dorsal capsulodesis

    Complete scapholunate tear with nonrepairable dorsal ligament


    but a normally aligned scaphoid

    Ligament reconstruction with tendon graft


    ( dorsal capsulodesis)
    Dorsal capsulodesis

    Complete scapholunate tear with nonrepairable tissue and a


    reducible rotatory subluxation of the scaphoid

    Ligament reconstruction with tendon graft


    ( dorsal capsulodesis)
    Dorsal capsulodesis

    Complete scapholunate tear with irreducible malalignment but


    no evidence of cartilage degeneration

    Partial carpal fusion

    Complete scapholunate tear with irreducible malalignment and


    cartilage degeneration

    Motion-preserving procedure (proximal row


    carpectomy [or four-corner fusion)
    Total wrist fusion

    because of their low specificity for ligamentous injuries.


    MRI and magnetic resonance and CT arthrography are
    the principal imaging techniques for diagnosing tears of
    the wrist ligaments. Recent studies reported CT arthrography to be more accurate than 1.5-tesla (T) MRI
    and magnetic resonance arthrography for detecting
    tears of the scapholunate and lunotriquetral ligaments.
    In general, there is improvement in the diagnostic capability and quality of 3.0-T MRI compared with 1.5-T
    MRI;15 however, arthroscopy remains the gold standard
    for diagnosis.
    The treatment of scapholunate instability continues
    to be an ongoing challenge for hand surgeons because
    outcomes have been inconsistent. Partial tears can be
    managed with immobilization or arthroscopic dbridement. Complete ligament disruption requires reduction
    and pinning, and primary dorsal ligament repair or ligament reconstruction. The authors of a 2006 study
    proposed six stages of scapholunate dissociation and
    described a treatment algorithm based on these stages16
    (Table 1).

    2011 American Academy of Orthopaedic Surgeons

    Lunate and Perilunate Dislocations


    Lunate and perilunate instability patterns are uncommon and represent injuries from high-energy trauma.
    The common defining feature is capitate dislocation
    from the distal articulation of the lunate. In lunate dislocation, the lunate is completely displaced from its
    fossa (and capitate) and comes to rest volar to the distal
    radius (Figure 3, A). In a perilunate dislocation, the relationship between the distal radius and lunate is maintained, but the capitate assumes a position dorsal to the
    lunate (Figure 3, B). Variations in this injury spectrum
    can involve a pure ligamentous disruption around the
    lunate (lesser arc injury) or a combination of bony and
    ligamentous structures (greater arc injury).
    Young men are most prone to these injuries and often have associated injuries that may require more urgent attention. Closed reduction should be attempted
    for acute dislocations to prevent median nerve compression. Patients with progressive median nerve symptoms should be treated with a carpal tunnel release; direct digital pressure on the lunate (through an extended
    carpal tunnel incision) should readily reduce the dislocation. Definitive treatment requires open repair of the
    scapholunate interosseous ligament (some surgeons
    also repair the lunotriquetral interosseous ligament)

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Lunotriquetral Dissociation
    Lunotriquetral interosseous ligament tears usually occur in combination with other intercarpal or radiocarpal ligament injuries, such as lunate or perilunate dislocations. Isolated injuries have been reported from a fall
    on a pronated, extended, and radially deviated hand or
    with the wrist in flexion. Provocative maneuvers, such
    as the ballottement maneuver, and shuck and shear
    tests may be positive. Radiographs may show evidence
    of carpal instability with flexion of the lunate (such as
    the volar intercalated segmental instability pattern).
    Magnetic resonance arthrography may show a dye leak
    at the lunotriquetral joint; however, similar to other
    soft-tissue injuries about the wrist, arthroscopy remains

    the best method for assessing the tear. Immobilization


    is used to treat stable lunotriquetral ligament tears.
    Midcarpal corticosteroid injection or arthroscopic dbridement of the lunotriquetral interosseous ligament
    may be considered for patients with persistent symptoms and normal carpal alignment. The treatment of an
    unstable lunotriquetral ligament can range from pinning the joint to direct repair or reconstruction of the
    ligament to limited fusions with the goal of correcting
    rotational malalignment of the proximal carpal row.

    355

    Section 3: Upper Extremity

    Figure 3

    A, Lateral radiograph of a wrist with lunate


    dislocation. The lunate is completely displaced
    from the fossa and is volar to the remainder of
    the carpus and distal radius. B, Lateral radiograph of a wrist with perilunate dislocation. The
    lunate remains in contact with the lunate fossa
    of the distal radius but the capitate is dislocated
    from the lunate and is sitting dorsal to the lunate. (Courtesy of Virak Tan, MD, Newark, NJ.)

    with intercarpal K-wire fixation. Surgical exposure for


    this injury can be through a single dorsal incision or a
    combined volar-dorsal approach. Great arc injuries are
    treated with fracture fixation and suture augmentation
    of the ligaments if they are ruptured or attenuated.
    Poor results can be expected after open injury or delayed treatment, and a primary proximal row carpectomy should be considered.

    Distal Radius Fractures

    3: Upper Extremity

    Distal radius fractures are the most common fractures


    of the upper limb and account for approximately 20%
    of all fractures. A large percentage of these injuries occur in older women with osteoporosis. Despite the myriad of treatment options, restoration of painless function of the injured wrist remains the ultimate goal.
    Plain radiographs (PA, true, fossa lateral, and oblique
    views) are usually sufficient to assess the initial displacement, angulation, and articular involvement. A
    CT scan, if needed, may be helpful in delineating the
    extent of articular disruption.
    The management of distal radius fractures should be
    individualized on the basis of the fracture pattern, degree of displacement, other associated injuries, the patients activity level, and the surgeons experience and
    preference. Despite the enthusiasm for internal fixation,
    closed reduction and immobilization should be attempted for most distal radius fractures that have minimal metaphyseal comminution and articular incongruity. Surgery is generally indicated for fractures that are
    open, unstable, have 2 mm or more of articular displacement, or those that are a part of a multitraumatic
    injury. The advantage of closed reduction and casting
    of distal radius fractures is its nonsurgical nature; how356

    Orthopaedic Knowledge Update 10

    ever, there is a known risk of secondary displacement


    (up to 89% in patients older than 65 years) as seen on
    radiographs.17 Predictors for redisplacement include increasing age, metaphyseal comminution, and shortening at presentation.17,18 In older patients, some degree
    of malalignment of the distal radius is well tolerated.
    Several studies found no relationship between anatomic
    position at healing and functional outcomes.19,20
    The surgical treatment of distal radius fractures has
    become commonplace, although conclusive scientific
    evidence of improved patient outcomes is lacking. Surgical fixation is typically recommended for fractures
    with postreduction radial shortening of more than 3
    mm, dorsal tilt greater than 10, or intra-articular displacement of more than 2 mm.21 The following conclusions can be reached from the literature on distal radius
    fractures.22 (1) Closed management or percutaneous
    pinning alone has worse radiographic outcomes than
    external fixation augmented with percutaneous pins.
    (2) Internal fixation yields radiographic and clinical results that are at least comparable with augmented external fixation. (3) Because internal fixation produces
    radiographic results comparable to external fixation,
    internal fixation can be expected to provide radiographic results that are better than those of casting or
    percutaneous pinning.
    The trend in surgical fixation is away from percutaneous pinning and external fixation, and toward internal fixation. Advocates of internal fixation suggest that
    fractures of the distal radius, like other periarticular
    fractures, are best treated by internal fixation that is
    sufficiently stable to allow immediate active motion of
    the wrist while maintaining alignment. Internal fixation, especially with volar fixed-angle locking plates, is
    seemingly the preferred treatment for most displaced or
    unstable distal radius fractures. Currently, there are
    more than 30 implant designs available worldwide. Although the use of volar plates and low-profile dorsal
    plates may decrease complications related to hardware
    prominence, these implants do not entirely eliminate
    complications. Additionally, there also has been an increased focus on contracture of the pronator quadratus
    as a cause of limited forearm rotation after fixation
    with a volar plate. Although locked plating is an acceptable form of treatment of distal radial fractures, it
    should be realized that data are lacking indicating clear
    superiority of one treatment modality over another.
    The American Academy of Orthopaedic Surgeons
    work group on the treatment of distal radius fractures
    has summarized the clinical practice guidelines for
    treating distal radius fractures21 (Table 2).

    Distal Radioulnar Joint


    The ulnar side of the wrist contains important anatomic structures that contribute to stability yet allow
    for motion of the distal radioulnar joint (DRUJ). The
    prime stabilizers of the DRUJ are the dorsal and volar
    radioulnar ligaments and the triangular fibrocartilage.
    The diagnosis of instability can be made with plain radiographs, although dynamic CT with contralateral

    2011 American Academy of Orthopaedic Surgeons

    Chapter 28: Hand and Wrist Trauma

    Table 2

    AAOS Clinical Practice Guideline on the Treatment of Distal Radius Fractures


    Strength of
    Recommendation

    Recommendation
    We are unable to recommend for or against performing nerve decompression when nerve
    dysfunction persists after reduction.

    Inconclusive

    We are unable to recommend for or against casting as definitive treatment for unstable
    fractures that are initially adequately reduced.

    Inconclusive

    We suggest surgical fixation for fractures with postreduction radial shortening > 3 mm, dorsal Moderate
    tilt > 10, or intra-articular displacement or step-off > 2 mm as opposed to cast fixation.
    We are unable to recommend for or against any one specific surgical method for fixation of
    distal radius fractures.

    Inconclusive

    We are unable to recommend for or against surgical treatment for patients older than 55
    years with distal radius fractures.

    Inconclusive

    We are unable to recommend for or against locking plates in patients older than 55 years
    who are treated surgically.

    Inconclusive

    We suggest rigid immobilization in preference to removable splints when using nonsurgical


    treatment for the management of displaced distal radius fractures.

    Moderate

    The use of removable splints is an option when treating minimally displaced distal radius
    fractures.

    Weak

    We are unable to recommend for or against immobilization of the elbow in patients treated
    with cast immobilization.

    Inconclusive

    Arthroscopic evaluation of the articular surface is an option during surgical treatment of


    intra-articular distal radius fractures.

    Weak

    Surgical treatment of associated ligament injuries (SLIL injuries, LT, or TFCC tears) at the time
    of radius fixation is an option.

    Weak

    Arthroscopy is an option in patients with distal radius intra-articular fractures to improve


    diagnostic accuracy for wrist ligament injuries, and CT is an option to improve diagnostic
    accuracy for patterns of intra-articular fractures.

    Weak

    We are unable to recommend for or against the use of supplement bone grafts or substitutes
    when using locking plates.

    Inconclusive

    We are unable to recommend for or against the use of bone graft (autograft or allograft) or
    bone graft substitutes for the filling of a bone void as an adjunct to other surgical
    treatments.

    Inconclusive

    In the absence of reliable evidence, it is the opinion of the work group that distal radius
    fractures that are treated nonsurgically be followed by ongoing radiographic evaluation
    for 3 weeks and at cessation of immobilization.

    Consensus

    We are unable to recommend whether two or three K-wires should be used for distal radius
    fracture fixation.

    Inconclusive

    We are unable to recommend for or against using the occurrence of distal radius fractures to
    predict future fragility fractures.

    Inconclusive

    We suggest that all patients with distal radius fractures receive a postreduction true lateral
    radiograph of the carpus to assess DRUJ alignment.

    Moderate

    In the absence of reliable evidence, it is the opinion of the work group that all patients with
    distal radius fractures and unremitting pain during follow-up be reevaluated.

    Consensus

    A home exercise program is an option for patients prescribed therapy after distal radius
    fracture.

    Weak

    In the absence of reliable evidence, it is the opinion of the work group that patients perform
    active finger motion exercises following diagnosis of distal radius fractures.

    Consensus

    We suggest that patients do not need to begin early wrist motion routinely following stable
    fracture fixation.

    Moderate

    3: Upper Extremity

    We are unable to recommend for or against concurrent surgical treatment of DRUJ instability Inconclusive
    in patients with surgically treated distal radius fractures.

    (continued on next page)

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    357

    Section 3: Upper Extremity

    Table 2

    AAOS Clinical Practice Guideline on the Treatment of Distal Radius Fractures (continued)
    Strength of
    Recommendation

    Recommendation
    In order to limit complications when using external fixation, it is an option to limit the
    duration of fixation.

    Weak

    We are unable to recommend against overdistraction of the wrist when using an external
    fixator.

    Inconclusive

    We suggest adjuvant treatment of distal radius fractures with vitamin C for the prevention of Moderate
    disproportionate pain.
    Ultrasound and/or ice are options for adjuvant treatment of distal radius fractures.

    Weak

    We are unable to recommend for or against fixation of ulnar styloid fractures associated with Inconclusive
    distal radius fractures.
    We are unable to recommend for or against using external fixation alone for the
    management of distal radius fractures where there is depressed lunate fossa or four-part
    fracture (sagittal split).

    Inconclusive

    SLIL = scapholunate interosseous ligament, LT = lunotriquetral, TFCC = triangular fibrocartilage complex, DRUJ = distal radioulnar joint
    (Reproduced from the American Academy of Orthopaedic Surgeons: Clinical Practice Guideline on the Treatment of Distal Radius Fractures. Rosemont, IL, American
    Academy of Orthopaedic Surgeons, Dec 2009. http://www.aaos.org/research/guidelines/DRFguideline.asp.)

    stability caused by disruption of the radioulnar ligaments. However, a recent study concluded that an unrepaired ulnar styloid base fracture does not appear to
    influence function or outcome after plate fixation of a
    distal radial fracture.23

    Soft-Tissue and Vascular Injuries

    Figure 4

    A, Preoperative clinical photograph shows loss of


    the normal cascade of the ring and small fingers
    caused by disruption of the flexor tendons from
    a flexor tendon laceration. B, The cascade is restored after primary repair of the flexor tendons. (Courtesy of Virak Tan, MD, Newark, NJ.)

    Trauma to the hand and wrist can result in injury to


    multiple structures depending on the injury mechanism.
    Tendons, joints, and bone are at risk with blunt
    trauma, whereas skin, blood vessels, and nerves may be
    injured by sharp lacerations. Partial tendon disruption
    from a closed injury may be difficult to diagnose with
    physical examination; therefore, MRI or ultrasound
    may be needed.

    Extensor Tendon Injuries

    3: Upper Extremity

    wrist comparison is more accurate. DRUJ instability


    most commonly results from a fracture of the distal radius. When the instability is purely ligamentous, it usually can be reduced by closed manipulation; the forearm can be immobilized in the position of stability for
    4 weeks. Dorsal instability (the distal ulna is dorsal to
    the distal radius) is usually stable when the forearm is
    in supination, and vice versa for instability in the volar
    direction. If the DRUJ is highly unstable, pinning
    across the joint with 0.062-inch K-wires or repair of
    the radioulnar ligaments should be considered.
    In the setting of a distal radius fracture, anatomic reduction to re-create a concentric sigmoid notch is an
    important factor in determining DRUJ stability. The
    conventional practice has been to fix associated ulnar
    styloid base fractures because of the potential DRUJ in358

    Orthopaedic Knowledge Update 10

    The treatment of extensor tendon injuries is largely dependent on the location and type of injury. Closed injury
    to the central slip (PIP boutonnire deformity) or terminal extensor tendon (distal interphalangeal mallet finger)
    should be managed with splinting; in rare instances,
    surgery will be needed. Injury to the radial sagittal band
    can cause subluxation of the extensor digitorum communis ulnarly, which can be managed with splinting or
    surgery to centralize the tendon over the MCP joint.
    More proximal extensor tendon lacerations require
    direct repair with either figure-of-8 or core sutures.24

    Flexor Tendon Injuries


    Suspected flexor tendon injury warrants a careful examination to identify loss of active flexion strength or
    motion, and any associated digital nerve injury (Figure
    4). Injuries are classified by the anatomic zones. Zone I

    2011 American Academy of Orthopaedic Surgeons

    Chapter 28: Hand and Wrist Trauma

    injury is distal to the flexor digitorum sublimis insertion, and the flexor digitorum profundus is either
    avulsed from the distal phalanx or transected distal to
    the A4 pulley. Tendon avulsion (such as a jersey finger)
    should be reattached to its insertion site. Although suture anchors in the distal phalanx are increasing in
    popularity, the traditional pull-out suture tied over a
    button is acceptable.
    Zone II flexor tendon injuries occur between the A1
    and A4 pulleys. Both the flexor digitorum sublimis and
    flexor digitorum profundus (along with the digital neurovascular structures) can be involved. Tendon repair in
    this zone frequently requires working around the A2
    and A4 pulleys to avoid bowstringing. If the laceration
    occurs at either of these pulleys, repair with a smallcaliber monofilament suture is recommended at the end
    of the procedure. Both the flexor digitorum profundus
    and flexor digitorum sublimis should be repaired with
    core and epitendinous sutures. Studies have shown improved gliding when only one slip of the flexor digitorum sublimis is repaired.25 Numerous articles have been
    dedicated to the study of intrasynovial flexor tendon
    repair. Different suture techniques are described and
    many suture materials are available; however, it is believed that it is desirable to increase the number of core
    strands with stronger suture material, which leaves
    minimal suture bulk (from the knots). Great interest
    has been shown in reducing adhesions with various
    agents, but these agents generally remain experimental.
    Meticulous atraumatic handling of the tendon ends,
    precise suturing techniques, repair of the flexor tendon
    sheath, and early motion rehabilitation protocols reduce peritendinous adhesions. Although early controlled motion is widely accepted, a Cochrane review
    found insufficient evidence from published controlled
    trials to determine the best mobilization protocol.26
    Flexor tendon injuries that occur more proximally
    (zones III to V) are less common. Acute lacerations
    should be repaired, but tendon transfers may be required for attritional ruptures.

    Nerve Injuries

    2011 American Academy of Orthopaedic Surgeons

    High-Pressure Injection Injuries


    Despite a relatively benign appearing entry wound,
    high-pressure injection injuries may result in extensive
    soft-tissue damage. The nondominant index finger is
    most commonly involved. The force of the injection,
    the volume injected, the composition of the injected
    substance, and the latency from injury to treatment affect the degree of mechanical and chemical injury. Local tissue necrosis and vascular occlusion can lead to
    digit loss. Grease, chlorofluorocarbon, and water-based
    paints are relatively less destructive. Less severe injuries
    may be successfully treated nonsurgically with parenteral antibiotics, elevation, and early mobilization.28,29
    Industrial solvents and oil-based paints produce a high
    degree of tissue necrosis. An amputation rate of 50%
    was reported in one large study of oil-based paint injection injuries.30
    Emergent surgical dbridement and decompression
    is typically required following high-pressure injection
    injuries. A surgical delay of more than 10 hours from
    the time of injury was found to result in higher rates of
    amputation.31 Despite wide and aggressive initial surgical dbridement, it is generally not possible to remove
    all the injected material. Broad-spectrum antibiotic coverage is important because the necrotic tissue resulting
    from these injuries is a good culture medium for bacterial growth.

    Compartment Syndrome
    The hand can be divided into dorsal and volar interosseous compartments, thenar and hypothenar compartments, and a separate digital compartment. Compartment syndrome has many causes, including
    decreased compartment volume resulting from tight
    closure of fascial defects, the application of excessive
    traction to fractured limbs, and the use of tourniquets,
    tight dressings, or splints. Alternatively, increased content within the compartment caused by bleeding, postrevascularization changes, trauma, metabolic derangement, or fluid extravasation also can lead to
    compartment syndrome.
    It has been shown that no distinct fascia completely
    surrounds any of the intrinsic muscles of the hand. The
    unyielding nature of the surrounding skin, however,
    can contribute to the development of compartment syndrome. As in all limbs, compartment syndrome of the

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Traumatic peripheral nerve injuries are a heterogeneous


    group of disorders that commonly occur in conjunction
    with other soft-tissues trauma. When possible, primary
    repair of the nerve should be done within the first 2
    days after injury to achieve the best possible functional
    result. Urgent repair is not needed. The nerve ends
    should be trimmed back to healthy axons and reapproximated with epineural or group fascicular sutures.
    There should be minimal tension on the repair to allow
    for motion within 2 to 3 weeks.
    When primary end-to-end coaptation is not possible
    because of tension or gapping, autografting is the gold
    standard for treatment. However, because autografts
    result in donor-site deficits and are a limited resource,
    nerve graft substitutes have been developed. Biologic
    and synthetic axonal guidance channels (nerve conduits) are effective substitutes for short gaps (approximately up to 2 cm). For longer gaps, enhancement of

    the conduits with nerve growth factor, brain-derived


    neurotrophic factor, glial growth factor, Schwann cells,
    and segments of normal nerve tissue are being actively
    investigated. Future improvements may include engineered conduits that closely mimic the internal organization of an uninjured nerve.27
    Tendon transfer can supplement a motor nerve repair. If done early, the transfer can act as an internal
    splint to support function and prevent deformity during
    nerve recovery.

    359

    Section 3: Upper Extremity

    Figure 5

    A, Clinical photograph of multiple finger amputations caused by a table saw injury. The amputated part of the
    thumb was not salvageable, therefore orthotopic replantation of the amputated middle finger to the thumb and
    amputated index finger to the middle finger stump were performed. B and C, Clinical photographs taken 9
    months postoperatively. (Courtesy of Virak Tan, MD, Newark, NJ.)

    hand is a surgical emergency. If not treated within 24


    hours, contracture becomes established in a matter of
    days with muscle necrosis ultimately leading to fibrosis.
    Late changes in missed diagnoses of compartment syndrome vary with the compartment, but generally lead
    to a stiff hand and prolonged pain.

    Digital Replantation

    3: Upper Extremity

    Digital replantation is among the most technically challenging procedures for the hand surgeon. Educational,
    economic, and practical factors discourage many surgeons from attempting microsurgery.32 The procedures
    themselves are typically performed in large tertiary referral centers and academic institutions only.
    The criteria for digital replantation varies based on
    the experience of the surgeon, but the goals are return
    of function of the replanted part and low morbidity to
    the remainder of the limb and the patient as a whole.
    Survivability of the digit alone should not be the main
    indication. Typical indications include multiple digit
    traumatic amputations (Figure 5), thumb amputations,
    through-the-palm amputations, major limb replantation, and almost any level of digital amputation in a
    child. Single digit amputation distal to the flexor digitorum sublimis insertion is suitable for replantation
    after a careful discussion with the patient regarding
    potential morbidity and long-term functional expectations.
    Typical contraindications to replantation include severe mangling of the amputated part, segmental injury,
    serious comorbidities, and severely arteriosclerotic vessels. Digital replantation in patients with psychiatric
    comorbidities is typically contraindicated. Single digits,
    particularly border digits and digits proximal to the
    360

    Orthopaedic Knowledge Update 10

    flexor digitorum sublimis insertion, are relative contraindications for replantation.


    Patient selection may also be influenced by other risk
    factors. A large meta-analysis33 reported a worse prognosis in patients with a history of diabetes or smoking,
    those younger than 9 years, and patients with injuries
    caused by a crush or avulsion mechanism. Amputations
    of the distal phalanx and thumb, male sex, and ischemia time greater than 12 hours are associated with a
    somewhat worse prognosis. A history of alcohol use
    did not affect the prognosis. Regardless of the zone of
    injury, repair of as many vessels as possible is correlated with better implant survivability.34 Postoperative
    anemia, hemodilution, and the use of dextrans negatively affected digital implant survival rates.35

    Annotated References
    1.

    Collins AL, Timlin M, Thornes B, OSullivan T: Old


    principles revisited: Traction splinting for closed proximal phalangeal fractures. Injury 2002;33(3):235-237.

    2.

    Henry M: Soft tissue sleeve approach to open reduction


    and internal fixation of proximal phalangeal fractures.
    Tech Hand Up Extrem Surg 2008;12(3):161-165.
    The author describes specific technical aspects of optimizing soft-tissue management for open fixation of
    proximal phalanx fractures.

    3.

    Horton TC, Hatton M, Davis TR: A prospective randomized controlled study of fixation of long oblique
    and spiral shaft fractures of the proximal phalanx:
    Closed reduction and percutaneous Kirschner wiring
    versus open reduction and lag screw fixation. J Hand
    Surg Br 2003;28(1):5-9.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 28: Hand and Wrist Trauma

    4.

    Badia A, Riano F: A simple fixation method for unstable bony mallet finger. J Hand Surg Am 2004;29(6):
    1051-1055.

    5.

    McAuliffe JA: Dorsal fracture dislocation of the proximal interphalangeal joint. J Hand Surg Am 2008;
    33(10):1885-1888.
    This evidence-based medicine article discusses the best
    treatment of an unstable dorsal fracture-dislocation of
    the PIP joint.

    6.

    7.

    8.

    Dionysian E, Eaton RG: The long-term outcome of


    volar plate arthroplasty of the proximal interphalangeal
    joint. J Hand Surg Am 2000;25(3):429-437.
    Calfee RP, Kiefhaber TR, Sommerkamp TG, Stern PJ:
    Hemi-hamate arthroplasty provides functional reconstruction of acute and chronic proximal interphalangeal
    fracture-dislocations. J Hand Surg Am 2009;34(7):
    1232-1241.
    The authors report on 33 patients treated with autologous hemihamate bone graft for reconstructing a PIP
    fracture-dislocation. They conclude that the procedure
    is valuable for treating severe injuries.
    Katolik LI, Friedrich J, Trumble TE: Repair of acute ulnar collateral ligament injuries of the thumb metacarpophalangeal joint: A retrospective comparison of pullout sutures and bone anchor techniques. Plast Reconstr
    Surg 2008;122(5):1451-1456.
    Two cohorts (30 patients each) were treated with repair
    of the thumb MCP ulnar collateral ligament with either
    an intraosseous suture anchor or a pull-out suture tied
    over a button. Both methods were effective, but the cohort treated with the suture anchor had improved range
    of motion and pinch strength at follow-up.
    Carlsen BT, Moran SL: Thumb trauma: Bennett fractures, Rolando fractures, and ulnar collateral ligament
    injuries. J Hand Surg Am 2009;34(5):945-952.
    The authors of this review article summarize recent advancements in the realm of thumb trauma.

    10.

    Langhoff O, Andersen K, Kjaer-Petersen K: Rolandos


    fracture. J Hand Surg Br 1991;16(4):454-459.

    11.

    Boles CA: Wrist, scaphoid fractures and complications.


    eMedicine:
    Medscape.
    http://emedicine.com/radio/
    topic747.htm. Accessed September 30, 2010.
    Scaphoid fractures are discussed in this review article.

    12.

    13.

    Yin ZG, Zhang JB, Kan SL, Wang P: Treatment of acute


    scaphoid fractures: Systematic review and metaanalysis. Clin Orthop Relat Res 2007;460:142-151.
    The results of a meta-analysis showed that the surgical
    treatment of acute nondisplaced or minimally displaced
    scaphoid waist fractures does not provide greater benefits regarding nonunion rate, return to work, grip
    strength, range of wrist motion, or patient satisfaction
    than nonsurgical treatment.
    Vinnars B, Pietreanu M, Bodestedt A, Ekenstam F, Gerdin B: Nonoperative compared with operative treatment

    2011 American Academy of Orthopaedic Surgeons

    14.

    Demirkan F, Calandruccio JH, DiAngelo D: Biomechanical evaluation of flexor tendon function after
    hamate hook excision. J Hand Surg [Br] 2003;28(1):
    138-143.

    15.

    Magee T: Comparison of 3-T MRI and arthroscopy of


    intrinsic wrist ligament and TFCC tears. AJR Am J
    Roentgenol 2009;192(1):80-85.
    This study showed that 3-T MRI is sensitive and specific
    for detecting wrist ligament tears.

    16.

    Garcia-Elias M, Lluch AL, Stanley JK: Three-ligament


    tenodesis for the treatment of scapholunate dissociation:
    Indications and surgical technique. J Hand Surg Am
    2006;31(1):125-134.

    17.

    Makhni EC, Ewald TJ, Kelly S, Day CS: Effect of patient age on the radiographic outcomes of distal radius
    fractures subject to nonoperative treatment. J Hand
    Surg Am 2008;33(8):1301-1308.
    The authors evaluated 124 nonsurgically treated distal
    radius fractures at union. The displacement rate was associated with increasing patient age.

    18.

    Mackenney PJ, McQueen MM, Elton R: Prediction of


    instability in distal radial fractures. J Bone Joint Surg
    Am 2006;88(9):1944-1951.

    19.

    Jaremko JL, Lambert RG, Rowe BH, Johnson JA, Majumdar SR, Lambert RG: Do radiographic indices of
    distal radius fracture reduction predict outcomes in
    older adults receiving conservative treatment? Clin Radiol 2007;62(1):65-72.
    Seventy-four patients (older than 50 years) with nonsurgically managed distal radius fractures were enrolled in
    a prospective cohort study. Self-reported outcomes were
    not related to the acceptability of radiographic fracture reduction.

    20.

    Synn AJ, Makhni EC, Makhni MC, Rozental TD, Day


    CS: Distal radius fractures in older patients: Is anatomic
    reduction necessary? Clin Orthop Relat Res 2009;
    467(6):1612-1620.
    In a study of 53 patients (older than 55 years) with distal radius fractures, the authors reported no relationship
    between anatomic reduction, as evidenced by radiographic outcomes, and subjective or objective functional
    outcomes. Level of evidence: II.

    21.

    Guideline on the Treatment of Distal Radius Fractures.


    American Academy of Orthopaedic Surgeons Web site.
    http://www.aaos.org/Research/guidelines/
    DRFguideline.asp. Accessed September 30, 2010.
    The AAOS workgroup presents their guideline on the
    treatment of distal radius fractures.

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    9.

    of acute scaphoid fractures: A randomized clinical trial.


    J Bone Joint Surg Am 2008;90(6):1176-1185.
    This randomized study did not show improved benefits
    of internal fixation compared with nonsurgical treatment for acute nondisplaced or minimally displaced
    scaphoid fractures at 10-year follow-up. Level of evidence: I.

    361

    Section 3: Upper Extremity

    22.

    Chen NC, Jupiter JB: Management of distal radial fractures. J Bone Joint Surg Am 2007;89(9):2051-2062.
    The authors discuss the management of distal radial
    fractures in this review article.

    23.

    Souer JS, Ring D, Matschke S, Audige L, Marent-Huber


    M, Jupiter JB; AOCID Prospective ORIF Distal Radius
    Study Group: Effect of an unrepaired fracture of the ulnar styloid base on outcome after plate-and-screw fixation of a distal radial fracture. J Bone Joint Surg Am
    2009;91(4):830-838.
    Two cohorts of 76 matched patients (fracture of the ulnar styloid base versus no ulnar fracture) were retrospectively analyzed. The authors found that not fixing
    the ulnar styloid base fracture did not appear to influence function or outcome after plate fixation of a distal
    radial fracture.

    24.

    Soni P, Stern CA, Foreman KB, Rockwell WB: Advances in extensor tendon diagnosis and therapy. Plast
    Reconstr Surg 2009;123(2):52e-57e.
    The authors present a summary of a literature review of
    extensor tendon injury articles published since 1989.

    25.

    Tang JB, Xie RG, Cao Y, Ke ZS, Xu Y: A2 pulley incision or one slip of the superficialis improves flexor tendon repairs. Clin Orthop Relat Res 2007;456:121-127.
    In a chicken model, incision of the pulley or partial
    flexor digitorum superficialis resection improved outcomes of tendon repairs.

    26.

    de Ruiter GC, Malessy MJ, Yaszemski MJ, Windebank


    AJ, Spinner RJ: Designing ideal conduits for peripheral
    nerve repair. Neurosurg Focus 2009;26(2):E5.
    The authors present a review article that discusses the
    ideal nerve conduit for peripheral nerve repair.

    Goetting AT, Carson J, Burton BT: Freon injection injury to the hand: A report of four cases. J Occup Med
    1992;34(8):775-778.

    29.

    Snarski JT, Birkhahn RH: Non-operative management


    of a high-pressure water injection injury to the hand.
    CJEM 2005;7(2):124-126.

    30.

    Mirzayan R, Schnall SB, Chon JH, Holtom PD, Patzakis


    MJ, Stevanovic MV: Culture results and amputation
    rates in high-pressure paint gun injuries of the hand.
    Orthopedics 2001;24(6):587-589.

    31.

    Stark HH, Ashworth CR, Boyes JH: Paint-gun injuries


    of the hand. J Bone Joint Surg Am 1967;49(4):637-647.

    32.

    Payatakes AH, Zagoreos NP, Fedorcik GG, Ruch DS,


    Levin LS: Current practice of microsurgery by members
    of the American Society for Surgery of the Hand.
    J Hand Surg Am 2007;32(4):541-547.
    A survey of members of the American Society for Surgery of the Hand showed that 44% of surgeons do not
    perform replantation surgery. Reasons for not performing replantations included busy elective schedules
    (51%), inadequate confidence in performing replantations (39%), and disappointment in results (23%).

    33.

    Chung KC, Watt AJ, Kotsis SV, Margaliot Z, Haase SC,


    Kim HM: Treatment of unstable distal radial fractures
    with the volar locking plating system. J Bone Joint Surg
    Am 2006;88(12):2687-2694.

    34.

    Lee BI, Chung HY, Kim WK, Kim SW, Dhong ES: The
    effects of the number and ratio of repaired arteries and
    veins on the survival rate in digital replantation. Ann
    Plast Surg 2000;44(3):288-294.

    35.

    Ridha H, Jallali N, Butler PE: The use of dextran post


    free tissue transfer. J Plast Reconstr Aesthet Surg 2006;
    59(9):951-954.

    3: Upper Extremity

    27.

    Thien TB, Becker JH, Theis J-C: Rehabilitation after


    surgery for flexor tendon injuries in the hand. Cochrane
    Database
    Syst
    Rev
    2004;4:CD00397910.1002/
    14651858.CD003979.pub2.

    28.

    362

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 29

    Hand and Wrist Reconstruction


    Tamara D. Rozental, MD

    Dawn M. LaPorte, MD

    Posttraumatic Arthritis of the Wrist

    Scapholunate Advanced Collapse Wrist

    Dr. LaPorte or an immediate family member has stock or


    stock options held in Auxilium. Neither Dr. Rozental nor
    any immediate family member has received anything of
    value from or owns stock in a commercial company or
    institution related directly or indirectly to the subject of
    this chapter.

    2011 American Academy of Orthopaedic Surgeons

    Untreated scaphoid nonunions also can lead to posttraumatic wrist arthritis. Staging for scaphoid nonunion advanced collapse (SNAC) wrist is similar to
    staging for SLAC wrist except that the joint surface between the proximal scaphoid fragment and scaphoid
    fossa of the distal radius is preserved (Table 2).
    Treatment methods for SNAC wrist are similar to
    those for SLAC wrist. In the early stages, fixation of the
    nonunion and radial styloidectomy are attempted. Fixation with vascularized bone grafts is also an option
    and has met with varying success.4 Excision of the distal pole of the scaphoid can be performed in patients
    with distal nonunions and an intact midcarpal joint. In
    later stages of SNAC wrist, salvage procedures such as
    a proximal row carpectomy or four-corner fusion are
    preferred. Once the capitolunate joint is involved, a
    four-corner fusion or wrist arthrodesis achieves more
    predictable results.

    Arthritis at the Distal Radioulnar Joint


    Patients with arthritis at the distal radioulnar joint
    (DRUJ) typically present with pain over the dorsum of

    3: Upper Extremity

    Scapholunate advanced collapse (SLAC) wrist is the


    most common form of posttraumatic arthritis of the
    wrist and typically stems from disruption of the scapholunate interosseous ligament. This condition results
    in palmar rotatory subluxation of the scaphoid and abnormal wrist mechanics, leading to the development of
    degenerative changes in the radioscaphoid and capitolunate joints (Figure 1). Arthrosis progresses in a predictable fashion and is reflected in the radiographic
    staging of SLAC wrist (Table 1). The radiolunate articulation is typically spared.
    Once a SLAC wrist develops, reconstruction of the
    scapholunate ligament alone is no longer adequate to
    correct rotatory subluxation of the scaphoid and eliminate pain from underlying arthrosis. At this stage, a radial styloidectomy and/or scapholunate reconstruction
    is typically the procedure of choice. For stage II and III
    SLAC wrists, elimination of the radioscaphoid joint is
    necessary. This is usually accomplished through a proximal row carpectomy, scaphoid excision with fourcorner fusion, or partial or total radiocarpal fusions.1,2
    Stage IV SLAC wrists, with pancarpal involvement, are
    treated with a total wrist arthrodesis.
    Proximal row carpectomies can be performed in patients whose proximal capitate is intact (no evidence of
    degenerative changes). The procedure preserves motion
    and strength and results in good long-term outcomes.
    In some instances, conversion to a total wrist arthrodesis may be required. A scaphoid excision with fourcorner fusion (SLAC procedure) is a better alternative
    in patients with midcarpal joint involvement. Overall,
    both procedures lead to similar functional outcomes.2
    Traditionally, four-corner arthrodesis is believed to provide better short-term grip strength.3

    Scaphoid Nonunion Advanced Collapse Wrist

    Figure 1

    AP radiograph of the wrist in a patient with a


    stage II SLAC wrist. There is a large osteophyte
    at the radial styloid (arrowhead) and complete
    destruction of the radioscaphoid articulation.

    Orthopaedic Knowledge Update 10

    363

    Section 3: Upper Extremity

    Table 1

    Progression of SLAC Wrist Deformity


    Radiographic Stage

    Description

    Treatment Options

    Arthrosis between radial styloid and distal


    scaphoid

    Radial styloidectomy and scapholunate reconstruction

    II

    Arthrosis of entire radioscaphoid joint

    Proximal row carpectomy


    Four-corner fusion
    Radioscapholunate fusion

    III

    Arthrosis involving capitolunate joint with


    proximal migration of the capitate

    Proximal row carpectomy


    Four-corner fusion
    Total wrist arthrodesis

    IV

    Pancarpal arthrosis

    Total wrist arthrodesis


    Wrist arthroplasty (sedentary patients)

    Table 2

    Progression of SNAC Wrist Deformity


    Radiographic Stage

    Description

    Arthrosis between radial styloid and Radial styloidectomy and fixation of scaphoid nonunion
    distal scaphoid

    II

    Arthrosis of scaphocapitate joint

    Proximal row carpectomy


    Four-corner fusion

    III

    Capitolunate arthrosis

    Four-corner fusion
    Total wrist arthrodesis

    IV

    Pancarpal arthrosis (except


    radiolunate joint)

    Total wrist arthrodesis


    Wrist arthroplasty (sedentary patients)

    3: Upper Extremity

    the wrist and limitation of forearm rotation. No classification or radiographic staging is used for DRUJ arthrosis and treatment is typically aimed toward restoration
    of motion and pain relief. If conservative management is
    unsuccessful in patients with mild involvement, the patient may be treated with dbridement of the DRUJ
    and/or an ulnar shortening osteotomy to alter the contact surface of the joint. In patients with more advanced
    disease, options include resection of the entire ulnar head
    (Darrach resection), partial ulnar head resection (hemiresection with soft-tissue interposition), or arthrodesis of
    the DRUJ with resection of the proximal ulnar segment
    (Sauve-Kapandji procedure). More recently, prosthetic
    replacement of the ulnar head has been attempted with
    promising early results.5

    Osteoarthritis

    Thumb Carpometacarpal Joint


    The carpometacarpal (CMC) joint of the thumb is
    commonly affected by osteoarthritis (second only to the
    distal interphalangeal [DIP] joint). The anterior oblique
    ligament (beak ligament) is believed to be the primary
    stabilizing force of the CMC joint; deficiency leads to
    the typical pattern of arthrosis. Patients present with
    364

    Orthopaedic Knowledge Update 10

    Treatment Options

    pain at the base of the thumb and have difficulty with


    pinching and gripping activities. Most patients are initially treated conservatively, independent of the degree
    of involvement. Treatment consists of antiinflammatory drugs, splinting, activity modification,
    and corticosteroid injections.
    The Eaton classification system is used for radiographic staging of CMC joint arthritis (Table 3). For
    early stages, surgical treatment may consist of joint dbridement (open or arthroscopic) or metacarpal extension osteotomy.6 For later stages, there are a variety of
    described procedures, but all involve either partial or
    complete excision of the trapezium. Most commonly,
    patients are treated with trapezium excision (partial or
    complete), tendon interposition, and reconstruction of
    the anterior oblique ligament (with the flexor carpi radialis or abductor pollicis longus). Some surgeons prefer trapezium excision alone or excision and the insertion of an allograft spacer. Most described forms of
    CMC joint arthroplasty provide good results in terms
    of pain relief although pinch strength is never fully restored.7 Compensatory metacarpophalangeal hyperextension should be treated with metacarpophalangeal
    capsulodesis or arthrodesis. The scaphotrapezoid joint
    also should be evaluated. If degenerative changes are
    present, a partial trapeziectomy should be performed.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 29: Hand and Wrist Reconstruction

    Table 3

    Eaton Staging and Treatment Classification System for CMC Joint Arthritis
    Radiographic Stage

    Description

    Treatment Options

    Widened CMC joint

    CMC dbridement
    Ligament reconstruction
    Metacarpal osteotomy

    Joint space narrowing


    Mild subchondral sclerosis
    Osteophytes < 2 mm

    CMC dbridement
    Trapeziectomy tendon interposition
    Arthrodesis

    Joint space narrowing


    Sclerosis or cystic changes
    Osteophytes > 2 mm

    Trapeziectomy tendon interposition


    Arthrodesis

    Pantrapezial arthrosis

    Trapeziectomy tendon interposition


    Arthroplasty

    As a treatment alternative to procedures involving excision of the trapezium, trapeziometacarpal arthrodesis


    can result in reliable long-term results, helping to preserve pinch strength at the expense of some loss of
    thumb mobility.8 Arthrodesis has been recommended in
    young, active patients who have trapeziometacarpal arthritis and require strong pinch and grip strength.9

    Scaphotrapezial Trapezoid Joint


    Scaphotrapezial trapezoid joint arthritis may be present
    with or without concomitant CMC joint changes.
    Symptoms are similar to CMC joint arthritis and radiographs are often necessary to make the diagnosis. If
    conservative care is unsuccessful, patients can be treated
    with scaphotrapezial fusion if the CMC joint is intact.
    Distal pole scaphoid or scaphotrapezial trapezoid excision also can be considered for symptomatic scaphotrapezial arthritis. If the CMC joint is also involved, a trapezium excision with tendon interposition and partial
    trapezoid excision is the procedure of choice.

    Treatment involves resection of the cyst as well as removal of the underlying bone spur. For patients with
    more advanced disease, arthrodesis in 10 to 20 of
    flexion is the procedure of choice.10 At the PIP joint,
    mild osteoarthritis with contractures and nodular involvement can be treated with joint dbridement and
    collateral ligament excision. Options for more advanced osteoarthritis include arthroplasty or arthrodesis. Arthroplasty with silicone implants leads to good
    pain relief but is often complicated by implant fractures
    in the long term. Newer two-piece prostheses have been
    designed to address this problem but significant complications have been reported, including dislocations,
    extensor lag, and stiffness.11,12 Arthrodesis is the traditional option for the management of degenerative
    changes in the PIP joint. The optimal position for PIP
    joint fusion is 30 to 45 of flexion, in 5 increments
    from the index to the small finger. In general, arthroplasty is a better option for the long and ring fingers,
    whereas border digits (index and small finger) are best
    treated with arthrodesis.

    Metacarpophalangeal Joint

    Proximal and Distal Interphalangeal Joints


    Osteoarthritis of the proximal interphalangeal (PIP)
    joint and DIP joint is common and often associated
    with enlargement of the joints (Heberden nodes at the
    DIP joint and Bouchard nodes at the PIP joint). At the
    DIP joint, bone spurs often result in the formation of
    mucous cysts, which can drain and lead to infection.

    2011 American Academy of Orthopaedic Surgeons

    Osteonecrosis

    Kienbck Disease
    A patient with Kienbck disease or osteonecrosis of the
    lunate often presents with pain, limited range of motion, and weakness. The etiology is not well understood
    but is associated with mechanical factors (ulnar negative variance leading to increased loads) as well as vascular factors (single nutrient vessel and poor collateral
    circulation, elevated intraosseous pressure).13 Plain radiographs may show increased sclerosis but MRI may
    be required to make a definitive diagnosis (Figure 2).
    Kienbck disease is classified according to the Lichtman classification system (Table 4). Early stages of the
    disease are treated with joint-leveling procedures designed to decrease the mechanical load on the lunate,14
    with or without vascularized bone grafts from the distal radius. Once fixed scaphoid rotation occurs, the

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Metacarpophalangeal joint arthritis is most common in


    the thumb. If the CMC joint and interphalangeal joints
    are not involved, arthrodesis is typically the procedure
    of choice, although implants for joint arthroplasty are
    available. In the digits, metacarpophalangeal joint fusions are functionally limiting and arthroplasty is preferred. Options include silicone implants or newer pyrolytic carbon implants. In rheumatoid arthritis
    patients with ulnar drift, metacarpophalangeal joint arthroplasty should be accompanied by soft-tissue reconstruction and realignment of the extensor mechanism.

    365

    Section 3: Upper Extremity

    Figures 2

    A, AP radiograph of the wrist of a patient with stage IIIA Kienbck disease showing lunate sclerosis and collapse
    without rotation of the scaphoid. B, The corresponding T1-weighted MRI shows signal change in the entire
    lunate.

    Table 4

    Staging and Treatment of Kienbck Disease


    Radiographic Stage

    Description

    Treatment Options

    Stage I

    Normal radiographs
    Low signal on MRI

    Observation
    Activity modification/immobilization

    Stage II

    Lunate sclerosis without collapse

    Radial shortening for ulnar negative


    Capitate shortening for ulnar neutral/positive
    Vascularized grafts

    Stage IIIA

    Sclerosis with lunate collapse

    Radial shortening for ulnar negative


    Capitate shortening for ulnar neutral/positive
    Vascularized grafts

    Stage IIIB

    Lunate collapse with rotatory


    scaphoid deformity

    Scaphotrapezial arthrodesis
    Scaphocapitate arthrodesis
    Proximal row carpectomy

    Stage IV

    Radiocarpal and/or midcarpal


    arthrosis

    Proximal row carpectomy


    Wrist arthrodesis

    3: Upper Extremity

    scaphoid must be stabilized with a limited arthrodesis


    or treated with a proximal row carpectomy.15 If radiocarpal or midcarpal arthrosis is present, wrist fusion is
    the procedure of choice. Early in the disease process,
    MRI should be used to differentiate Kienbck disease
    from ulnar impaction. Kienbck disease involves the
    entire lunate, whereas ulnar impaction typically only
    affects the ulnar facet.

    Preiser Disease
    Preiser disease, or idiopathic osteonecrosis of the scaphoid, is much less common than Kienbck disease.16
    Radiographs or MRI may show sclerosis of the proxi366

    Orthopaedic Knowledge Update 10

    mal pole of the scaphoid without any evidence of fracture. Observation and immobilization may be effective
    in up to 20% of patients. Surgery includes vascularized
    grafting,17 scaphoid excision, and four-corner fusion or
    proximal row carpectomy.

    Osteonecrosis of the Capitate


    Patients with idiopathic osteonecrosis of the capitate, a
    rare condition, present with pain and limitation of motion. This condition can be posttraumatic or can be associated with steroid use or chemotherapy. Radiographs show sclerosis and fragmentation of the
    proximal pole of the capitate. Idiopathic osteonecrosis

    2011 American Academy of Orthopaedic Surgeons

    Chapter 29: Hand and Wrist Reconstruction

    of the capitate is initially treated with observation


    and/or immobilization. Excision of the avascular head
    of the capitate with tendon interposition can be used
    for recalcitrant cases. Other options are vascularized
    grafting or limited arthrodesis.

    Table 5

    Sites of Nerve Compression


    Nerve

    Sites of Compression

    Median

    Ligament of Struthers
    Lacertus fibrosus

    Nerve Compression Syndromes


    Although the term compression neuropathy suggests
    that the affected nerve is compressed by an anatomic
    structure, the cause of the compression is often multifactorial. There are several sites between the cervical
    spine and the hand where nerve compression is common (Table 5). Compression at one point on a peripheral nerve will lower the threshold for the occurrence of
    a compression neuropathy at a more proximal or distal
    level on the same nerve. This is referred to as a double
    crush phenomenon. Cervical radiculopathy in a patient
    with carpal tunnel syndrome is the most common manifestation of the double crush phenomenon; both sites
    of compression should be treated to achieve an optimal
    result.

    Median Nerve

    2011 American Academy of Orthopaedic Surgeons

    Pronator teres

    Pronator

    Flexor digitorum superficialis


    origin

    Anterior
    interosseous

    Flexor carpi radialis


    Gantzer muscle
    Ulnar

    Transverse carpal ligament

    Carpal tunnel

    Arcade of Struthers

    Cubital
    tunnel

    Intermuscular septum
    Medial epicondyle
    Cubital tunnel
    Anconeus epitrochlearis
    Flexor carpi ulnaris aponeurosis
    Radial

    Guyon canal

    Ulnar tunnel

    Fibrous band at radial head

    Posterior
    interosseous
    nerve

    Recurrent leash of Henry

    Radial tunnel

    Extensor carpi radialis brevis


    fibrous edge
    Arcade of Frohse (most common)
    proximal supinator
    Distal supinator
    Between extensor carpi radialis
    longus and extensor carpi
    radialis brevis

    Wartenberg

    lief. Patients who have temporary relief after injection


    are likely to have a good response to surgical carpal
    tunnel release. Surgical carpal tunnel release is recommended if symptoms persist. Improvement in symptoms can be anticipated in up to 98% of patients following surgery. Although treatment in elderly and
    diabetic patients has been controversial, studies support
    carpal tunnel release in both of these populations.19-21
    Carpal tunnel release can be performed via open or endoscopic techniques; there does not appear to be an appreciable difference in outcomes at 1 year postoperatively.22 No proven benefit to neurolysis of the median
    nerve or tenosynovectomy of the flexor tendons has
    been shown.23 Pillar pain, associated with a painful palmar scar at the site of transverse carpal ligament release, is the most common complication after carpal
    tunnel release. Persistent or recurrent carpal tunnel
    symptoms are likely caused by an incomplete release.
    The initial recommended treatment for recurrent or
    persistent carpal tunnel syndrome is revision surgery.24

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Carpal Tunnel Syndrome


    Compression neuropathy of the median nerve at the
    wrist is the most common compression neuropathy of
    the upper extremity and affects up to 10% of the general population. Carpal tunnel syndrome is primarily a
    clinical diagnosis. In addition to an accurate patient
    history, sensory examination with Semmes-Weinstein
    monofilaments (a threshold test) is considered to be the
    most sensitive test for detecting early disease. Manual
    motor testing of the upper extremity should be performed with attention to ascertaining the presence of
    thenar atrophy, which has a high predictive value in
    carpal tunnel syndrome. Provocative maneuvers, including the carpal compression test, the Phalen maneuver, and the Tinel sign can be helpful in establishing the
    diagnosis. The American Academy of Orthopaedic Surgeons (AAOS) Clinical Practice Guideline on the Diagnosis of Carpal Tunnel Syndrome recommends obtaining electrodiagnostic studies if clinical and/or
    provocative tests are positive and surgery is being considered18 (Table 6). However, many surgeons believe
    that the diagnosis can satisfactorily be made based on
    the clinical examination alone (Table 7). Good surgical
    outcome is correlated with a combination of positive
    clinical and electrodiagnostic tests. Although electrodiagnostic testing is generally considered the gold standard for assessing peripheral compression neuropathies, a negative nerve study does not universally rule
    out carpal tunnel syndrome, which may improve following carpal tunnel release.
    The initial treatment of mild or moderate carpal tunnel syndrome includes nighttime splinting to avoid
    flexion/extension and the use of nonsteroidal antiinflammatory drugs. Corticosteroid injection into the
    carpal canal also can be very effective for symptom re-

    Syndrome

    367

    Section 3: Upper Extremity

    Table 6

    AAOS Clinical Practice Guideline on the Diagnosis of Carpal Tunnel Syndrome: Summary of
    Recommendations
    Recommendation 1.1

    The physician should obtain an accurate patient history (level V, grade C).

    Recommendation 2.1

    The physician should perform a physical examination of the patient that may include:
    Personal characteristics (level V, grade C)
    Performing a sensory examination (level V, grade C)
    Performing a manual muscle testing of the upper extremity (level V, grade C)
    Performing provocative tests (level V, grade C), and/or
    Performing discriminatory tests for alternative diagnoses (level V, grade C)

    Recommendation 3.1a

    The physician may obtain electrodiagnostic tests to differentiate among diagnoses (level V, grade C)

    Recommendation 3.1b

    The physician may obtain electrodiagnostic tests in the presence of thenar atrophy and/or persistent
    numbness (Level V, grade C)

    Recommendation 3.1c

    The physician should obtain electrodiagnostic tests if clinical and/or preventive tests are positive and
    surgical management is being considered
    (level II and III, grade B)

    Recommendation 3.2

    If the physician orders electrodiagnostic tests, the testing protocol should follow the
    AAN/AANEM/AAPMR guidelines for diagnosis of carpal tunnel syndrome
    (level IV and V, grade C)

    Recommendation 3.3a

    The physician should not routinely evaluate patients suspected of having carpal tunnel syndrome
    with new technology, such as MRI, CT, and pressure-specified sensorimotor devices in the wrist and
    hand. (level V, grade C)

    Please note that recommendation 3.3 is not based on a systematic literature review. An additional abbreviated review was completed following the face-to-face meeting
    of the Work Group on February 24, 2007.
    AAN = American Academy of Neurology, AANEM = American Association of Neuromuscular and Electrodiagnostic Medicine, AAPMR = American Academy of Physical
    Medicine and Rehabilitation
    (Reproduced from the American Academy of Orthopaedic Surgeons: Clinical Practice Guideline on the Diagnosis of Carpal Tunnel Syndrome. Rosemont, IL, American
    Academy of Orthopaedic Surgeons, May 2007. Http://www.aaos.org/Research/guidelines/CTStreatmentguide.asp.)

    Table 7

    3: Upper Extremity

    Diagnostic Tests for Carpal Tunnel Syndrome


    Name of Test

    How Performed

    Condition Measured

    Positive Result

    Interpretation of
    Positive Result

    Phalen test

    Patient places elbows


    on table, forearms
    vertical, wrists flexed

    Paresthesia in response
    to position

    Numbness or tingling
    on radial side digits
    within 60 seconds

    Probable carpal tunnel


    syndrome (sensitivity
    0.75, specificity 0.47)

    Percussion test (Tinel


    sign)

    Examiner lightly taps


    Site of nerve lesion
    along median nerve
    at the wrist, proximal
    to distal

    Tingling response in
    fingers at site of
    compression

    Probable carpal tunnel


    syndrome if
    response is at the
    wrist (sensitivity
    0.60, specificity 0.67)

    Carpal tunnel
    compression test

    Direct compression of
    median nerve by
    examiner

    Paresthesias in response Paresthesias within 30


    to pressure
    seconds

    Probable carpal tunnel


    syndrome (sensitivity
    0.87, specificity 0.90)

    Hand diagram

    Patient marks sites of


    pain or altered
    sensation on the
    outline diagram of
    the hand

    Patients perception of
    site of nerve deficit

    Probable carpal tunnel


    syndrome (sensitivity
    0.96, specificity 0.73,
    negative predictive
    value of a negative
    test 0.91)

    Signs on palmar side of


    radial digits without
    signs in the palm

    (Data from Szabo RM: Nerve compression syndromes, in Hand Surgery Update 1. Rosemont, IL, American Academy of Orthopaedic Surgeons, 1996, pp 221-231.)

    An AAOS work group has provided a summary of


    recommendations for the treatment of carpal tunnel
    syndrome in a clinical practice guideline based on available evidence25 (Table 8).
    368

    Orthopaedic Knowledge Update 10

    Anterior Interosseous Nerve Syndrome


    A patient with anterior interosseous nerve syndrome
    presents with anterior forearm pain and weakness or
    motor loss of one or more of the flexor pollicis longus,

    2011 American Academy of Orthopaedic Surgeons

    Chapter 29: Hand and Wrist Reconstruction

    Table 8

    AAOS Clinical Practice Guideline on the Treatment of Carpal Tunnel Syndrome: Summary of
    Recommendations
    A course of nonsurgical treatment is an option in patients diagnosed with
    carpal tunnel syndrome. Early surgery is an option when there is clinical
    evidence of median nerve denervation or the patient elects to proceed
    directly to surgical treatment.

    (Grade C, level V)

    Recommendation 2

    We suggest another nonsurgical treatment or surgery when the current


    treatment fails to resolve the symptoms within 2 to 7 weeks.

    (Grade B, level I and II)

    Recommendation 3

    We do not have sufficient evidence to provide a specific treatment


    recommendations for carpal tunnel syndrome when found in association
    with the following conditions: diabetes mellitus, coexistent cervical
    radiculopathy, hypothyroidism, polyneuropathy, pregnancy, rheumatoid
    arthritis, and carpal tunnel syndrome in the workplace.

    (Inconclusive, No
    evidence found)

    Recommendation 4a

    Local steroid injection or splinting is suggested when treating patients with


    carpal tunnel syndrome, before considering surgery.

    (Grade B, level I and II)

    Recommendation 4b

    Oral steroids or ultrasound are options when treating patients with carpal
    tunnel syndrome.

    (Grade C, level II)

    Recommendation 4c

    We recommend carpal tunnel release as treatment of carpal tunnel syndrome. (Grade A, level I)

    Recommendation 4d

    Heat therapy is not among the options that should be used to treat patients
    with carpal tunnel syndrome.

    (Grade C, level II)

    Recommendation 4e

    The following treatments carry no recommendation for or against their use:


    activity modifications, acupuncture, cognitive behavioral therapy, cold laser,
    diuretics, exercise, electric stimulation, fitness, graston instrument,
    iontophoresis, laser, stretching, massage therapy, magnet therapy,
    manipulation, medications (including anticonvulsants, antidepressants, and
    nonsteroidal anti-inflammatory drugs), nutritional supplements,
    phonophoresis, smoking cessation, systemic steroid injection, therapeutic
    touch, vitamin B6 (pyridoxine), weight reduction, yoga.

    (Inconclusive, level II
    and V)

    Recommendation 5

    We recommend surgical treatment of carpal tunnel syndrome by complete


    division of the flexor retinaculum regardless of the specific surgical
    technique.

    (Grade A, level I and II)

    Recommendation 6

    We suggest that surgeons do not routinely use the following procedures when (Grade B, level I)
    (Grade C, level II)
    performing carpal tunnel release:
    (Inconclusive, level II
    Skin nerve preservation
    and V)
    Epineurotomy
    The following procedures carry no recommendation for or against use:
    Flexor retinaculum lengthening
    Internal neurolysis
    Tenosynovectomy
    Ulnar bursa preservation

    Recommendation 7

    The physician has the option of prescribing preoperative antibiotics for carpal
    tunnel surgery.

    (Grade C, level III)

    Recommendation 8

    We suggest that the wrist not be immobilized postoperatively after routine


    carpal tunnel surgery.
    We make no recommendation for or against the use of postoperative
    rehabilitation.

    (Grade B, level II)


    (Inconclusive, level II)

    Recommendation 9

    We suggest physicians use one or more of the following instruments when


    assessing patients responses to carpal tunnel syndrome treatment of
    research:
    Boston Carpal Tunnel Questionnaire (disease-specific)
    DASH: Disabilities of the Arm, Shoulder and Hand (region-specific; upper
    limb)
    MHQ: Michigan Hand Outcomes Questionnaire (region-specific;
    hand/wrist)
    PEM: Patient Evaluation Measure (region-specific; hand)
    SF-12 or SF-36 Medical Outcomes Short Form Health Survey (generic;
    physical health component for global health impact)

    (Grade B, level I, II, and


    III)

    3: Upper Extremity

    Recommendation 1

    (Reproduced from the American Academy of Orthopaedic Surgeons: Clinical Practice Guideline on the Treatment of Carpal Tunnel Syndrome. Rosemont, IL, Sept 2008.
    Http://www.aaos.org/Research/guidelines/CTStreatmentguide.asp.)

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    369

    Section 3: Upper Extremity

    Figure 4

    Figure 3

    Clinical photograph showing the characteristic hyperextension of the thumb interphalangeal


    joint and index finger DIP joint in a patient
    with anterior interosseous nerve syndrome.

    3: Upper Extremity

    index finger and/or long flexor digitorum profundus,


    and the pronator quadratus muscle. There is no clinically observable or measurable sensory loss, and if
    present, sensory involvement suggests other diagnoses.
    A partial palsy with isolated involvement of the flexor
    digitorum profundus to the index finger or the flexor
    pollicis longus can be seen. When attempting a tip to
    tip pinch, the distal joints hyperextend with the pinch
    creating pulp-to-pulp contact (Figure 3). The differential diagnosis of anterior interior nerve syndrome includes tendon rupture; proximal compression; or brachial neuritis/Parsonage-Turner syndrome, which often
    follows a viral illness. More than one third of cases are
    idiopathic. In many patients, anterior interior nerve
    syndrome resolves spontaneously; therefore, observation is recommended for a minimum of 3 to 6 months.
    If there is no improvement, surgical treatment may be
    indicated with a longitudinal/extensile exposure and
    neurolysis of the entire anterior interior nerve. If there
    is no electrodiagnostic evidence of reinnervation, a
    nerve transfer (radial to median) may be considered at
    7 to 10 months after surgery.26 Tendon transfers (brachioradialis to flexor pollicis longus and flexor digitorum profundus small/ring to index/long or extensor
    carpi radialis longus to index profundus) can be helpful
    in reestablishing pinch strength.
    Pronator Syndrome
    Pronator syndrome is a proximal entrapment of the
    median nerve that results in primarily sensory changes
    in the median nerve distribution in the hand and the
    palmar cutaneous distribution of the palm and thenar
    eminence. It is less common than carpal tunnel syndrome, is more common in women, and often occurs in
    the fifth decade of life. It has been associated with repetitive activities and in patients with well-developed
    forearm muscles, such as weight lifters. Provocative
    tests, which should reproduce symptoms in the median
    nerve distribution, include resisted forearm pronation,
    370

    Orthopaedic Knowledge Update 10

    Clinical photograph of a hand showing the Wartenberg sign. Ulnar deviation of the small finger
    occurs secondary to the unopposed force of the
    extensor digiti minimi in patients with advanced
    ulnar nerve compression.

    resisted elbow flexion with the forearm supinated, and


    resisted flexion of the long finger flexor digitorum superficialis. Electrodiagnostic studies are not reliable in
    diagnosing proximal median nerve compression. Nonsurgical management includes activity modification,
    nonsteroidal anti-inflammatory drugs, and splinting. If
    nonsurgical treatment fails (in approximately 50% of
    patients) and the clinical diagnosis is clear, surgical exploration and release of the nerve at all potential sites
    of compression is indicated.

    Ulnar Nerve
    Cubital Tunnel
    Compression of the ulnar nerve at the cubital tunnel is
    the second most common compression neuropathy after carpal tunnel syndrome. The diagnosis can often be
    made clinically. Physical examination findings include
    numbness and paresthesias in the small and ring finger
    and occasional pain at the medial elbow. The Tinel sign
    over the ulnar nerve at the cubital tunnel is often positive, but this test may be overly sensitive. More severe
    compression may result in motor changes, including atrophy of ulnar-innervated muscles, claw deformity of
    the small and ring fingers, and positive Froment and
    Wartenberg signs (Figure 4). Electrodiagnostic studies
    may be used to confirm the diagnosis and to evaluate
    other sites of nerve compression or other disease processes that may be present. Electromyographic changes
    in ulnar-innervated muscles are more sensitive than
    nerve conduction velocity studies in the early stages of
    the disorder.
    As in all other compression neuropathies, treatment
    outcomes are generally better before muscle atrophy
    develops. Nonsurgical management includes nighttime
    elbow extension splinting and education to avoid positioning that places the elbow in flexion or creates pressure on the ulnar nerve. If symptoms persist or progress, surgery may be indicated. Surgery may involve in
    situ decompression, medial epicondylectomy, or anterior transposition (subcutaneous, submuscular, or intramuscular). No significant difference has been reported

    2011 American Academy of Orthopaedic Surgeons

    Chapter 29: Hand and Wrist Reconstruction

    in outcomes between these procedures, although fewer


    complications have been observed in patients treated
    with in situ decompression.27 Endoscopically assisted
    cubital tunnel release with or without transposition
    also has been described with favorable early results.28
    The most common reasons for reoperation are inadequate decompression, perineural scarring, or tethering
    at the intermuscular septum or flexor carpi ulnaris fascia. Submuscular transposition has traditionally been
    preferred to revise a failed ulnar nerve procedure.29
    Ulnar Tunnel Syndrome
    The ulnar nerve divides in the Guyon canal at the hypothenar region of the wrist and can be compressed in
    this area. Compression at this level is uncommon and
    can be secondary to trauma (acute or repetitive); anomalous muscles; or space-occupying lesions such as ganglia (most commonly), thrombosis, or pseudoaneurysms. The anatomy is divided into three zones: zone 1
    is proximal to the bifurcation of the nerve and includes
    both sensory and motor fibers, zone 2 surrounds the
    motor branch distal to the bifurcation, and zone 3 encompasses the superficial sensory branches distal to the
    bifurcation. The site of compression impacts the presenting symptoms, which can include strictly motor,
    strictly sensory, or a mix of both motor and sensory
    loss. If a space-occupying lesion is suspected, MRI can
    identify the mass. The Allen test along with vascular
    testing, and in some cases ultrasound, can identify
    thrombosis of the ulnar artery. CT is the most costefficient method for evaluating the hook of the hamate
    fracture or fracture nonunion of the hook. When surgery is indicated, all three zones must be explored and
    released. Care should be taken to identify and release
    the deep motor branch of the ulnar nerve.

    Radial Nerve
    Compression of the radial nerve in the proximal forearm can result in motor weakness without pain (posterior interosseous nerve syndrome) or in pain without
    weakness (radial tunnel syndrome). Compression of the
    radial sensory nerve in the distal forearm (Wartenberg
    syndrome or cheiralgia paresthetica) can cause pain
    and, occasionally, sensory loss on the dorsal radial aspect of the distal forearm and hand.

    cated if there is no clinical improvement and no recovery from baseline measurements on repeat electrodiagnostic testing. In patients who have no return of
    function, nerve decompression or tendon transfer surgery should be considered.
    Radial Tunnel Syndrome
    Radial tunnel syndrome is characterized by pain without motor deficit. The pain is typically localized to the
    lateral aspect of the proximal forearm, and has been associated with lateral epicondylitis. Electrodiagnostic
    studies are usually negative. Nonsurgical management
    is appropriate in most patients. If nonsurgical treatment fails, surgical radial tunnel release may yield good
    outcomes.30 A recent study has reported good treatment results for radial tunnel syndrome with surgical
    decompression of the superficial branch of the radial
    nerve.31
    Wartenberg Syndrome (Cheiralgia Paresthetica)
    Radial sensory nerve entrapment at the distal forearm
    is characterized by pain. It may be related to closed
    trauma, laceration, or wearing a tight wristwatch or
    handcuffs. The nerve is compressed in pronation by the
    scissoring effect of the tendons of the brachioradialis
    and extensor carpi radialis longus. The physical examination will show a positive Tinel sign. Provocative testing includes wrist flexion and ulnar deviation and pronation. The Finkelstein maneuver places traction on the
    nerve and may increase symptoms. Electrodiagnostic
    testing is rarely useful in the diagnosis. Nonsurgical
    management includes splinting, activity modification,
    and local corticosteroid injections. Surgical release is
    occasionally needed if symptoms persist.

    Tendon Transfers
    Tendon transfers can provide an alternative to functional deficits secondary to nerve palsy. Adherence to
    certain principles is critical for successful tendon transfer surgery (Table 9). Planning for tendon transfer surgery requires identifying the key lost functions and the
    motor resources available to treat the deficit(s).

    Radial Nerve Palsy

    2011 American Academy of Orthopaedic Surgeons

    Radial nerve palsy is the most common indication for


    tendon transfer in the upper extremity. It can be classified as a high (radial nerve proper) or a low (posterior
    interosseous nerve syndrome) palsy. It is important to
    maintain full passive range of motion in the hand and
    wrist before proceeding with tendon transfer. Nonsurgical treatment includes wrist splint immobilization (including the metacarpophalangeal joints in extension) or
    a dynamic splint. Early tendon transfers can be considered as an internal splint as opposed to definitive
    treatment. Although there are several tendon transfer
    options to treat radial nerve palsy deficits, all generally
    include using the pronator teres to the extensor carpi
    radialis brevis for wrist extension in high radial nerve

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    Posterior Interosseous Nerve Syndrome


    Posterior interosseous nerve syndrome results in weakness of the muscles without clinically measurable loss
    of sensory function. This syndrome may occur spontaneously, after trauma, or may present secondary to a
    mass at the elbow. The diagnosis is based on clinical
    examination findings and electrodiagnostic testing.
    MRI is indicated to evaluate the possible presence of a
    space-occupying lesion. A baseline electromyogram
    should be obtained at 3 to 4 weeks after onset of symptoms and a repeat electromyogram should be obtained
    after 4 to 5 months if there is no return of function. Although posterior interosseous nerve syndrome resolves
    spontaneously in many instances, surgery may be indi-

    371

    Section 3: Upper Extremity

    Table 9

    Principles of Tendon Transfer Surgery


    One tendon, one function

    A split transfer will only function to the shortest excursion of the recipient tendons.

    Straight line of pull

    A straight line between motor and recipient maximizes function of the transfer.

    Similar excursion

    Donor excursion should approximate recipient excursion.

    Similar strength

    Donor strength should approximate recipient strength.

    Expendable donor

    Transferred tendons should not sacrifice existing function.

    Tissue equilibrium

    Tendon transfer surgery should be done at a time when surrounding soft tissue and
    bone is healed and mature.

    Joint mobility

    Soft-tissue maturity includes the correction of contracture. Range of motion of affected


    joints must be maximized prior to transfer.

    Synergy

    Tendon transfers that take advantage of the stabilization effect of antagonistic muscles
    result in improved recipient function.

    Tenodesis

    The normal tenodesis effect of the hand enhances the function of tendon transfers.
    Wrist fusion should be a measure of last resort as this compromises the results of
    tendon transfers.

    Power versus positional motors

    The use of weaker transfers for position and stronger transfers for power uses available
    motor resources more efficiently.

    From Dorf ER, Chhabra AB: Tendon transfer surgery, in Trumble TE, Budoff JE, eds: Hand Surgery Update IV. Rosemont, IL, American Society for Surgery of the
    Hand, 2007, pp 439-453.

    palsy, the palmaris longus to extensor pollicis longus


    for thumb extension, and either the flexor carpi ulnaris
    or flexor carpi radialis to the extensor digitorum communis for finger extension.
    One area of controversy is when to explore radial
    nerve palsy associated with a humeral fracture. Because
    many patients with closed injuries will achieve full recovery of the radial nerve without surgical treatment,
    nonsurgical management is recommended. A baseline
    electrodiagnostic study may be obtained at 3 to 4
    weeks after injury. If there is no evidence of return of
    function of the brachioradialis or radial wrist extensor
    by 4 to 5 months, a repeat electrodiagnostic study can
    be obtained for comparison with the baseline study. If
    there is no evidence of recovery, surgical treatment may
    be indicated. In patients with open fractures or fractures with vascular injury, the radial nerve should be
    explored acutely. Indications for nerve exploration for
    radial nerve palsy occurring after fracture manipulation
    remain controversial.
    3: Upper Extremity

    Median Nerve Palsy


    Median nerve injuries are classified as high or low
    based on whether the lesion is proximal or distal to the
    origin of the anterior interosseous nerve in the proximal forearm. The benefits and prognosis of tendon
    transfer surgery are largely influenced by the quality of
    hand sensation, function in the uninvolved hand, and
    patient motivation.
    Low Median Nerve Palsy
    Low median nerve palsy is the second most common
    reason for tendon transfer in the upper extremity after
    radial nerve palsy. Thumb opposition, largely motored
    372

    Orthopaedic Knowledge Update 10

    by the abductor pollicis brevis, is the primary functional loss in low median nerve palsy. Surgery is indicated when loss of thumb opposition causes a functional deficit for the patient. There are four reliable
    tendon transfers for opposition (opponensplasties): the
    flexor digitorum superficialis of the ring finger opponensplasty (Boyes transfer), the extensor indicis proprius opponensplasty, abductor digiti minimi or Huber
    transfer, and the palmaris longus or Camitz procedure.
    The extensor indicis proprius and flexor digitorum
    superficialis-ring finger are most commonly selected.
    The Huber transfer is most beneficial in pediatric patients with congenital hypoplastic thumb because it
    also improves the hands appearance by increasing the
    bulk of the thenar musculature. The Camitz procedure
    is most commonly performed for loss of opposition secondary to severe carpal tunnel syndrome.
    High Median Nerve Palsy
    In high median nerve palsy, along with loss of thumb
    opposition, flexion is also lost in the thumb, index finger, and long finger. Patients may also have loss of active pronation. In high median nerve palsy, thumb opposition is typically provided by transfer of the
    extensor indicis proprius as previously described. Alternatively, the extensor digiti minimi or extensor carpi ulnaris can be used for opponensplasty. As useful sensory
    recovery is often unlikely in these cases, opponensplasty may not benefit the patient. The preferred
    method to restore index and long finger flexion is a
    side-to-side transfer of the small and ring finger flexor
    digitorum profundus to the index and long flexor digitorum profundus. Flexor pollicis longus function is typically restored through transfer of the brachioradialis.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 29: Hand and Wrist Reconstruction

    Ulnar Nerve Palsy


    Ulnar nerve palsy is characterized by loss of function of
    ulnar-innervated musculature as well as deformity and
    contractures. A high ulnar nerve palsy is distinguished
    from a low ulnar nerve palsy by ring and small finger
    flexor digitorum profundus involvement. The primary
    deformity seen with ulnar nerve deficit is clawing,
    which results from an imbalance between the intrinsic
    and extrinsic muscles.
    Low Ulnar Nerve Palsy
    An injury to the ulnar nerve below the elbow results in
    loss of power pinch, abduction of the small finger, and
    clawing. Although tendon transfers typically improve
    function, they can also correct deformity in ulnar nerve
    palsy. The deficit in power pinch is a result of paralysis
    of the adductor pollicis and the first dorsal interosseous
    muscles. With this functional loss, patients compensate
    by using the extensor pollicis longus to adduct the
    thumb and the flexor pollicis longus to flex the thumb
    interphalangeal joint against the index finger (the compensation is known as the Froment sign). The unopposed extension force of the extensor digiti minimi results in ulnar deviation of the small finger. Clawing
    results because the intrinsic muscles are not functioning
    to flex the metacarpophalangeal joints and extend the
    interphalangeal joints. Tendon transfers for correcting
    clawing must pass volar to the transverse metacarpal
    ligament to flex the proximal phalanx. Many different
    motors have been used to correct clawing, including the
    extensor carpi radialis longus, extensor carpi radialis
    brevis, and palmaris longus. The grafts are attached by
    either a two- or four-tailed graft to the A2 pulleys or
    the radial lateral bands of the small and ring digits or
    all four digits. Power pinch can be restored with a
    Smith transfer (using extensor carpi radialis brevis) or
    with flexor digitorum superficialis of the ring finger.
    Abduction of the small finger (Wartenberg sign) can be
    corrected with transfer of the ulnar insertion of extensor digiti minimi to the radial collateral ligament or A1
    pulley of the small finger.

    Combined Nerve Palsies


    Combined nerve palsies lead to significant disability. A
    combination of low median and low ulnar nerve injury

    2011 American Academy of Orthopaedic Surgeons

    Ulnar Wrist Pain


    The differential diagnosis of ulnar-sided wrist pain includes arthritis, fracture, and instability, along with
    nerve, tendon, and vascular injuries.

    Triangular Fibrocartilage Complex


    The triangular fibrocartilage complex (TFCC) is a major stabilizer of the DRUJ and of the ulnar carpus. It is
    composed of a central articular disk, dorsal and volar
    radioulnar ligaments, a meniscus homolog, the ulnar
    collateral ligament, and the sheath of the extensor carpi
    ulnaris.32 The central disk extends from the sigmoid
    notch of the radius to its insertion at the base of the ulnar styloid. The vascular supply extends to the peripheral 10% to 40% of the TFCC with the central component being avascular.33
    Palmer34 divided TFCC injuries into traumatic (type
    I) and degenerative (type II) categories. Injuries are further classified by the location of the tear and the articular pathology (Table 10). Plain radiographs should be
    obtained and the ulnar variance evaluated (a zero rotation PA view is best). A dynamic PA grip view with the
    forearm in pronation also is helpful. MRI may show
    tears and signal changes at the ulnar part of the lunate,
    which are consistent with ulnocarpal impaction. The
    sensitivity of MRI arthrography for detecting TFCC
    tears ranges from 74% to 100%. Dedicated wrist coils,
    high-resolution pulsed sequences, and high-strength
    magnets can increase diagnostic sensitivity.
    Arthroscopy is the most accurate modality in diagnosing lesions of the TFCC and can help to directly
    evaluate the size and stability of a tear and detect coincident ligament or chondral injuries. Arthroscopy is indicated for patients with symptomatic TFCC injuries
    after failed conservative treatment (typically wrist
    splinting and activity modification for several months).
    Wrist arthroscopy should include midcarpal portals be-

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    High Ulnar Nerve Palsy


    Loss of function of the ring and small finger flexor digitorum profundus is the primary distinguishing deficit
    between low and high ulnar nerve palsy. Clawing will
    not be as pronounced in high ulnar nerve palsy as in
    low ulnar nerve palsy because the extrinsic flexors are
    not functioning. Restoring DIP flexion in the small and
    ring fingers is achieved via side-to-side transfer between
    the long, ring, and small finger flexor digitorum profundus muscles as is the case in a high median nerve
    palsy. Extensor carpi radialis brevis transfer should be
    used to treat the deficit in power pinch because flexor
    digitorum superficialis transfer will further weaken grip
    strength.

    is the most common of these combined palsies. Function in this combined nerve palsy is most impacted by
    the loss of thumb adduction and opposition, thumb to
    index finger pinch, intrinsics, and sensibility. Sensibility
    may be restored through transfer of a dorsal metacarpal artery flap with superficial radial nerve innervated
    skin from the index finger proximal phalanx to the palmar surface of the thumb. Combined high median and
    high ulnar nerve palsy is the second most common
    combined nerve injury and results in even greater loss
    of function. Clawing of all four fingers occurs because
    of the imbalance between the extrinsic flexors and extensors. The goals of surgery are to help restore simple
    grasp and key pinch. A volar neurovascular cutaneous
    island flap from the ring finger may be used to achieve
    sensation for pinch. A recent study has reported promising results with nerve transfers in the hand and upper
    extremity and has indicated that there may be an increasing role for nerve transfer in treating motor and
    sensory deficits.26

    373

    Section 3: Upper Extremity

    Table 10

    Classification and Treatment of TFCC Injuries


    Type

    Description

    Traumatic Tears

    IA

    Isolated central TFCC tear; no instability

    Nonsurgical or arthroscopic dbridement of unstable


    portion: leave at least 2 mm peripherally to avoid
    instability

    IB

    Peripheral tear at base of ulnar styloid; mild DRUJ


    instability; may have extensor carpi ulnaris instability

    Arthroscopic repair of TFCC tear; if ulnar styloid


    ununited with tear, need open procedure:
    pathognomonic finding is loss of triangular
    fibrocartilage normal tension as determined with a
    probe

    IC

    TFCC disruption from the ulnar extrinsic ligaments

    Arthroscopic reefing or tenodesis procedure; open


    repair for large defectcan augment with a strip of
    flexor carpi ulnaris

    ID

    Radial detachment of the TFCC from the sigmoid notch of


    the distal radius

    Open radial-sided TFCC repair; Munster cast for 4


    weeks if TFCC repair

    II

    Degenerative Tears Associated With Ulnar Impaction

    IIA

    TFCC wear without perforation or chondromalacia

    Arthroscopic evaluation and synovectomy; open ulnar


    shortening

    IIB

    TFCC wear with chondromalacia of the lunate or ulna

    Same as IIA

    IIC

    Perforation of TFCC with lunate chondromalacia

    Dbridement of central tear and arthroscopic wafer


    versus open ulnar shortening osteotomy

    IID

    TFCC perforation with ulna and/or lunate chondromalacia


    and lunotriquetral ligament injury but without carpal
    instability (no volar intercalated segmental instability)

    TFCC dbridement and arthroscopic wafer (open ulnar


    shortening if lunotriquetral unstable)

    IIE

    TFCC perforation with arthritic changes involving ulna and


    lunate; lunotriquetral ligament injury

    Ulnar shortening osteotomy with lunotriquetral


    dbridement; lunotriquetral pinning if unstable after
    ulnar shortening

    cause these are more sensitive than radiocarpal arthroscopy for evaluating scapholunate and lunotriquetral
    ligament instability.35

    Treatment

    Annotated References
    1.

    Chung KC, Watt AJ, Kotsis SV: A prospective outcomes


    study of four-corner wrist arthrodesis using a circular
    limited wrist fusion plate for stage II scapholunate advanced collapse wrist deformity. Plast Reconstr Surg
    2006;118(2):433-442.

    2.

    Mulford JS, Ceulemans LJ, Nam D, Axelrod TS: Proximal row carpectomy vs four corner fusion for scapholunate (Slac) or scaphoid nonunion advanced collapse
    (Snac) wrists: A systematic review of outcomes. J Hand
    Surg Eur Vol 2009;34(2):256-263.
    The authors present a meta-analysis comparing proximal row carpectomy and four-corner fusion. Outcomes
    were similar in both groups.

    3.

    Cohen MS, Kozin SH: Degenerative arthritis of the


    wrist: Proximal row carpectomy versus scaphoid excision and four-corner arthrodesis. J Hand Surg Am
    2001;26(1):94-104.

    4.

    Jones DB Jr, Brger H, Bishop AT, Shin AY: Treatment


    of scaphoid waist nonunions with an avascular proximal pole and carpal collapse: A comparison of two vascularized bone grafts. J Bone Joint Surg Am 2008;
    90(12):2616-2625.

    Degenerative Ulnocarpal Impaction

    3: Upper Extremity

    Chronic overloading of the ulnocarpal joint can lead to


    ulnocarpal impaction, which may include wear of the
    ulnar head, lunate, triquetrum, and/or TFCC. Patients
    will present with reports of ulnar-sided wrist pain and
    possibly swelling or decreased range of motion. Pain is
    increased with ulnar deviation, especially when combined with pronation and supination. Positive ulnar
    variance is a known risk factor for ulnar impaction
    syndrome because of the resultant increase in ulnocarpal loading. Degenerative ulnocarpal impaction can be
    developmental or acquired, static or dynamic. Several
    months of nonsurgical treatment should be attempted
    before surgery is considered. Surgical treatment involves an ulnar shortening osteotomy or partial distal
    ulna resection (arthroscopic wafer or hemiresection arthroplasty) to decrease force transmission through the
    ulnar side of the wrist. Newer techniques for ulnar
    shortening use subcondylar osteotomies, require less
    surgical exposure, and may achieve more rapid healing
    in metaphyseal rather than diaphyseal bone.36
    374

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 29: Hand and Wrist Reconstruction

    This retrospective review compares distal radial pedicle


    grafts to medial femoral condyle grafts for scaphoid
    nonunions with an avascular proximal pole. Union rates
    and time to healing were better for medial femoral condyle grafts. Level of evidence: III.
    5.

    6.

    Greenberg JA: Reconstruction of the distal ulna: Instability, impaction, impingement, and arthrosis. J Hand
    Surg Am 2009;34(2):351-356.
    The authors present a review of the etiology and treatment options for distal radioulnar joint pathology.
    Parker WL, Linscheid RL, Amadio PC: Long-term outcomes of first metacarpal extension osteotomy in the
    treatment of carpal-metacarpal osteoarthritis. J Hand
    Surg Am 2008;33(10):1737-1743.
    A small retrospective review of metacarpal osteotomies
    for early and moderate CMC arthritis showed good outcomes at an average 9-year follow-up.

    7.

    Shuler MS, Luria S, Trumble TE: Basal joint arthritis of


    the thumb. J Am Acad Orthop Surg 2008;16(7):418423.
    The authors present a comprehensive review of treatment modalities for CMC joint arthritis.

    8.

    Rizzo M, Moran SL, Shin AY: Long-term outcomes of


    trapeziometacarpal arthrodesis in the management of
    trapeziometacarpal arthritis. J Hand Surg Am 2009;
    34(1):20-26.
    The authors report on a large retrospective review of
    patients treated with CMC arthrodesis. Improvements
    in pinch and grip strength as well as average pain scores
    were reported. Despite the development of arthritis in
    adjacent joints, patient satisfaction scores were excellent
    several years postoperatively. Level of evidence: IV.
    Klimo GF, Verma RB, Baratz ME: The treatment of trapeziometacarpal arthritis with arthrodesis. Hand Clin
    2001;17(2):261-270.

    10.

    Tomaino MM: Distal interphalangeal joint arthrodesis


    with screw fixation: Why and how. Hand Clin 2006;
    22(2):207-210.

    11.

    Chung KC, Ram AN, Shauver MJ: Outcomes of pyrolytic carbon arthroplasty for the proximal interphalangeal joint. Plast Reconstr Surg 2009;123(5):1521-1532.
    A prospective evaluation of pyrolytic carbon implants
    for PIP arthritis revealed improvements in grip and
    pinch strength as well as functional outcome scores. Implant squeaking and dislocation were the most common
    complications.

    12.

    Jennings CD, Livingstone DP: Surface replacement arthroplasty of the proximal interphalangeal joint using
    the PIP-SRA implant: Results, complications, and revisions. J Hand Surg Am 2008;33(9):1565, e1-e11.
    The authors present a retrospective review of PIP joint
    arthroplasties performed with surface replacement arthroplasty implants. Although range of motion did not
    improve, pain scores were significantly better. The complication rate was 26%. Loosening in noncemented

    2011 American Academy of Orthopaedic Surgeons

    13.

    Bonzar M, Firrell JC, Hainer M, Mah ET, McCabe SJ:


    Kienbck disease and negative ulnar variance. J Bone
    Joint Surg Am 1998;80(8):1154-1157.

    14.

    Watanabe T, Takahara M, Tsuchida H, Yamahara S, Kikuchi N, Ogino T: Long-term follow-up of radial shortening osteotomy for Kienbock disease. J Bone Joint
    Surg Am 2008;90(8):1705-1711.
    The authors present results of a follow-up questionnaire
    administered to patients treated with radial shortening osteotomy for Kienbock disease. Most patients reported
    mild pain and little functional loss. Level of evidence: IV.

    15.

    Croog AS, Stern PJ: Proximal row carpectomy for advanced Kienbcks disease: Average 10-year follow-up.
    J Hand Surg Am 2008;33(7):1122-1130.
    A long-term follow-up of proximal row carpectomies
    for Kienbck disease showed reliable results and minimal functional limitations. Patients with more advanced
    disease were more likely to require conversion to arthrodesis. Level of evidence: IV.

    16.

    Kalainov DM, Cohen MS, Hendrix RW, Sweet S, Culp


    RW, Osterman AL: Preisers disease: Identification of
    two patterns. J Hand Surg Am 2003;28(5):767-778.

    17.

    Moran SL, Cooney WP, Shin AY: The use of vascularized grafts from the distal radius for the treatment of
    Preisers disease. J Hand Surg Am 2006;31(5):705-710.

    18.

    Keith MW, Masear V, Chung K, et al: Diagnosis of carpal tunnel syndrome. J Am Acad Orthop Surg 2009;
    17(6):389-396.
    The authors discuss the clinical practice guideline for diagnosis of carpal tunnel syndrome developed by AAOS.

    19.

    Weber RA, Rude MJ: Clinical outcomes of carpal tunnel


    release in patients 65 and older. J Hand Surg Am 2005;
    30(1):75-80.

    20.

    Hobby JL, Venkatesh R, Motkur P: The effect of age


    and gender upon symptoms and surgical outcomes in
    carpal tunnel syndrome. J Hand Surg Br 2005;30(6):
    599-604.

    21.

    Thomsen NO, Cederlund R, Rosn I, Bjrk J, Dahlin


    LB: Clinical outcomes of surgical release among diabetic
    patients with carpal tunnel syndrome: Prospective
    follow-up with matched controls. J Hand Surg Am
    2009;34(7):1177-1187.
    The authors report on a prospective, consecutive
    matched series of diabetic and nondiabetic patients
    treated with carpal tunnel release. Diabetic patients had
    the same beneficial outcome as nondiabetic patients.
    Level of evidence: I.

    22.

    Keith MW, Masear V, Amadio PC, et al: Treatment of


    carpal tunnel syndrome. J Am Acad Orthop Surg 2009;
    17(6):397-405.

    Orthopaedic Knowledge Update 10

    3: Upper Extremity

    9.

    prostheses was the most common reason for revision


    surgery. Level of evidence: IV.

    375

    Section 3: Upper Extremity

    Clinical practice guidelines for the treatment of carpal


    tunnel syndrome are discussed. Nine specific recommendations are made.
    23.

    24.

    25.

    26.

    27.

    3: Upper Extremity

    28.

    376

    Scholten RJ, Gerritsen AA, Uitdehaag BM, van Geldere


    D, de Vet HC, Bouter LM: Surgical treatment options
    for carpal tunnel syndrome. Cochrane Database Syst
    Rev 2004;4(4):CD003905.

    29.

    Vogel RB, Nossaman BC, Rayan GM: Revision anterior


    submuscular transposition of the ulnar nerve for failed
    subcutaneous transposition. Br J Plast Surg 2004;57(4):
    311-316.

    30.

    Lee JT, Azari K, Jones NF: Long term results of radial


    tunnel release: The effect of co-existing tennis elbow,
    multiple compression syndromes and workers compensation. J Plast Reconstr Aesthet Surg 2008;61(9):10951099.

    Amadio PC: Interventions for recurrent/persistent carpal


    tunnel syndrome after carpal tunnel release. J Hand
    Surg Am 2009;34(7):1320-1322.
    This case report-based article presents an algorithm for
    evaluation and treatment recommendations for recurrent or persistent carpal tunnel syndrome.
    Guideline on the Treatment of Carpal Tunnel Syndrome. American Academy of Orthopaedic Surgeons
    Web
    site.
    http://www.aaos.org/research/guidelines/
    CTStreatmentguide.asp. Accessed October 5, 2010.
    The AAOS work group recommendations on the guideline for treating carpal tunnel syndrome are summarized. A list of the work group members also is provided.
    Brown JM, Mackinnon SE: Nerve transfers in the forearm and hand. Hand Clin 2008;24(4):319-340, v.
    This review article presents nerve transfer options for
    restoring motor and sensory deficits in each nerve in the
    hand and forearm.
    Zlowodzki M, Chan S, Bhandari M, Kalliainen L, Schubert W: Anterior transposition compared with simple
    decompression for treatment of cubital tunnel syndrome: A meta-analysis of randomized, controlled trials. J Bone Joint Surg Am 2007;89(12):2591-2598.
    The authors present a meta-analysis of randomized controlled studies evaluating the efficacy of simple decompression of the ulnar nerve compared with anterior
    transposition. Results showed no significant difference
    in motor nerve conduction velocities or clinical outcome
    scores between the two procedures.
    Ahcan U, Zorman P: Endoscopic decompression of the
    ulnar nerve at the elbow. J Hand Surg Am 2007;32(8):
    1171-1176.
    In a retrospective review of endoscopically assisted ulnar nerve decompression at the elbow, the authors reported only one complication (hematoma). All patients
    had electrophysiologic improvement after surgery, were
    satisfied with the procedure, and returned to full activities within 3 weeks.

    Orthopaedic Knowledge Update 10

    The authors of this retrospective analysis of outcomes of


    radial tunnel release at an average of 57 months after
    surgery reported better outcomes in patients with radial
    tunnel pathology alone compared with patients with additional pathologies.
    31.

    Bolster MA, Bakker XR: Radial tunnel syndrome: Emphasis on the superficial branch of the radial nerve.
    J Hand Surg Eur Vol 2009;34(3):343-347.
    In a study reporting results on 12 patients with radial
    tunnel syndrome treated with surgical decompression of
    the superficial branch of the radial nerve, 11 patients
    were satisfied with the results.

    32.

    Palmer AK, Werner FW: The triangular fibrocartilage


    complex of the wrist: Anatomy and function. J Hand
    Surg Am 1981;6(2):153-162.

    33.

    Bednar MS, Arnoczky SP, Weiland AJ: The microvasculature of the triangular fibrocartilage complex: Its clinical significance. J Hand Surg Am 1991;16(6):11011105.

    34.

    Palmer AK: Triangular fibrocartilage complex lesions: A


    classification. J Hand Surg Am 1989;14(4):594-606.

    35.

    Hofmeister EP, Dao KD, Dao KD, Glowacki KA, Shin


    AY: The role of midcarpal arthroscopy in the diagnosis
    of disorders of the wrist. J Hand Surg Am 2001;26(3):
    407-414.

    36.

    Slade JF III, Gillon TJ: Osteochondral shortening osteotomy for the treatment of ulnar impaction syndrome:
    A new technique. Tech Hand Up Extrem Surg 2007;
    11(1):74-82.
    A new technique for ulnar shortening osteotomy is described that preserves the articular surface of the distal
    ulna. The osteotomy is secured with headless compression screws and, therefore, complications associated
    with plating are avoided.

    2011 American Academy of Orthopaedic Surgeons

    This page intentionally left blank

    This page intentionally left blank

    Chapter 30

    Fractures of the Pelvis and


    Acetabulum
    Henry Claude Sagi, MD

    Frank A. Liporace, MD

    Introduction

    Current Issues and Controversies in the


    Treatment of Pelvic Ring Injuries
    Four controversies concerning the treatment of pelvic
    ring injuries currently exist. (1) Malunion of one
    hemipelvis may result in leg length inequality, mechan-

    Initial Evaluation and Management of


    Patients With Pelvic Fractures

    Dr. Sagi or an immediate family member serves as a


    board member, owner, officer, or committee member of
    the Orthopaedic Trauma Association of the American
    Academy of Orthopaedic Surgeons; is a member of a
    speakers bureau or has made paid presentations on behalf of Stryker, Smith & Nephew, and AO; serves as a
    paid consultant to or is an employee of Smith &
    Nephew, Synthes, and Stryker; and has received research
    or institutional support from Smith & Nephew, Synthes,
    and Stryker. Dr. Liporace or an immediate family member is a member of a speakers bureau or has made paid
    presentations on behalf of DePuy, A Johnson & Johnson
    Company, Osteotech, Synthes, and Smith & Nephew;
    serves as a paid consultant to or is an employee of
    DePuy, A Johnson & Johnson Company, Osteotech, Synthes, and Smith & Nephew; serves as an unpaid consultant to AO; and has received research or institutional
    support from Synthes and Smith & Nephew.

    Established standard prehospital transport protocols


    and emergency department management algorithms
    have documented benefit and should be followed to decrease patient morbidity and mortality. The multiply injured patient is at risk for thoracic, intra-abdominal,
    soft-tissue, pelvic, and extremity hemorrhage, and requires a coordinated multidisciplinary team approach.
    The most common injuries associated with pelvic fractures are chest injury in up to 63% of patients, long
    bone fractures in 50%, brain and abdominal injury
    (spleen, liver, bladder, and urethra) in 40%, and spine
    fractures in 25%.2
    Injuries to the bladder and urethra have a reported
    incidence of 15% to 20% (21% in males and 8% in females). Bladder and urethral trauma occur with relatively equal frequency (approximately 7%). When pelvic fractures are accompanied by bladder rupture,
    associated mortality can be as high as 22% to 34% because of the significant force required to rupture a hollow viscus within the pelvis. The clinical finding most

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    Traumatic pelvic and acetabular fractures result from


    high-energy accidents such as motor vehicle crashes,
    auto-pedestrian collisions, falls, and crush injuries. Because of the great forces that are required to disrupt the
    pelvic ring, traumatic pelvic fractures and the accompanying visceral and soft-tissue injuries are associated
    with diverse outcomes. Prior to the 1980s, there was a
    substantial lack of both clinical and scientific information regarding the biomechanics and techniques for stabilization of pelvic ring disruptions. Modern strategies
    and philosophies regarding surgical and nonsurgical
    treatment of injuries to the pelvic ring continue to
    evolve to include early open reduction and internal fixation to restore normal anatomic relationships in hopes
    of improving functional outcomes.

    ical low back pain, sitting imbalance, dyspareunia, and


    bowel and/or bladder dysfunction. However, the exact
    relationship of pelvic malunion to functional outcome
    remains unclear.
    (2) Ligamentous injuries (symphyseal disruptions
    and sacroiliac (SI) joint dislocations) heal less predictably than fractures and may result in chronic pain secondary to pelvic instability. Accurately identifying
    those injuries that exhibit sufficient ligamentous instability to warrant surgical stabilization remains difficult.
    (3) Completely unstable injuries of the posterior ring
    managed with posterior fixation should be supplemented with some form of anterior fixation to improve
    stability and restore the normal loading response of the
    unstable hemipelvis.1 However, this may depend on
    whether the anterior injury is ligamentous (symphysis)
    or bony (ramus).
    (4) Anatomic reduction and stable fixation is more
    critical for the unstable posterior pelvic ring than anterior. However, considerable debate exists regarding the
    order of fixation and reduction maneuvers as it pertains to the nature and extent of posterior injury.

    379

    Section 4: Lower Extremity

    Table 1

    Clinical Findings That May Be Present in


    Patients With a Pelvic Fracture
    External rotation of one or both extremities
    Limb-length discrepancy
    Scrotal, labial, and/or perineal ecchymosis
    Urethral, vaginal, and/or rectal bleeding
    Neurologic deficit

    4: Lower Extremity

    consistently observed after bladder or urethral injury is


    gross hematuria, which is present in approximately
    95% of patients; most bladder ruptures are extraperitoneal.3
    Gastrointestinal injuries and open pelvic fractures
    are seen in 4% to 5% of patients with pelvic fracture,
    and significantly increase the incidence of deep pelvic
    and soft-tissue infection, osteomyelitis, mortality, and
    long-term disability. Diverting colostomy and distal
    washout are performed to reduce the chance of pelvic
    wound infection when damage to the anal sphincter
    with a perineal laceration exists or fecal soiling of an
    open perineal wound that communicates with the fracture is possible. Diverting colostomy should be performed within the first 6 to 8 hours following injury to
    reduce the incidence of sepsis and death.4
    Modern evaluation of a patient with blunt abdominal and pelvic trauma routinely involves the use of
    plain radiographs; CT of the chest, abdomen, and pelvis; diagnostic peritoneal lavage (DPL); and focused abdominal sonography for trauma (FAST) examination
    for free fluid and bleeding within the peritoneal and
    preperitoneal cavities. The sequence of assessments outlined in the Advanced Trauma Life Support course and
    handbook is helpful for organizing an approach to
    managing potentially unstable trauma patients.5 Table
    1 lists the clinical findings that may be present in patients with a pelvic fracture.
    Persistent pelvic hemorrhage and hemodynamic instability despite appropriate fluid resuscitation is usually the
    result of coagulopathy and/or pelvic arterial bleeding and
    requires urgent intervention to prevent ongoing blood
    loss, shock, and death. In a recent review of the German
    Trauma Registry, the rate of mortality directly attributable to pelvic injury and hemorrhage was 7%.6
    External compression devices such as inflatable garments, pelvic binders/sheets applied over the greater
    trochanters, and external fixators are generally the first
    line of intervention for persistent hypotension after appropriate fluid resuscitation in a patient with pelvic
    fracture and no other potential source of hemorrhage.
    Internal rotation and adduction of the lower extremities (if possible) can be helpful in reducing external rotation deformities of the pelvic ring. Anterior pelvic external fixation frames function by internally rotating an
    externally rotated (open book) hemipelvis around a
    sufficiently intact posterior ring that functions as a
    380

    Orthopaedic Knowledge Update 10

    hinge. With skillful placement of the pins and lateral to


    medial translation of the hemipelvis, some control of
    the posterior ring is also possible.
    For patients who present in shock and/or have persistent hemodynamic instability despite pelvic compression, appropriate resuscitation and exclusion of thoracic, abdominal, and extremity hemorrhage,
    laparotomy with pelvic packing or angiography should
    be considered. The basic tenets are well outlined in the
    practice management guidelines promulgated by the
    Eastern Association for the Surgery of Trauma.7
    The use of transfemoral angiography with selective
    embolization of injured arteries should be based on initial response to resuscitation and the presence of a contrast blush on CT. Necrosis of pelvic viscera, sexual
    dysfunction, and soft-tissue necrosis (particularly gluteal) are potential complications seen with aggressive
    angiography, particularly with bilateral internal iliac arterial occlusion in patients who have had large extensile
    exposures.8 For those patients in extremis, pelvic packing may be preferable to taking a desperately ill, unstable patient to the angiography suite.9
    Radiologic Evaluation
    Apart from the standard AP pelvic radiograph taken as
    part of the traditional trauma series, radiologic evaluation of the pelvic ring should include the inlet and outlet projections. The pelvic inlet view is obtained with the
    x-ray beam directed caudally approximately 40 to 60
    to the radiographic film. The inlet view is helpful in imaging external or internal rotation of the hemipelvis, diastasis of the SI joint, and impaction fractures of the sacral ala. The pelvic outlet is obtained by directing the
    x-ray beam approximately 30 to 60 cephalad to the radiographic film. The outlet view is helpful in imaging
    cephalad vertical shift of the hemipelvis and the location of sacral fractures relative to the foramina. CT is
    performed routinely using 2- to 3-mm axial sections (or
    3 mm of vertical travel per 360 rotation of the gantry
    in a spiral CT). Images with this resolution should disclose most injuries and allow for good-qualtiy threedimensional and multiplanar reconstructions.

    Classification of Pelvic Fractures


    The Young and Burgess classification scheme,10 currently the most widely used, focuses on the mechanism
    of injury and represents further refinement and modification of the work performed by Pennal and Tile.11
    These two classification schemes are summarized in Tables 2 and 3.

    Nonsurgical Treatment of Pelvic Ring Injuries


    The following injury patterns can be considered sufficiently stable to warrant a trial of nonsurgical care:
    nondisplaced or minimally displaced ramus fractures;
    symphyseal disruptions with less than 2.5 cm of widening (anteroposterior compression injury); and impacted
    sacral fractures without cephalad displacement or excessive internal rotation of the hemipelvis (lateral
    compression injury).

    2011 American Academy of Orthopaedic Surgeons

    Chapter 30: Fractures of the Pelvis and Acetabulum

    Table 2

    Table 3

    Young and Burgess Classification Scheme

    Pennal and Tile Classification Scheme

    Lateral Compression (LC type): rami fractures plus:

    Type A: Pelvic Ring Stable

    LC I: sacral fracture on side of impact (usually impacted


    fracture).

    A1: fractures not involving the ring (ie, avulsions, iliac wing
    or crest fractures).

    LC II: crescent fracture on side of impact.

    A2: stable minimally displaced fractures of the pelvic ring

    LC III: type I or II injury on side of impact with contra-lateral


    open book injury.

    Type B: Pelvic Ring Rotationally Unstable, Vertically Stable

    Anteroposterior Compression (APC type): symphysis


    diastasis or rami fractures plus:

    B2: lateral compression, ipsilateral

    APC I: minor opening of symphysis and SI joint anteriorly


    (SI, STL, and SSL intact)

    APC III: complete disruption of SI joint and all supporting


    ligaments

    B3: lateral compression, contralateral or bucket-handle type


    injury
    Type C: Pelvic Ring Rotationally and Vertically Unstable
    C1: unilateral

    4: Lower Extremity

    APC II: opening of anterior SI (sacrospinous and


    sacrotuberous ligaments), intact posterior SI ligaments

    B1: open book

    C2: bilateral
    C3: associated with acetabular fracture

    Vertical Shear (VS type)


    Vertical displacement of hemipelvis with symphysis diastasis
    or rami fractures anteriorly
    Iliac wing fracture, sacral facture or SI dislocation posteriorly
    Combination (CM type): any combination of above injuries

    Although some authors have used single-leg stance


    views to diagnose occult instability in the subacute or
    chronic setting, these tests have limited utility in the
    acute phase of the injury.12,13 Examination under anesthesia with dynamic intraoperative stress fluoroscopic
    views can be used to diagnose occult instability of the
    pelvic ring; however, the tolerable ranges of motion of
    the pelvic ring under stress examination are not well
    defined (Figure 1). Some lateral compression injuries of
    the sacrum in patients with good bone quality may be
    treated successfully in some circumstances with immediate weight bearing as tolerated without the risk of
    further displacement. Because the consequences of
    malunion can significantly affect function and quality
    of life for patients, a course of nonsurgical care requires
    a compliant patient and frequent serial physical and radiographic examinations to detect early displacement.

    Indications for Surgical Reduction and


    Fixation of Anterior Pelvic Ring Injuries
    The indications for surgical reduction and fixation of
    anterior pelvic ring injuries include symphyseal dislocations demonstrating greater than 2.5 cm of diastasis
    (implying disruption of the sacrospinous and sacrotuberous ligaments) with static or dynamic (examination
    under anesthesia) imaging; augmentation of posterior
    fixation in vertically displaced unstable pelvic ring injuries; a locked symphysis; pain and immobility; or the
    presence of tilt fractures.
    External Anterior Fixation
    Some of the more frequent complications that have limited the use of external fixation devices for definitive

    2011 American Academy of Orthopaedic Surgeons

    treatment of unstable pelvic injuries include pin site


    complications, interference with abdominal access,
    their cumbersome nature, inability to maintain accurate
    reductions, and bladder entrapment.14 However, when
    formal open reduction and internal fixation is contraindicated by open pelvic fractures, contaminated abdominal incisions, or complex bladder and urethral injuries, external fixation may be a good treatment
    option. Recent biomechanical studies have demonstrated that supra-acetabular frames15 (Figure 2) are
    similar to traditional iliac crest frames in resisting flexion and extension but superior in resisting internal and
    external rotation.16 Five-millimeter Schanz pins for
    both constructs have been shown to be significantly
    stronger than 4-mm pins.17
    Open Reduction and Internal
    Fixation of Symphyseal Disruptions
    One recent study has shown a higher rate of fixation failure and pelvic malunion with two-hole symphyseal plating, recommending a plating configuration that has at
    least two points of fixation on either side of the symphysis.18 Dual plating and multiplanar symphyseal plates
    have not been shown to offer improved stability in biomechanical studies and are currently used only in revision or failed fixation cases.19 The role of locking plates
    for symphyseal fixation remains undefined. Four- and
    six-hole precontoured symphyseal plates with 3.5- or
    4.5-mm cortical screws are the constructs most commonly used by most pelvic reconstruction surgeons (Figure 3).
    Open Reduction and Internal
    Fixation of Ramus Fractures
    Many ramus fractures can be treated nonsurgically because of the surrounding periosteal sleeve that enhances
    stability and provides rapid, predictable bony healing.
    Surgical fixation of widely displaced ramus fractures
    should be considered for augmenting posterior fixation

    Orthopaedic Knowledge Update 10

    381

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 1

    A, Technique for examination under anesthesia of pelvic ring. B, Preoperative static film of pelvic ring injury.
    C, Intraoperative dynamic stress view of the pelvis showing an unstable pelvic ring.

    Figure 2

    A, Clinical photograph of a supra-acetabular pelvic external fixator. B, Radiograph demonstrating pin placement for
    the supra-acetabular frame.

    constructs to increase the stability of the pelvic ring.


    Where indicated, the use of percutaneously placed intramedullary ramus screws can be considered for stabilization of the anterior pelvic ring. Medially located
    fractures can be stabilized with a retrograde ramus
    screw, whereas those fractures located laterally near the
    pubic root may be better treated with an anterior column screw20 (Figure 4).

    Indications for Surgical Reduction and


    Fixation of Posterior Pelvic Ring Injuries

    Figure 3

    382

    Radiograph demonstrating multihole symphyseal


    plating.

    Orthopaedic Knowledge Update 10

    The indications for surgical reduction and fixation of


    posterior pelvic ring injuries are: displaced iliac wing
    fractures that enter and exit both the crest and greater
    sciatic notch or sacroiliac (SI) joint (crescent fractures);
    disruption of the posterior SI ligaments, resulting in
    multiplanar instability of the SI joint; nonimpacted,
    comminuted sacral fractures; any posterior ring injury
    that has demonstrated or has the propensity for cepha-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 30: Fractures of the Pelvis and Acetabulum

    Radiograph demonstrating the use of both anterior column (right) and retrograde rami screws
    (left) for anterior pelvic fixation.

    Figure 5

    Radiograph demonstrating typical fixation for an


    iliac wing fracture.

    Figure 6

    Radiograph demonstrating typical fixation construct for a crescent fracture associated with a
    small crescent fragment and SI joint instability.

    4: Lower Extremity

    Figure 4

    lad (vertical) displacement; and U-shaped sacral fractures with spinal-pelvic dissociation.
    Iliac Wing Fractures and Fracture-Dislocations
    (Crescent Fractures)
    A single pelvic reconstruction plate or lag screw along
    the crest supplemented with a second reconstruction
    plate or lag screw at the level of the pelvic brim (anterior approach) or sciatic buttress (posterior approach)
    will usually suffice in neutralizing deforming forces until healing has occurred21 (Figure 5).
    Iliac wing fractures are more often associated with
    open wounds than other pelvic ring injuries and may be
    associated with entrapped bowel.22 Careful examination of the wound and evaluation of the CT scan for
    subcutaneous air or entrapped bowel is imperative.
    Early reconstruction of the ilium and serial dbridements with open packing and delayed closure, along
    with appropriate prophylactic antibiotic therapy, is recommended.
    Iliac wing fractures that enter the SI joint (crescent
    fractures) result in disruption of some or all of the SI
    ligaments.23 Reduction of crescent fractures involving
    only a small portion of the SI joint are treated similar
    to extra-articular iliac wing fractures, and no iliosacral
    screws are needed. Standard fixation involves a superiorly placed pelvic reconstruction plate along the iliac
    crest with supplemental lag screws from the posterior
    inferior iliac spine (PIIS) into the sciatic buttress just
    above the greater notch. With smaller crescent fragments, the degree of SI joint instability increases and
    the injury behaves more like an SI dislocation; consideration must be given to supplemental fixation with SI
    screws or plates (Figure 6).
    SI Joint Dislocations
    The SI joint can be reduced from either an anterior or
    posterior direction. With significant vertical displace-

    2011 American Academy of Orthopaedic Surgeons

    ment of the hemipelvis, forceful traction may be required, and recent studies have reported that rigidly
    stabilizing the patient to the operating room table using
    some form of table-skeletal fixation24,25 helps considerably in achieving either open or indirect percutaneous
    closed reductions.
    Although biomechanical studies26 have not shown
    significant superiority of either iliosacral screw fixation, transiliac fixation, or anterior SI plating, iliosacral
    screws remain the workhorse for posterior pelvic ring
    stabilization because they can be applied in either the
    prone or supine position, and in open or percutaneous
    situations of severe soft-tissue damage when closed reduction is possible.27,28
    Commonly used iliosacral screws are cannulated
    with diameters of 6.5, 7.3, or 8.0 mm made of titanium

    Orthopaedic Knowledge Update 10

    383

    Section 4: Lower Extremity

    Lateral (A), inlet (B), and outlet (C) radiographic views demonstrating appropriate positioning and trajectory of an
    SI screw for an SI dislocation.

    4: Lower Extremity

    Figure 7

    Figure 9

    Figure 8

    Radiograph demonstrating the use of a


    transsacral screw for fixation of a vertical sacral
    fracture.

    or stainless steel. Long thread lengths with purchase in


    the sacral body and promontory offer the greatest resistance to pullout.29 The SI screw should be directed as
    close to the superior end plate and anterior aspect of S1
    to avoid the upper sacral nerve root tunnel (Figure 7).
    A second iliosacral screw can be placed into S1 or S2 if
    purchase of the first SI screw is thought to be suboptimal or considerable instability of the pelvic ring exists.30 Currently available data from biomechanical
    studies suggest increased stability with a second iliosacral screw for SI dislocations, with a second screw
    into the S2 vertebral body being superior to a second
    screw into S1.1,31
    Vertical Sacral Fractures
    In addition to pelvic instability, vertical sacral fractures
    may result in varying degrees of neurologic deficit.32 The
    indications for reduction and stabilization of vertical sa384

    Radiograph demonstrating the use of triangular


    osteosynthesis for stabilization of a vertically
    unstable transforaminal sacral fracture.

    Orthopaedic Knowledge Update 10

    cral fractures include vertical or cephalad instability in


    the case of a vertical shear sacral fracture; comminuted,
    nonimpacted sacral alar fractures; and impacted sacral
    fractures from lateral compression injuries with excessive internal rotation and pelvic deformity.
    Stabilization of most sacral fracture reductions is
    usually accomplished with one or two iliosacral screws
    placed posteriorly.33 One study has shown that anatomic reduction of the fracture is important for improving fracture stability and increasing the diameter of
    the safe corridor for iliosacral screw placement.34 Another recent publication has advocated the use of a
    transsacral screw that crosses the sacrum to gain
    purchase in the contralateral ilium35 (Figure 8). There
    are no published biomechanical studies demonstrating
    superiority of transsacral screws over standard iliosacral screws.
    An increased risk of loss of reduction in vertical sacral fractures treated with iliosacral screws alone when
    associated with severe comminution, osteoporotic

    2011 American Academy of Orthopaedic Surgeons

    Chapter 30: Fractures of the Pelvis and Acetabulum

    Role of Surgical Navigation in the


    Treatment of Pelvic Fractures
    Due to the inherent difficulties in fiducial positioning
    and obtaining image quality sufficient for tracking and
    navigation, surgical navigation systems for pelvic fixation have not had the same popularity and utility as
    pedicle screws and arthroplasty. Several preliminary reports have examined iliosacral screw placement in cadaver pelves demonstrating improved or equal accuracy
    with a substantial decrease in radiation exposure to the
    surgeon.43,44 Surgical navigational systems still add considerable time to the procedure and should not be used
    in place of experience and knowledge of threedimensional pelvic anatomy.

    Radiograph demonstrating the use of a spinalpelvic construct to stabilize an unstable


    U-shaped sacral fracture with spinal-pelvic
    dissociation.

    bone, or disruption of the L5/S1 facet joint has been


    noted by some authors.36 Spinal-pelvic constructs, such
    as triangular osteosynthesis, have been implemented in
    these situations to help minimize the occurrence of late
    displacement and malunion. Spinal-pelvic constructs
    have been shown to be superior both biomechanically
    and clinically to SI screws alone for maintaining reduction in comminuted sacral fractures37-39 (Figure 9). Patients are able to fully bear weight within a few weeks
    of surgery. Prominent and symptomatic fixation, delayed union and nonunion, lumbosacral scoliosis, and
    the need for later removal are the most commonly encountered problems.40
    Sacral nerve root decompression may be required
    when the patient presents with sacral radiculopathy
    and the preoperative CT scan shows nerve root impingement. When necessary, decompression can be performed directly through the fracture and a sacral
    laminectomy is generally not required.40
    U-Shaped Sacral Fractures: Spinal Pelvic Dissociation
    U-shaped sacral fractures result in dissociation of the
    spine from the pelvic ring (spinal-pelvic dissociation),
    and pelvic ring stability is generally not affected.
    Rather than unilateral radiculopathy, these patients
    present neurologically with cauda equina lesions. Lateral pelvic or lumbosacral radiographs with sagittal
    and coronal CT reconstructions are critical in identifying this injury pattern. Some authors advocate in situ
    bilateral SI screw fixation alone for impacted, stable injuries without significant kyphosis or neurologic deficit.41 However, U-shaped sacral fractures with spinalpelvic dissociation and cauda equina syndrome
    commonly require reduction, decompression and some
    form of bilateral posterior spinal-pelvic fixation construct to control kyphotic deformity and allow early
    mobilization of the patient42 (Figure 10).

    2011 American Academy of Orthopaedic Surgeons

    4: Lower Extremity

    Figure 10

    Internal Degloving Soft-Tissue Injuries


    Serial drainage, dbridement, and vacuum-assisted closure of the wound before formal open reduction and
    internal fixation is generally advocated by most trauma
    surgeons; however, percutaneous drainage and lavage
    may be appropriate in select cases.45,46

    Outcome Studies for Pelvic Fractures


    Certain outcome studies47,48 support the position that
    the long-term functional results are improved if reduction with less than 1 cm of combined displacement of
    the posterior ring is obtained, particularly with pure
    dislocations of the SI complex. Fractures of the posterior ring tend to have better postoperative function
    than dislocations that rely on scar formation and ligamentous healing.49 However, pure dislocations of the SI
    joint that heal with a solid bony ankylosis have not
    demonstrated improved outcome over those without
    ankylosis.50 Despite anatomic reduction, however, other
    studies have shown that a substantial number of patients continue to have poor outcomes, with chronic
    posterior pelvic pain.51,52 Males frequently report erectile dysfunction and females frequently report dyspareunia, urinary difficulty, and pregnancy-related issues
    with an increase in the need for cesarean section.53-56
    Outcome after pelvic fracture is associated with significantly higher mortality in the elderly: 12.3% versus
    2.3% in the younger age groups, despite equal need for
    transfusion and similar injury patterns.57 Fewer than
    50% of patients with severe pelvic fractures return to
    their previous level of function and work status and the
    majority of patients sustain persistent impairment in
    both the physical and mental components of the Short
    Form-36 questionnaire.

    Current Issues and Controversies in the


    Treatment of Acetabular Fractures
    Acetabular fractures are fairly rare injuries, with an annual incidence of approximately 0.003%.58 Most of
    these injuries occur in a bimodal age distribution, with
    young adults more frequently suffering high-energy injuries (for example, motor vehicle accidents and falls
    from heights) and the elderly sustaining low-energy in-

    Orthopaedic Knowledge Update 10

    385

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 11

    A, The external and internal aspects of the innominate bone showing the anterior and posterior columns and
    ischiopubic rami. B, Schematic representation of the Letournel and Judet classification. (A reproduced with permission from Baumgaertner MR, Tornetta P III, eds: Orthopaedic Knowledge Update: Trauma 3. Rosemont, IL,
    American Academy of Orthopaedic Surgeons, 2005, pp 259269. B reproduced with permission from Fischgrund
    JS, ed: Orthopaedic Knowledge Update 9. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2008, pp
    389397.)

    jury mechanisms (for example, falls from standing position).

    Evaluation and Initial Management


    Prior to deciding whether surgical treatment is indicated,
    an understanding of the local anatomy and radiographic
    portrayal of the fracture is required. The two-column
    concept was developed to elucidate a better understanding of the complex surrounding osseous anatomy and its
    radiographic corollaries responsible for supporting the
    asymmetric, hemispherical acetabulum. As a result, the
    Letournel classification of acetabular fractures was developed59 (Figure 11) and has been shown to have substantial reliability (kappa >0.7) when used by surgeons
    386

    Orthopaedic Knowledge Update 10

    who treat acetabular fractures regularly or who interpret


    images.60 Plain radiographic analysis should include an
    AP pelvic radiograph with associated Judet views (45
    obturator and iliac oblique views). A supplementary CT
    scan, often with coronal and sagittal or even threedimensional reconstructions, can be very helpful. When
    combined with an AP radiograph, CT has been postulated to increase the interobserver reliability of classification over an AP radiograph combined with Judet
    views.61 A recent analysis of 11 computer-reconstructed
    radiographs from CT scans determined that these radiographs were effective in supplying necessary data and
    more esthetically pleasing than standard plain radiographs. Computer-reconstructed radiographs have the

    2011 American Academy of Orthopaedic Surgeons

    Chapter 30: Fractures of the Pelvis and Acetabulum

    Surgical Timing and Bleeding


    Assuming the patient is medically stable to undergo
    surgery, some authors have historically waited 3 to 5
    days after injury to perform definitive treatment. Also,
    it has been anecdotally postulated that less bleeding occurs from fracture surfaces during surgery when delayed, but cessation of fracture bleeding most reliably
    occurs with reduction and fixation. No specific evidence exists to support that delayed fixation decreases
    intraoperative bleeding. Many surgeons incorporate the
    use of cell-saver technology in an effort to decrease the
    requirement of allogenic blood transfusion. In a recent
    analysis of 186 acetabular surgeries in which 60 of the
    patients had a cell-saver, a significant difference in the
    rates of intraoperative and postoperative transfusion
    received by patients was not determined. The cell-saver
    group averaged a 282% greater cost in blood-related
    charges.64 Certain acetabular fractures have an increased need for blood transfusion within the first 24
    hours after admission. In a retrospective review of 289
    acetabular fractures, both-column, anterior column,
    anterior column/posterior hemitransverse, and T-type
    fractures had a 56% incidence of requiring transfusion
    within 24 hours of admission compared to 28% for
    other fracture types.65
    It must be recognized that there has been variability
    within the literature when defining early fixation of
    acetabular fractures, which has ranged from 24 hours
    to 2 weeks.66 Another recent series evaluated 68 patients with isolated injuries of the femur, pelvis/
    acetabulum, or spine. Preoperatively, those with femoral shaft fractures exhibited the highest levels of
    interleukin-6 and -8, but those with pelvic and acetab-

    2011 American Academy of Orthopaedic Surgeons

    ular injuries exhibited similar levels of interleukin 24


    hours after surgery as those with surgically treated femur fractures. This finding was not dependent on the
    duration of the procedure.67

    Indications
    If the patient is deemed medically and psychologically
    fit to undergo surgical treatment, the following questions must be answered when determining whether surgical treatment or nonsurgical management with or
    without skeletal traction is appropriate.
    (1) Is there articular (wall or columnar) displacement, how much, and where in the acetabulum?
    (2) If displaced, is there secondary congruence?
    (3) Is the fracture stable?
    (4) Can the fracture be appropriately fixed based
    on factors such as bone quality and excessive
    impaction?
    (5) Does the surgeon or institution have the expertise
    and experience to adequately treat the fracture?
    Many surgeons quantify the intact weight-bearing
    dome on radiographs by evaluating the roof-arc angle
    on the AP and Judet views. It has been postulated that
    a fracture that lies within a roof-arc of <45 on any of
    the three standard acetabular radiographs involves the
    weight-bearing dome. If displacement is unacceptable,
    reduction and fixation are required.68 A recent study
    evaluating what CT findings correlate to this superior
    weight-bearing dome has determined that on the axial
    cuts, the superior 10 mm represents this area of importance.69 Biomechanical analyses have suggested that the
    significance of the roof-arc angle is not the same on all
    three standard acetabular radiographs.70,71 With certain
    both-column fractures that maintain secondary congruence, nonsurgical treatment may be considered with approximately 85% acceptable results.72 It should be
    noted that with secondary congruence, the stress concentration during simulated single-leg stance increases
    substantially in the dome adjacent to the area of the
    fracture line.73 The presence of articular displacement
    must be considered before nonsurgical treatment is undertaken. A recent review of 32 patients treated nonsurgically with more than 3 mm of articular incongruity yielded only 56% good to excellent results.74
    Although posterior wall fractures are most common
    clinically,59 they are often difficult to treat. Concomitant hip dislocation, femoral head injury, intra-articular
    fragments, patient age older than 55 years, and marginal impaction all have a significant effect on results
    and have only fair interobserver agreement when classifying these additional factors.75-77 Determining displacement and potential instability also play a role
    when considering surgical management of posterior
    wall fractures. Gross instability after closed reduction
    with subluxation occurring with 40 of hip flexion,
    intra-articular osteochondral fragments that are not
    isolated small avulsions within the fovea, and fractures
    that involve more than 50% of the posterior wall are
    absolute indications for surgical intervention. A recent
    review of 10 years of acetabular fractures seen at a level

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    potential to overcome patient-related factors (for example, discomfort, bowel gas, or overlying osseous structures) when positioning for standard radiographic
    views.62
    The propensity for associated nonskeletal injury in
    patients with acetabular fractures, especially from highenergy mechanisms, should not be overlooked. A recent
    study indicated that when correlating Letournel classification of the fracture with the force vector most likely
    responsible for the fracture, a statistically significant
    higher association with retroperioneal hematomas, visceral injuries, and vascular injuries occurred with patterns that resulted from a lateral loading. Although
    posterior hip dislocations in isolation have a relatively
    impressive rate of osteonecrosis of the femoral head,
    those associated with an acetabular fracture do not
    necessarily correlate with a poor prognosis and have
    been shown to have a 71% rate of good to excellent results when appropriately managed.63 Impaction fractures of the femoral head also can occur and can have
    implications on prognosis. These fractures often occur
    concomitantly with dislocation or with significant medialization of the femoral head to the ilioischial line
    (protrusio) as seen with many associated fracture patterns. The implication of injury to the femoral head is
    significant when considering prognosis.63

    387

    Section 4: Lower Extremity

    4: Lower Extremity

    1 trauma center yielded a 26% rate of intra-articular


    osteochondral fragments when postreduction CT scan
    was evaluated.78 When determining percentage of posterior wall involvement on axial CT scan to define instability, multiple measurement methods have been proposed, with the resultant conclusion that fractures
    involving less than 20% of the posterior wall are most
    likely stable, those involving 20% to 50% have intermediate risk of instability with justification for fluoroscopic stress examination, and those involving more
    than 50% are unstable. A recent study discusses a modified method that accounts for measurement at the level
    of the largest posterior wall defect and accounts for
    marginal impaction. When calculating the percentage
    of posterior wall involvement and tendency to be stable, intermediate risk, or unstable, there was a resultant
    100% specificity, sensitivity, and positive predictive
    value.79
    It is clear that anatomic reduction with stable fixation is the goal. The ability to accurately assess reduction quality does have variability between plain radiograph and CT scan. One study evaluated patients in
    whom received radiographs and CT scan were performed postoperatively to evaluate quality of reduction
    as well as interobserver and intraobserver agreement.
    Although plain radiography was only 75% sensitive at
    detecting residual articular displacement, the added
    cost and radiation exposure of postoperative routine
    CT scans could not be justified because altering postoperative management was not necessary in any of the 20
    cases reviewed.80

    Choices of Surgical Approach


    Surgical treatment of acetabular fractures is with the
    Kocher-Langenbeck, ilioinguinal, or in selected cases,
    the extended iliofemoral approach. Variants to these as
    well as the option for percutaneous supplementary or
    definitive treatment may also be used. Direction of displacement, the ability to reduce the fracture and apply
    adequate fixation, and surgeon experience will dictate
    the approach chosen.
    The Kocher-Langenbeck approach is recommended
    for posterior wall, posterior column, transverse,
    transverse-posterior wall, and some T-type fractures. It
    allows direct access to the posterior column and posterior wall safely from the superior aspect of the greater
    sciatic notch to the ischial tuberosity. Through the
    greater sciatic notch, reduction clamp access and digital
    palpation of the quadrilateral surface can be conducted. Care must be taken to surgically preserve any
    blood supply to the femoral head that has not been
    traumatized by the injury with preservation of the
    quadratus femoris.81
    A modification of the Kocher-Langenbeck approach
    with the addition of a trochanteric digastric osteotomy
    will allow more superior and anterior exposure when
    addressing fracture patterns that require access for reduction and fixation that is proximal to the superior
    aspect of the greater sciatic notch and decrease the risk
    of affecting the neurovascular supply to the abductors
    388

    Orthopaedic Knowledge Update 10

    through inadvertent stretch injury. The ilioinguinal approach is advocated for anterior column, anterior wall,
    anterior column with associated posterior hemitransverse, both-column, and certain T-type or transverse
    fractures. Access to the pelvic brim, internal iliac fossa,
    iliac crest, and anterior SI joint are possible.81 In an effort to directly buttress the quadrilateral plate and
    avoid the inadvertent potential complications of a hernia and external iliac vessel injury with the ilioinguinal
    approach, the modified Stoppa approach with or without the lateral window of the ilioinguinal approach has
    been advocated.82,83 A retrospective review of 55 patients treated by two experienced pelvic/acetabular surgeons yielded an 89% good to excellent radiographic
    result, with a relatively low complication rate.84 Another review of 25 patients yielded similar results with
    up to 95% satisfactory to anatomic reductions and
    highlighted the versatility of this approach to address
    acetabular and pelvic ring injuries85 (Figure 12). The
    extended iliofemoral approach has been advocated for
    complex acetabular fractures that are being operated
    on more than 21 days after injury, fractures that have a
    transtectal transverse component or T-type fracture
    with dome involvement, both-column fractures with
    extension to the sacroiliac joint, or fractures requiring
    simultaneous anterior and posterior columnar exposure.63,86,87 This seemingly morbid approach yields acceptable results based on quality of articular reduction,
    although heterotopic ossification can be more prevalent
    than with the other approaches discussed.86,88,89

    New Technologies and Techniques


    Recently, the ability to acquire three-dimensional (3-D)
    CT reconstructions, computer navigation, 3-D fluoroscopy, and improved visualization with two-dimensional
    fluoroscopy have contributed to better preoperative
    planning and percutaneous/limited open reduction and
    fixation techniques.90-95 In an early series of limited
    open reduction with percutaneous fixation, acceptable
    reductions were obtained in all young patients, within
    an average of 3 mm of anatomic reduction in elderly
    patients. Surgical time averaged 75 minutes and blood
    loss averaged 50 mL. All of the younger patients went
    on to union with an average Harris hip score of 96.
    These techniques have also been used in elderly patients
    with minimally displaced acetabular fractures to improve early mobilization in an effort to avoid
    immobility-associated medical complications. A recent
    evaluation of 21 elderly patients with minimally or
    nondisplaced acetabular fractures underwent percutaneous fluoroscopically guided columnar screw fixation
    with no reported complications. Patients were allowed
    mobilization the first day after surgery and were bearing weight as tolerated at 4 weeks. At an average
    follow-up of 3.5 years, no radiographic evidence of degenerative changes, hardware failure, or fracture displacement was seen.96 The use of these techniques requires a detailed understanding of the anatomy as well
    as a willingness and ability to convert to standard open

    2011 American Academy of Orthopaedic Surgeons

    Chapter 30: Fractures of the Pelvis and Acetabulum

    4: Lower Extremity

    Figure 12

    A, Preoperative AP pelvic radiograph of both-column fracture. B through D, Postoperative AP and Judet views after open reduction with internal fixation via a modified Stoppa approach in conjunction with the lateral window
    of the ilioinguinal. Note intrapelvic supplementary fixation.

    surgery if appropriate reduction and stability is not attainable.

    Specific Considerations
    Construct Stability and Supplementation
    Adequacy of fixation is always a concern. The ability
    to match the need for stable fixation with technical and
    anatomic limitations can be challenging. Each fracture
    pattern in conjunction with comminution, patient factors, and surgeon experience play a role in making this
    determination. A combination of fragment-specific
    3.5-mm screws with reconstruction plates for buttress
    effect is commonly used. With plate fixation the concept of near-near and far-far screw positioning relative
    to the fracture site provides the greatest stability.97
    Frequently, transverse acetabular fractures are approached through a single incision yet involve both columns. Therefore, fixation options are dictated by the surgical exposure with or without percutaneous screw
    supplementation. In terms of biomechanical stability, the
    combination of posterior column plating with anterior
    column screw fixation provides a significantly stiffer
    construct than posterior plate fixation alone or isolated

    2011 American Academy of Orthopaedic Surgeons

    anterior and posterior column screw fixation or screw


    and wire fixation.97,98 In some patients, anterior column
    width or fracture geometry may preclude anterior column screw fixation from the posterior approach. A recent evaluation of 35 patients with a minimum 18month follow-up showed that isolated posterior column
    fixation with dual plating did not yield statistically different radiographic or clinical results when compared to
    posterior column plating combined with anterior column
    screw fixation.99 An alternative to supplementing isolated posterior plating for transverse fractures is the use
    of locked plates, which have been shown to provide results similar to more traditional fixation methods in
    terms of resisting displacement under cyclical loading.100
    Locked plating may also be beneficial in the treatment
    of patients with osteopenia. In an effort to provide additional stability in the presence of marginal impaction
    that has been reduced, subchondral minifragment specific fixation has been used to supplement buttress plating with 93% good to excellent results at a mean
    follow-up of 35 months.101 For smaller posterior wall
    fragments that are not amenable to lag screw fixation,
    spring plates have also been used.102,103

    Orthopaedic Knowledge Update 10

    389

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 13

    A, Preoperative axial CT of a 72-year-old woman with an acetabular fracture showing femoral head impaction,
    multiple intra-articular osteochondral fragments, osteopenia, and severe comminution. B, Postoperative AP pelvic
    radiograph of limited columnar fixation in conjunction with bone grafting and total arthroplasty with cage.

    Dome Impaction/Arthroplasty
    Osteopenia causes complications during acetabular fixation. Initial radiographic signs reveal known problems
    when treating these patients. Most significantly, superomedial dome impaction can result in a gull wing
    sign that precludes consistent long-term results with internal fixation.104 Elderly patients and those with osteopenia, femoral head impaction, endogenous obesity,
    more than 40% cartilage abrasion, and extensive impaction may have better results with columnar fixation
    and total hip arthroplasty done acutely.77 Outcome
    after early fixation and late hip arthroplasty is predictably poor.105,106Revision acetabular surgery delayed longer than 3 weeks when persistent instability concomitant with femoral head pathology is present yields poor
    results, especially in the elderly.107 Limited fixation has
    been advocated in conjunction with these acute total
    hip arthroplasties to limit the undesired complication
    of significant superomedial migration of the hip center,
    which could result in premature loosening and poor results.77 With a mean follow-up of 8.1 years and 79%
    good to excellent results, the average subsidence in one
    series was 3 mm medial and 2 mm vertical in the first 6
    weeks. Ultimately, cup position stabilized and there
    were no instances of premature loosening using combined limited fixation and acute total hip arthroplasty.108 A recent series of 18 patients using similar
    techniques, with an average age of 72 years and average follow-up of 3.9 years, yielded a mean Harris hip
    score of 88, minimal cup migration, no loosening, and
    one acute revision within 3 weeks.76 Initial cup stability,
    when supplemented by limited fixation, may be an issue in certain situations. Combining limited fixation
    with cage reconstruction and cemented polyethylene
    liners may help achieve treatment goals (Figure 13). Elderly patients and those with osteopenia, acetabular
    fractures, and significant impaction remain challenging
    to treat.
    390

    Orthopaedic Knowledge Update 10

    Complications
    Acetabular fracture surgery requires a detailed understanding of the local anatomy. Complications can be
    quite severe and such surgery should be performed by
    those who have had adequate training and experience.
    Appropriate prophylaxis can be implemented to limit
    the incidence of certain predictable complications.
    Wound infection, nerve injury, posttraumatic arthritis,
    osteonecrosis, heterotopic bone formation, and thromboembolic complications (discussed in the pelvis section) are most commonly associated with acetabular
    fractures.63,109 Alterations in gait patterns affecting the
    hip, knee, and ankle, regardless of approach, have been
    discussed in the literature.110
    Long-term single-surgeon series have shown infection rates between 2% and 5%.63,111 Considerations of
    the surrounding soft tissues, approach, and timing play
    a significant role.112 Obesity has been shown to contribute to the propensity for infection, thromboembolic
    events, and increased intraoperative blood loss.113-115
    Morbid obesity carries a relative risk of 2.6 when considering overall complication rate. A recent series
    showed a statistically significant increase in total surgical time, hospital stay, and complication rate (63%) in
    morbidly obese patients. Although not a statistically
    significant finding, morbidly obese patients also had increased positioning time and estimated intraoperative
    blood loss.114
    Nerve injury can involve the sciatic, superior gluteal,
    femoral, ilioinguinal, lateral femoral cutaneous, and
    obturator nerves.116 Large series rates of iatrogenically
    induced sciatic nerve injury have been shown to range
    from 2% to 6%.63,117 Nerve injury may occur from the
    injury or surgical manipulation. Although fracture pattern or surgical approach may intuitively lead to suspicion of what nerve may be injured, these are not without deviation. A recent report of two cases with sciatic
    nerve palsy found entrapment in the posterior colum-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 30: Fractures of the Pelvis and Acetabulum

    3.

    Cass AS: The multiple injured patient with bladder


    trauma. J Trauma 1984;24(8):731-734.

    4.

    Brenneman FD, Katyal D, Boulanger BR, Tile M, Redelmeier DA: Long-term outcomes in open pelvic fractures. J Trauma 1997;42(5):773-777.

    5.

    American College of Surgeons Committee on Trauma:


    Advanced Trauma Life Support for Doctors, ed 6,
    1997.

    6.

    Hauschild O, Strohm PC, Culemann U, et al: Mortality


    in patients with pelvic fractures: Results from the German pelvic injury register. J Trauma 2008;64(2):
    449-455.
    The authors provide a review of more than 4,000 patients from 23 different hospitals over two segments of
    time, 1991-1993 (prior to well-organized prehospital
    and in-hospital resuscitative algorithms) and 1998-2000
    (after establishment of such). Mortality directly attributable to the pelvic fracture decreased from 11% to 7%
    despite similar Injury Severity Scores.

    7.

    DiGiacomo JC, Bonadies JA, Cole FJ, et al: Practice


    management guidelines for hemorrhage in pelvic fracture: Eastern Association for the Surgery of Trauma
    (EAST), Winston-Salem, North Carolina. 2001. http://
    www.east.org/tpg/pelvis.pdf. Accessed January 5, 2010.

    8.

    Velmahos GC, Toutouzas KG, Vassiliu P, et al: A prospective study on the safety and efficacy of angiographic
    embolization for pelvic and visceral injuries. J Trauma
    2002;53(2):303-308, discussion 308.

    9.

    Cothren CC, Osborn PM, Moore EE, Morgan SJ, Johnson JL, Smith WR: Preperitonal pelvic packing for
    hemodynamically unstable pelvic fractures: A paradigm shift. J Trauma 2007;62(4):834-839, discussion
    839-842.
    The authors describe the results of a team approach
    (critical care and orthopaedic trauma surgeons) to peritoneal and pelvic packing in hemodynamically unstable
    patients with pelvic fracture. In this series of 29 patients, blood loss and the need for both angiography
    and transfusion were decreased with preperitoneal pelvic packing.

    10.

    Young JW, Burgess AR, Brumback RJ, Poka A: Pelvic


    fractures: Value of plain radiography in early assessment
    and management. Radiology 1986;160(2):445-451.

    11.

    Pennal GF, Tile M, Waddell JP, Garside H: Pelvic disruption: Assessment and classification. Clin Orthop
    Relat Res 1980;151(151):12-21.

    12.

    Garras DN, Carothers JT, Olson SA: Single-leg-stance


    (flamingo) radiographs to assess pelvic instability: How
    much motion is normal? J Bone Joint Surg Am 2008;
    90(10):2114-2118.
    Serial pelvic radiographs were taken in healthy men and
    multiparous and nulliparous women to identify the normal range of motion at the symphysis. Multiparous
    women had the most motion, and up to 5 mm of motion
    at the symphysis was considered within normal limits.

    Annotated References
    1.

    Sagi HC, DiPasquale T: Biomechanical analysis of fixation for vertically unstable sacroiliac dislocations with
    iliosacral screws and symphyseal plating. J Orthop
    Trauma 2004;18(3):138-143.

    2.

    Demetriades D, Karaiskakis M, Toutouzas K, Alo K,


    Velmahos G, Chan L: Pelvic fractures: Epidemiology
    and predictors of associated abdominal injuries and outcomes. J Am Coll Surg 2002;195(1):1-10.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    nar component of a both-column fracture requiring release through a Kocher-Langenbeck approach and ultimate improvement of symptomatology.118 Lower
    extremity positioning with the hip extended and knee
    flexed may decrease the incidence of sciatic nerve injury
    when undergoing a posterior approach to the acetabulum. Heterotopic ossification (HO) prophylaxis can
    help decrease the risk of delayed nerve entrapment.
    Electromyography has been shown to be superior to
    somatosensory-evoked potential monitoring in detecting intraoperative sciatic nerve compromise, but utility
    and consistent results in terms of decreasing iatrogenic
    intraoperative nerve injury are limited.119-121
    HO is a known complication of acetabular fractures
    and their associated surgical interventions ,which seem
    to be more prevalent after extended iliofemoral approaches compared to the Kocher-Langenbeck or ilioinguinal approach. HO has been shown to adversely affect
    outcome.122,123 Necrotic gluteus minimus muscle has
    been postulated to contribute to HO. Dbridement of necrotic gluteus minimus muscle has been suggested as a
    means of decreasing the incidence of HO after the
    Kocher-Langenbeck approach.124 Prophylaxis with indomethacin or one low dose of irradiation (700 800 cGy)
    within 3 days of surgery has been shown to provide prophylaxis, but questions remain about the relative effectiveness of these treatments.125 A recent meta-analysis
    yielded 5 appropriate prospective studies with a total of
    384 patients, which showed a significantly lower incidence of HO in patients treated with radiation (3%) as
    opposed to indomethacin (9%) for prophylaxis.126
    Posttraumatic arthritis can result from traumatic
    cartilage damage, osteochondral loss, intra-articular
    fragements or hardware, and imperfect surgical reductions. Also, development of arthritis, aside from causing pain, may be related to hip muscle weakness.127 Detection of intra-articular hardware can be done with
    the aid of fluoroscopy and even adjunctive intraoperative auscultation with an esophageal stethoscope.128
    Clinical and radiographic results closely correlate. Anatomic reductions are considered to have less than 2
    mm of displacement, imperfect reductions have 2 to 3
    mm of displacement, and poor reductions have more
    than 3 mm of displacement. With anatomic reduction,
    an approximately 75% rate of good to excellent results
    can be expected. The rate of anatomic reduction decreases with increased fracture complexity, patient age,
    and the interval between the injury and the reduction.

    391

    Section 4: Lower Extremity

    13.

    14.

    4: Lower Extremity

    15.

    16.

    17.

    18.

    392

    Siegel J, Tornetta P III: Single-leg-stance radiographs in


    the diagnosis of pelvic instability. J Bone Joint Surg Am
    2008;90(10):2119-2125.
    Radiographic examination of 38 patients with pelvic
    pain for greater than 6 weeks was done. The authors attempted to correlate radiographic findings of instability
    (>5 mm of motion using flamingo views) with visual analog scores; no correlation was found.
    Mason WT, Khan SN, James CL, Chesser TJ, Ward AJ:
    Complications of temporary and definitive external fixation of pelvic ring injuries. Injury 2005;36(5):599-604.

    21.

    Switzer JA, Nork SE, Routt ML Jr: Comminuted fractures of the iliac wing. J Orthop Trauma 2000;14(4):
    270-276.

    22.

    Charnley GJ, Dorrell JH: Small bowel entrapment in an


    iliac wing fracture. Injury 1993;24(9):627-628.

    23.

    Borrelli J JR, Koval KJ, Helfet DL: Operative stabilization of fracture dislocations of the sacroiliac joint. Clin
    Orthop Relat Res 1996;329:141-146.

    24.

    Lefaivre KA, Starr AJ, Reinert CM: Reduction of displaced pelvic ring disruptions using a pelvic reduction
    frame. J Orthop Trauma 2009;23(4):299-308.

    Gnsslen A, Pohlemann T, Krettek C: [A simple supraacetabular external fixation for pelvic ring fractures]. Oper Orthop Traumatol 2005;17(3):296-312.
    Archdeacon MT, Arebi S, Le TT, Wirth R, Kebel R,
    Thakore M: Orthogonal pin construct versus parallel
    uniplanar pin constructs for pelvic external fixation: A
    biomechanical assessment of stiffness and strength.
    J Orthop Trauma 2009;23(2):100-105.
    The authors present a biomechanical comparison of traditional iliac crest external fixators, supra-acetabular
    fixators, and orthogonal pin fixators (combination of iliac crest and supra-acetabular pins) in a cadaver study.
    Orthogonal constructs were stiffer in resisting flexion
    and extension, whereas supra-acetabular constructs
    were superior in resisting internal and external rotation.
    Ponsen KJ, Joosse P, Van Dijke GA, Snijders CJ: External fixation of the pelvic ring: An experimental study on
    the role of pin diameter, pin position, and parasymphyseal fixator pins. Acta Orthop 2007;78(5):648-653.
    The authors present a cadaver biomechanical study that
    showed increased external fixation frame stiffness with
    pin diameters of 8 mm as well as the addition of supraacetabular pins to an iliac crest construct.
    Sagi HC, Papp S: Comparative radiographic and clinical
    outcome of two-hole and multi-hole symphyseal plating. J Orthop Trauma 2008;22(6):373-378.
    A retrospective review of 92 patients treated with multihole and two-hole symphyseal plates is presented.
    Two-hole symphyseal plates were associated with a
    higher rate of loss of reduction, pelvic malunion, and
    fixation failure.

    19.

    Simonian PT, Schwappach JR, Routt ML Jr, Agnew SG,


    Harrington RM, Tencer AF: Evaluation of new plate designs for symphysis pubis internal fixation. J Trauma
    1996;41(3):498-502.

    20.

    Starr AJ, Nakatani T, Reinert CM, Cederberg K: Superior pubic ramus fractures fixed with percutaneous
    screws: What predicts fixation failure? J Orthop
    Trauma 2008;22(2):81-87.
    The authors describe a technique for retrograde ramus
    screws in pelvic fractures and report a 15% complication rate in 82 patients. Elderly female patients with
    fractures medial to the lateral border of the foramen
    were predicted to have the greatest chance of failure of
    retrograde ramus screws.

    Orthopaedic Knowledge Update 10

    The authors present a technical description and report


    of 35 patient consecutive series for the use of pelvic reduction frame for closed or percutaneous reduction of
    displaced pelvic ring injuries.
    25.

    Matta JM, Yerasimides JG: Table-skeletal fixation as an


    adjunct to pelvic ring reduction. J Orthop Trauma
    2007;21(9):647-656.
    A technical description of table-skeletal fixation for applying greater amounts of traction in the reduction of
    pelvic ring injuries is presented.

    26.

    Yinger K, Scalise J, Olson SA, Bay BK, Finkemeier CG:


    Biomechanical comparison of posterior pelvic ring fixation. J Orthop Trauma 2003;17(7):481-487.

    27.

    Keating JF, Werier J, Blachut P, Broekhuyse H, Meek


    RN, OBrien PJ: Early fixation of the vertically unstable
    pelvis: The role of iliosacral screw fixation of the posterior lesion. J Orthop Trauma 1999;13(2):107-113.

    28.

    Carlson DA, Scheid DK, Maar DC, Baele JR, Kaehr


    DM: Safe placement of S1 and S2 iliosacral screws: The
    vestibule concept. J Orthop Trauma 2000;14(4):264269.

    29.

    Kraemer W, Hearn T, Tile M, Powell J: The effect of


    thread length and location on extraction strengths of iliosacral lag screws. Injury 1994;25(1):5-9.

    30.

    Moed BR, Geer BL: S2 iliosacral screw fixation for disruptions of the posterior pelvic ring: A report of 49
    cases. J Orthop Trauma 2006;20(6):378-383.
    A retrospective review of posterior pelvic fixation using
    iliosacral screws placed into the S2 vertebral segment is
    presented. All screws were safely placed and there were
    no iatrogenic nerve injuries. Loss of reduction occurred
    in 4%.

    31.

    van Zwienen CM, van den Bosch EW, Snijders CJ,


    Kleinrensink GJ, van Vugt AB: Biomechanical comparison of sacroiliac screw techniques for unstable pelvic
    ring fractures. J Orthop Trauma 2004;18(9):589-595.

    32.

    Denis F, Davis S, Comfort T: Sacral fractures: An important problem. Retrospective analysis of 236 cases. Clin
    Orthop Relat Res 1988;227:67-81.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 30: Fractures of the Pelvis and Acetabulum

    33.

    Simonain PT, Routt C Jr, Harrington RM, Tencer AF:


    Internal fixation for the transforaminal sacral fracture.
    Clin Orthop Relat Res 1996;323(323):202-209.

    34.

    Reilly MC, Bono CM, Litkouhi B, Sirkin M, Behrens


    FF: The effect of sacral fracture malreduction on the
    safe placement of iliosacral screws. J Orthop Trauma
    2003;17(2):88-94.
    Beaul PE, Antoniades J, Matta JM: Trans-sacral fixation for failed posterior fixation of the pelvic ring. Arch
    Orthop Trauma Surg 2006;126(1):49-52.

    36.

    Griffin DR, Starr AJ, Reinert CM, Jones AL, Whitlock


    S: Vertically unstable pelvic fractures fixed with percutaneous iliosacral screws: Does posterior injury pattern
    predict fixation failure? J Orthop Trauma 2003;17(6):
    399-405.

    37.

    38.

    39.

    40.

    Schildhauer TA, Ledoux WR, Chapman JR, Henley


    MB, Tencer AF, Routt ML Jr: Triangular osteosynthesis
    and iliosacral screw fixation for unstable sacral fractures: A cadaveric and biomechanical evaluation under
    cyclic loads. J Orthop Trauma 2003;17(1):22-31.
    Sagi HC, Militano U, Caron T, Lindvall E: A comprehensive analysis with minimum 1-year follow-up of vertically unstable transforaminal sacral fractures treated
    with triangular osteosynthesis. J Orthop Trauma 2009;
    23(5):313-319, discussion 319-321.
    A technical description and case series of 40 patients
    followed both clinically and radiographically are presented. The study shows the reliability of triangular fixation in maintaining reduction of comminuted sacral
    fractures, but complications such as iatrogenic nerve injury (13%), L5/S1 scoliosis (16%), delayed union
    (25%), and symptomatic fixation requiring removal
    (95%) were common.
    Schildhauer TA, Josten C, Muhr G: Triangular osteosynthesis of vertically unstable sacrum fractures: A new
    concept allowing early weight-bearing. J Orthop
    Trauma 1998;12(5):307-314.

    Collinge C, Coons D, Tornetta P, Aschenbrenner J:


    Standard multiplanar fluoroscopy versus a fluoroscopically based navigation system for the percutaneous insertion of iliosacral screws: A cadaver model. J Orthop
    Trauma 2005;19(4):254-258.

    44.

    Day AC, Stott PM, Boden RA: The accuracy of


    computer-assisted percutaneous iliosacral screw placement. Clin Orthop Relat Res 2007;463:179-186.
    The authors report on a cadaver accuracy study in 10
    specimens during which iliosacral screws were placed
    using surgical navigation and conventional multiplanar
    fluoroscopy. Accuracy with navigation was as good as
    that of conventional methods, deviations in the intended
    path with navigation occurred only in dysmorphic sacra, and radiation exposure was decreased.

    45.

    Hak DJ, Olson SA, Matta JM: Diagnosis and management of closed internal degloving injuries associated
    with pelvic and acetabular fractures: The MorelLavalle lesion. J Trauma 1997;42(6):1046-1051.

    46.

    Tseng S, Tornetta P III: Percutaneous management of


    Morel-Lavallee lesions. J Bone Joint Surg Am 2006;
    88(1):92-96.

    47.

    Dujardin FH, Hossenbaccus M, Duparc F, Biga N,


    Thomine JM: Long-term functional prognosis of posterior injuries in high-energy pelvic disruption. J Orthop
    Trauma 1998;12(3):145-150, discussion 150-151.

    48.

    Tornetta P III, Matta JM: Outcome of operatively


    treated unstable posterior pelvic ring disruptions. Clin
    Orthop Relat Res 1996;329(329):186-193.

    49.

    Cole JD, Blum DA, Ansel LJ: Outcome after fixation of


    unstable posterior pelvic ring injuries. Clin Orthop
    Relat Res 1996;329(329):160-179.

    50.

    Mullis BH, Sagi HC: Minimum 1-year follow-up for patients with vertical shear sacroiliac joint dislocations
    treated with iliosacral screws: Does joint ankylosis or
    anatomic reduction contribute to functional outcome?
    J Orthop Trauma 2008;22(5):293-298.

    Sagi HC: Technical aspects and recommended treatment


    algorithms in triangular osteosynthesis and spinopelvic
    fixation for vertical shear transforaminal sacral fractures. J Orthop Trauma 2009;23(5):354-360.
    The author describes the technical aspects to applying
    the technique of spinal-pelvic fixation contructs relative
    to vertical shear sacral fractures, with the specific intent
    of maintaining reduction and avoiding potential complications and pitfalls.

    Patients with pure SI dislocations treated with iliosacral


    screws were followed up after a minimum of 1 year for
    both functional outcome testing and CT. No correlation
    was made between the degree of ankylosis and functional outcome; however, magnitude of combined displacement was correlated with outcome, confirming
    some earlier studies.

    41.

    Nork SE, Jones CB, Harding SP, Mirza SK, Routt ML


    Jr: Percutaneous stabilization of U-shaped sacral fractures using iliosacral screws: Technique and early results. J Orthop Trauma 2001;15(4):238-246.

    51.

    Gustavo Parreira J, Coimbra R, Rasslan S, Oliveira A,


    Fregoneze M, Mercadante M: The role of associated injuries on outcome of blunt trauma patients sustaining
    pelvic fractures. Injury 2000;31(9):677-682.

    42.

    Schildhauer TA, Bellabarba C, Nork SE, Barei DP,


    Routt ML Jr, Chapman JR: Decompression and lumbopelvic fixation for sacral fracture-dislocations with
    spino-pelvic dissociation. J Orthop Trauma 2006;20(7):
    447-457.

    52.

    Nepola JV, Trenhaile SW, Miranda MA, Butterfield SL,


    Fredericks DC, Riemer BL: Vertical shear injuries: Is
    there a relationship between residual displacement and
    functional outcome? J Trauma 1999;46(6):1024-1029,
    discussion 1029-1030.

    2011 American Academy of Orthopaedic Surgeons

    4: Lower Extremity

    35.

    43.

    Orthopaedic Knowledge Update 10

    393

    Section 4: Lower Extremity

    53.

    Pohlemann T, Gnsslen A, Schellwald O, Culemann U,


    Tscherne H: Outcome after pelvic ring injuries. Injury
    1996;27(suppl 2):B31-B38.

    54.

    Ramirez JI, Velmahos GC, Best CR, Chan LS, Demetriades D: Male sexual function after bilateral internal iliac artery embolization for pelvic fracture. J Trauma
    2004;56(4):734-739, discussion 739-741.
    Copeland CE, Bosse MJ, McCarthy ML, et al: Effect of
    trauma and pelvic fracture on female genitourinary, sexual, and reproductive function. J Orthop Trauma 1997;
    11(2):73-81.

    56.

    Cannada LK, Barr J: Pelvic fractures in woment of


    childbearing age. Clin Orthop Relat Res 2010;468(7):
    1781-1789.
    The authors completed a review of 71 women of childbearing age who sustained pelvic fractures. There was a
    high incidence of genitourinary complaints (49%) in
    this population; 38% of women had pain with sexual
    intercourse. Twenty-six women had children after their
    pelvic fracture: 38% delivered vaginally and 62% had a
    cesarean section. Four of the women who delivered vaginally had surgical fixation of their pelvic fracture. The
    rate of cesarean section was more than double standard
    norms, but the authors found that vaginal delivery after
    a pelvic fracture, even with surgical fixation sparing the
    public symphysis, is possible.

    4: Lower Extremity

    55.

    394

    57.

    Obrien DP, Luchette FA, Pereira SJ, et al: Pelvic fracture in the elderly is associated with increased mortality.
    Surgery 2002;132(4):710-714, discussion 714-715.

    58.

    Laird A, Keating JF: Acetabular fractures: A 16-year


    prospective epidemiological study. J Bone Joint Surg Br
    2005;87(7):969-973.

    59.

    Letournel E: Acetabulum fractures: Classification and


    management. Clin Orthop Relat Res 1980;151 :81-106.

    60.

    Beaul PE, Dorey FJ, Matta JM: Letournel classification


    for acetabular fractures: Assessment of interobserver
    and intraobserver reliability. J Bone Joint Surg Am
    2003;85-A(9):1704-1709.

    61.

    Ohashi K, El-Khoury GY, Abu-Zahra KW, Berbaum


    KS: Interobserver agreement for Letournel acetabular
    fracture classification with multidetector CT: are standard Judet radiographs necessary? Radiology 2006;
    241(2):386-391.

    62.

    Borrelli J Jr, Peelle M, McFarland E, Evanoff B, Ricci


    WM: Computer-reconstructed radiographs are as good
    as plain radiographs for assessment of acetabular fractures. Am J Orthop (Belle Mead NJ) 2008;37(9):455459, discussion 460.
    This study evaluated 11 retrospectively identified patients with displaced acetabular fractures. Five orthopaedic surgeons with various trauma experience evaluated computer-generated radiographic acetabular series
    from information gathered on CT scan and overall were
    pleased with the provided information.

    Orthopaedic Knowledge Update 10

    63.

    Matta JM: Fractures of the acetabulum: accuracy of reduction and clinical results in patients managed operatively within three weeks after the injury. J Bone Joint
    Surg Am 1996;78(11):1632-1645.

    64.

    Scannell BP, Loeffler BJ, Bosse MJ, Kellam JF, Sims SH:
    Efficacy of intraoperative red blood cell salvage and autotransfusion in the treatment of acetabular fractures.
    J Orthop Trauma 2009;23(5):340-345.
    This recent analysis of 186 acetabular surgeries in which
    60 of the patients had cell-saver could not yield a significant difference in the rates of intraoperative and postoperative transfusion received by patients. The cell-saver
    group averaged a 282% greater cost in blood-related
    charges.

    65.

    Magnussen RA, Tressler MA, Obremskey WT, Kregor


    PJ: Predicting blood loss in isolated pelvic and acetabular high-energy trauma. J Orthop Trauma 2007;21(9):
    603-607.
    In a retrospective review of 289 acetabular fractures,
    both-column, anterior column, anterior column posterior hemitransverse, and T-type fractures had a 56% incidence of receiving transfusion within 24 hours of admission compared to 28% for other fracture types.

    66.

    Katsoulis E, Giannoudis PV: Impact of timing of pelvic


    fixation on functional outcome. Injury 2006;37(12):
    1133-1142.

    67.

    Pape HC, Griensven MV, Hildebrand FF, et al; Epoff


    Study group: Systemic inflammatory response after extremity or truncal fracture operations. J Trauma 2008;
    65(6):1379-1384.
    This prospective multicenter, nonrandomized, cohort
    study evaluated 68 patients with truncal or extremity
    fractures. Patients were separated into three groups: spine
    fractures; pelvic or acetabular fractures; and femur fractures. Perioperative concentrations of IL-6 and IL-8 were
    evaluated during a 24-hour period and set in relation with
    the duration of surgery and degree of blood loss.

    68.

    Matta JM, Anderson LM, Epstein HC, Hendricks P:


    Fractures of the acetabulum: A retrospective analysis.
    Clin Orthop Relat Res 1986;205:230-240.

    69.

    Olson SA, Matta JM: The computerized tomography


    subchondral arc: A new method of assessing acetabular
    articular continuity after fracture (a preliminary report).
    J Orthop Trauma 1993;7(5):402-413.

    70.

    Vrahas MS, Widding KK, Thomas KA: The effects of


    simulated transverse, anterior column, and posterior
    column fractures of the acetabulum on the stability of
    the hip joint. J Bone Joint Surg Am 1999;81(7):966974.

    71.

    Chuckpaiwong B, Suwanwong P, Harnroongroj T:


    Roof-arc angle and weight-bearing area of the acetabulum. Injury 2009;40(10):1064-1066.
    The purpose of this cadaver study was to identify exactly the medial, anterior, and posterior roof-arc angles
    that cross the weight bearing dome. Twenty cadaver

    2011 American Academy of Orthopaedic Surgeons

    Chapter 30: Fractures of the Pelvis and Acetabulum

    fulness of computed tomography following open reduction and internal fixation of acetabular fractures. J Orthop Surg (Hong Kong) 2006;14(2):127-132.

    hips had simulated transverse fractures created and radiographs obtained. The average medial, anterior, and
    posterior roof-arc angles were 46, 52, 61, respectively.
    Tornetta P III: Non-operative management of acetabular
    fractures. The use of dynamic stress views. J Bone Joint
    Surg Br 1999;81(1):67-70.

    73.

    Levine RG, Renard R, Behrens FF, Tornetta P III: Biomechanical consequences of secondary congruence after
    both-column acetabular fracture. J Orthop Trauma
    2002;16(2):87-91.

    74.

    Sen RK, Veerappa LA: Long-term outcome of conservatively managed displaced acetabular fractures. J Trauma
    2009;67(1):155-159.
    This review of 32 patients with displaced acetabular
    fractures (>3 mm) treated nonsurgically evaluated longterm follow-up ( 2 years). In 18 of 32 patients, fracture
    reduction was achieved along with a good to excellent
    clinical score.

    75.

    76.

    Patel V, Day A, Dinah F, Kelly M, Bircher M: The value


    of specific radiological features in the classification of
    acetabular fractures. J Bone Joint Surg Br 2007;89(1):
    72-76.
    Thirty sets of radiographs and CT scans were analyzed
    by six observers on two separate occasions with only a
    moderate interobserver and intraobserver agreement between description of associated issues with the acetabular fracture, as well as the fracture itself.
    Boraiah S, Ragsdale M, Achor T, Zelicof S, Asprinio
    DE: Open reduction internal fixation and primary total
    hip arthroplasty of selected acetabular fractures. J Orthop Trauma 2009;23(4):243-248.
    This retrospective series of 18 patients using similar
    techniques, with an average age of 72 years and average
    follow-up of 3.9 years, yielded a mean Harris hip score
    of 88, minimal cup migration, no loosening, and one
    acute revision within 3 weeks.

    77.

    Mears DC, Velyvis JH, Chang CP: Displaced acetabular


    fractures managed operatively: indicators of outcome.
    Clin Orthop Relat Res 2003;407:173-186.

    78.

    Pascarella R, Maresca A, Reggiani LM, Boriani S: Intraarticular fragments in acetabular fracture-dislocation.


    Orthopedics 2009;32(6):402.
    Three hundred seventy-three acetabular fractures were
    reviewed over a 10-year period; 127 had a fracturedislocation. In 45 cases, postreduction CT displayed
    intra-articular bony fragments that were not consistently defined on plain radiograph, thus, supporting
    postreduction CT scans in these patients.

    79.

    Moed BR, Ajibade DA, Israel H: Computed tomography as a predictor of hip stability status in posterior
    wall fractures of the acetabulum. J Orthop Trauma
    2009;23(1):7-15.

    80.

    OShea K, Quinlan JF, Waheed K, Brady OH: The use-

    2011 American Academy of Orthopaedic Surgeons

    81.

    Templeman DC, Olson S, Moed BR, Duwelius P, Matta


    JM: Surgical treatment of acetabular fractures. Instr
    Course Lect 1999;48:481-496.

    82.

    Qureshi AA, Archdeacon MT, Jenkins MA, Infante A,


    DiPasquale T, Bolhofner BR: Infrapectineal plating for
    acetabular fractures: A technical adjunct to internal fixation. J Orthop Trauma 2004;18(3):175-178.

    83.

    Jakob M, Droeser R, Zobrist R, Messmer P, Regazzoni


    P: A less invasive anterior intrapelvic approach for the
    treatment of acetabular fractures and pelvic ring injuries. J Trauma 2006;60(6):1364-1370.

    84.

    Cole JD, Bolhofner BR: Acetabular fracture fixation via


    a modified Stoppa limited intrapelvic approach: Description of operative technique and preliminary treatment results. Clin Orthop Relat Res 1994;305 :112123.

    85.

    Ponsen KJ, Joosse P, Schigt A, Goslings JC, Luitse JS:


    Internal fracture fixation using the Stoppa approach in
    pelvic ring and acetabular fractures: Technical aspects
    and operative results. J Trauma 2006;61(3):662-667.

    86.

    Griffin DB, Beaul PE, Matta JM: Safety and efficacy of


    the extended iliofemoral approach in the treatment of
    complex fractures of the acetabulum. J Bone Joint Surg
    Br 2005;87(10):1391-1396.

    87.

    Johnson EE, Matta JM, Mast JW, Letournel E: Delayed


    reconstruction of acetabular fractures 21-120 days following injury. Clin Orthop Relat Res 1994;305 :20-30.

    88.

    Alonso JE, Davila R, Bradley E: Extended iliofemoral


    versus triradiate approaches in management of associated acetabular fractures. Clin Orthop Relat Res 1994;
    305:81-87.

    89.

    Stckle U, Hoffmann R, Sdkamp NP, Reindl R, Haas


    NP: Treatment of complex acetabular fractures through
    a modified extended iliofemoral approach. J Orthop
    Trauma 2002;16(4):220-230.

    90.

    Rommens PM: Is there a role for percutaneous pelvic


    and acetabular reconstruction? Injury 2007;38(4):463477.
    This article reviews the indications and techniques as
    well as indications for incorporating percutaneous pelvic and acetabular reduction and fixation techniques
    into the complex algorithm of treating these injuries.

    91.

    Starr AJ, Jones AL, Reinert CM, Borer DS: Preliminary


    results and complications following limited open reduction and percutaneous screw fixation of displaced fractures of the acetabulum. Injury 2001;32(Suppl 1):
    SA45-SA50.

    92.

    Rosenberger RE, Dolati B, Larndorfer R, Blauth M,


    Krappinger D, Bale RJ: Accuracy of minimally invasive

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    72.

    395

    Section 4: Lower Extremity

    navigated acetabular and iliosacral fracture stabilization


    using a targeting and noninvasive registration device.
    Arch Orthop Trauma Surg 2010;130(2):223-230.
    The accuracy of guide pin placement was evaluated in
    12 patients with a noninvasive targeting and registration
    device for treatment of acetabular fractures and iliosacral fractures. Accuracy of the target and starting
    and ending points was within 2.8 to 3.9 mm. The authors concluded that this method was effective in stabilizing the injuries described.

    4: Lower Extremity

    93.

    94.

    Kendoff D, Gardner MJ, Citak M, et al: Value of 3D


    fluoroscopic imaging of acetabular fractures comparison to 2D fluoroscopy and CT imaging. Arch Orthop
    Trauma Surg 2008;128(6):599-605.
    In 24 cadaver acetabuli, the authors compared the accuracy of three-dimensional fluoroscopic imaging in evaluating acetabular fracture displacement and implant
    placement with fluoroscopy and CT scans. Its sensitivity
    and specificity for evaluating intraoperative hardware
    was greater than two-dimensional fluoroscopy and
    equivalent to CT scan.
    Cimerman M, Kristan A: Preoperative planning in pelvic and acetabular surgery: The value of advanced computerised planning modules. Injury 2007;38(4):442449.
    Poperative planning of bone fragment reduction, plate
    contouring, and hardware placement using a computergenerated model from preoperative CT scans were helpful before pelvic and acetabular surgery in 10 cases.

    101. Giannoudis PV, Tzioupis C, Moed BR: Two-level reconstruction of comminuted posterior-wall fractures of the
    acetabulum. J Bone Joint Surg Br 2007;89(4):503-509.
    In an effort to provide further stability in the presence of
    marginal impaction that has been reduced, subchondral
    minifragment specific fixation was used by the authors
    in 29 acetabular fractures to supplement buttress plating, with 93% good to excellent results at a mean
    follow-up of 35 months.
    102. Richter H, Hutson JJ, Zych G: The use of spring plates
    in the internal fixation of acetabular fractures. J Orthop
    Trauma 2004;18(3):179-181.
    103. Mast JW: Techniques of open reduction and fixation of
    acetabular fractures, in Tile M, Helfet DL, Kellam JF,
    eds: Fractures of the Pelvis and Acetabulum, ed 3. Philadelphia, PA, Lippincott Williams & Wilkins, 2003, pp
    632-633.
    104. Anglen JO, Burd TA, Hendricks KJ, Harrison P: The
    gull sign: A harbinger of failure for internal fixation
    of geriatric acetabular fractures. J Orthop Trauma
    2003;17(9):625-634.

    95.

    Starr AJ, Reinert CM, Jones AL: Percutaneous fixation


    of the columns of the acetabulum: A new technique.
    J Orthop Trauma 1998;12(1):51-58.

    105. Mears DC: Surgical treatment of acetabular fractures in


    elderly patients with osteoporotic bone. J Am Acad Orthop Surg 1999;7(2):128-141.

    96.

    Mouhsine E, Garofalo R, Borens O, et al: Percutaneous


    retrograde screwing for stabilisation of acetabular fractures. Injury 2005;36(11):1330-1336.

    106. Pagenkopf E, Grose A, Partal G, Helfet DL: Acetabular


    fractures in the elderly: Treatment recommendations.
    HSS J 2006;2(2):161-171.

    97.

    Shazar N, Brumback RJ, Novak VP, Belkoff SM: Biomechanical evaluation of transverse acetabular fracture
    fixation. Clin Orthop Relat Res 1998;352 :215-222.

    98.

    Chang JK, Gill SS, Zura RD, Krause WR, Wang GJ:
    Comparative strength of three methods of fixation of
    transverse acetabular fractures. Clin Orthop Relat Res
    2001;392 :433-441.

    107. Dean DB, Moed BR: Late salvage of failed open reduction and internal fixation of posterior wall fractures of
    the acetabulum. J Orthop Trauma 2009;23(3):180-185.
    The outcome of late revision surgery was retrospectively
    reviewed in a series of four patients with posterior wall
    fractures having recurrent hip instability after failed initial open reduction and internal fixation. Three of four
    patients ultimately required arthroplasty.

    99.

    Giordano V, do Amaral NP, Pallottino A, Pires e Albuquerque R, Franklin CE, Labronici PJ: Operative treatment of transverse acetabular fractures: is it really necessary to fix both columns? Int J Med Sci 2009;6(4):
    192-199.
    This recent evaluation of 35 patients with a minimum
    18-month follow-up showed that isolated posterior column fixation with dual plating did not yield statistically
    different radiographic or clinical results when compared
    to posterior column plating combined with anterior column screw fixation.

    100. Mehin R, Jones B, Zhu Q, Broekhuyse H: A biomechanical study of conventional acetabular internal frac-

    396

    ture fixation versus locking plate fixation. Can J Surg


    2009;52(3):221-228.
    In a biomechanical study, the authors found that locked
    plating provides similar strength when compared to
    conventional plating plus interfragmentary screw for
    fixing transverse acetabular fractures in terms of resisting displacement under cyclical loading.

    Orthopaedic Knowledge Update 10

    108. Mears DC, Velyvis JH: Acute total hip arthroplasty for
    selected displaced acetabular fractures: Two to twelveyear results. J Bone Joint Surg Am 2002;84-A(1):1-9.
    109. Letournel E, Judet R: Fractures of the Acetabulum,
    ed 2. New York, NY, Springer-Verlag, 1993, pp 535562.
    110. Engsberg JR, Steger-May K, Anglen JO, Borrelli J Jr: An
    analysis of gait changes and functional outcome in patients surgically treated for displaced acetabular fractures. J Orthop Trauma 2009;23(5):346-353.
    According to a review of kinematic data, patients surgically treated for acetabular fractures, regardless of the

    2011 American Academy of Orthopaedic Surgeons

    Chapter 30: Fractures of the Pelvis and Acetabulum

    open approach used, had alterations in gait patterns and


    strength at all joints of the affected extremity.
    111. Letournel E, Judet R: Fractures of the Acetabulum, ed
    2. New York, NY, Springer-Verlag, 1993, pp 535-537.
    112. Hak DJ, Olson SA, Matta JM: Diagnosis and management of closed internal degloving injuries associated
    with pelvic and acetabular fractures: The MorelLavalle lesion. J Trauma 1997;42(6):1046-1051.

    120. Helfet DL, Anand N, Malkani AL, et al: Intraoperative


    monitoring of motor pathways during operative fixation of acute acetabular fractures. J Orthop Trauma
    1997;11(1):2-6.
    121. Haidukewych GJ, Scaduto J, Herscovici D Jr , Sanders
    RW, DiPasquale T: Iatrogenic nerve injury in acetabular
    fracture surgery: a comparison of monitored and unmonitored procedures. J Orthop Trauma 2002;16(5):
    297-301.
    122. Triantaphillopoulos PG, Panagiotopoulos EC, Mousafiris C, Tyllianakis M, Dimakopoulos P, Lambiris EE:
    Long-term results in surgically treated acetabular fractures through the posterior approaches. J Trauma 2007;
    62(2):378-382.

    114. Porter SE, Russell GV, Dews RC, Qin Z, Woodall J Jr ,


    Graves ML: Complications of acetabular fracture surgery in morbidly obese patients. J Orthop Trauma
    2008;22(9):589-594.
    Morbid obesity carries a relative risk of 2.6 when overall complication rate is considered. A recent series
    showed a statistically significant increase in total operative time, hospital stay, and complication rate (63%) in
    morbidly obese patients. Although not a statistically significant finding, morbidly obese patients also had increased positioning time and estimated intraoperative
    blood loss.

    The authors reviewed results from 75 patients treated


    with open reduction and internal fixation of displaced
    acetabular fractures through a posterior approach. The
    patients average follow-up was 12.5 years. Results were
    good to excellent in 80% and there was a definite correlation between radiographic and clinical results. The
    most frequent complication was HO (40%). Posttraumatic arthrosis was seen in 10.7% and osteonecrosis in
    8%.

    115. Karunakar MA, Shah SN, Jerabek S: Body mass index


    as a predictor of complications after operative treatment
    of acetabular fractures. J Bone Joint Surg Am 2005;
    87(7):1498-1502.
    116. Routt ML Jr: Surgical treatment of acetabular fractures,
    in Browner BD, Jupiter JB, Levine AM, Trafton PG,
    Krettek C, eds: Skeletal Trauma, ed 4. Philadelphia, PA,
    Saunders, 2009, pp 1207-1208.
    117. Letournel E, Judet R: Fractures of the Acetabulum ed 2.
    New York, NY, Springer-Verlag, 1993. pp 537-539.
    118. Dunbar RP Jr , Gardner MJ, Cunningham B, Routt ML
    Jr : Sciatic nerve entrapment in associated both-column
    acetabular fractures: A report of 2 cases and review of
    the literature. J Orthop Trauma 2009;23(1):80-83.
    This case report cites two cases in which the sciatic
    nerve was found entrapped in the posterior column
    component of a both-column fracture requiring surgical
    release. Both patients had return of nerve function after
    release.
    119. Issack PS, Helfet DL: Sciatic nerve injury associated
    with acetabular fractures. HSS J 2009;5(1):12-18.
    This review outlines the potential causes of sciatic nerve
    injury from acetabular fractures, their treatment, and
    long-term sequelae. The authors discuss the superior results of sensory as opposed to motor function return
    with release.

    2011 American Academy of Orthopaedic Surgeons

    4: Lower Extremity

    113. Russell GV Jr , Nork SE, Chip Routt ML Jr : Perioperative complications associated with operative treatment
    of acetabular fractures. J Trauma 2001;51(6):10981103.

    123. Murphy D, Kaliszer M, Rice J, McElwain JP: Outcome


    after acetabular fracture: Prognostic factors and their
    inter-relationships. Injury 2003;34(7):512-517.
    124. Rath EM, Russell GV Jr , Washington WJ, Routt ML Jr:
    Gluteus minimus necrotic muscle debridement diminishes heterotopic ossification after acetabular fracture
    fixation. Injury 2002;33(9):751-756.
    125. Burd TA, Lowry KJ, Anglen JO: Indomethacin compared with localized irradiation for the prevention of
    heterotopic ossification following surgical treatment of
    acetabular fractures. J Bone Joint Surg Am 2001;
    83(12):1783-1788.
    126. Blokhuis TJ, Frlke JP: Is radiation superior to indomethacin to prevent heterotopic ossification in acetabular fractures?: A systematic review. Clin Orthop Relat
    Res 2009;467(2):526-530.
    This meta-analysis of studies evaluating indomethacin in
    comparison with radiation for HO prophylaxis supports
    radiation therapy as the preferred method for preventing HO after surgical fixation of acetabular fractures.
    127. Matta JM, Olson SA: Factors related to hip muscle
    weakness following fixation of acetabular fractures. Orthopedics 2000;23(3):231-235.
    128. Anglen JO, DiPasquale T: The reliability of detecting
    screw penetration of the acetabulum by intraoperative
    auscultation. J Orthop Trauma 1994;8(5):404-408.

    Orthopaedic Knowledge Update 10

    397

    Chapter 31

    Hip Trauma
    Brian H. Mullis, MD

    Jeffrey Anglen, MD, FACS

    Introduction

    Hip Dislocations
    Traumatic hip dislocations are high-energy injuries and
    are associated with other systemic and musculoskeletal

    Dr. Mullis or an immediate family member serves as a


    board member, owner, officer, or committee member of
    Wishard Hospital and the Orthopaedic Trauma Association and has received research or institutional support
    from Amgen and Synthes. Dr. Anglen or an immediate
    family member serves as a board member, owner, officer, or committee member of the American Board of Orthopaedic Surgery, the American College of Surgeons,
    and the Orthopaedic Trauma Association; has received
    royalties from Biomet; serves as a paid consultant to or
    is an employee of Stryker; and has received research or
    institutional support from Stryker.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    Injury to the hip, particularly fracture of the proximal


    femur, is a common and increasing cause of hospitalization, morbidity, and even mortality. In 2004, there were
    more than 320,000 hospital admissions in the United
    States because of hip fractures, with more than
    500,000 hip fractures per year projected by 2040.1 Approximately 4% of all deaths from injury in the United
    States are caused by hip fractures, and roughly 50% of
    fractures that lead to mortality are hip fractures.2 In the
    younger population (generally defined as age younger
    than 65 years), hip fracture is usually caused by a highenergy injury, and mortality may result from associated
    injuries. The hip injury itself also can be a source of
    lifelong disability. In the elderly population, in whom
    hip fracture usually results from a low-energy mechanism such as a fall, mortality may ensue from associated
    medical comorbidities that are exacerbated by injuryrelated immobility or complications. In either population, the treatment decisions made by the orthopaedic
    surgeon may have a significant impact on the patients
    outcome.
    Hip trauma can consist of dislocation of the joint
    with or without associated fracture of the femur or acetabulum, or fracture of the proximal femur. Although
    fractures of the acetabulum are technically hip fractures, they will not be discussed in this chapter.

    injuries in up to 75% of patients.3 Dislocations may be


    simple (or not associated with a fracture), or may be
    more complex fracture-dislocations.4 The rate of posttraumatic arthritis following a simple dislocation is up
    to 26% and can approach 90% in more complex
    fracture-dislocations.5 This rate is particularly concerning because hip dislocation injuries often occur in
    young patients.
    Given the inherent stability of the hip, a large force
    is needed to cause a dislocation. One of the more common mechanisms is a dashboard injury sustained during a motor vehicle collision in which the femoral head
    is driven posteriorly. There may also be an associated
    posterior wall or femoral head fracture. Other injury
    mechanisms include falls from a height, pedestrianmotor vehicle collisions, industrial accidents, and athletic
    injuries. Posterior dislocations accounts for 90% of all
    dislocations and are typically caused by a high-energy,
    axial load on the femur through a flexed and adducted
    hip.6 Anterior dislocations are caused by an external
    rotation force in an abducted hip. A central dislocation
    describes protrusio of the femoral head associated with
    an acetabulum fracture.
    Because there is a high association of other injuries
    in patients with hip dislocations, it is important that
    the Advanced Trauma Life Support (ATLS) protocols
    be followed before the focus turns to the musculoskeletal injuries. Up to 90% of patients will have visible
    swelling around the knee, with up to 25% of patients
    having significant internal knee derangement such as a
    cruciate or collateral ligament tear.7
    A hip dislocation can typically be diagnosed based
    on the patients physical examination. A patient with a
    posterior dislocation typically presents with a flexed,
    adducted, and internally rotated leg. An anterior dislocation results in an externally rotated leg with slight
    flexion and abduction. It is important to perform a detailed neurovascular examination before reduction is
    attempted. Typically, a plain radiograph of the pelvis is
    sufficient to make the diagnosis, but a cross-table lateral or frog-lateral radiograph should always be obtained in patients with pain and without an obvious
    dislocation or fracture based on the AP radiograph. A
    posterior dislocation is suggested by loss of congruency
    of the femoral head in the acetabulum, a lesser trochanter that is poorly visualized because of the internally rotated femur, and a femoral head that appears
    smaller than the contralateral side (Figure 1). Alternatively, a lesser trochanter seen in full profile with a
    399

    Section 4: Lower Extremity

    4: Lower Extremity

    larger femoral head suggests an anterior dislocation. If


    a femoral neck fracture is suspected, a CT scan before
    reduction is reasonable to prevent displacement of a
    possible fracture.
    Closed reduction is typically achieved by traction in
    line with the deformity, with the patient under adequate sedation. Following reduction, an AP plain radiograph and CT scan of the pelvis are typically obtained
    to confirm a concentric reduction. A nonconcentric reduction indicates the presence of a loose body within
    the joint and warrants surgical removal. Ideally, this
    would be done urgently because of the pressure on the
    articular cartilage from the osteochondral loose body
    fragment. However, some surgeons believe that skeletal

    traction is adequate to relieve pressure on the joint if


    surgery must be delayed. Even in the presence of a concentric reduction, loose bodies may be present that are
    too small to detect with CT.8,9
    If closed reduction is unsuccessful, open reduction
    must be performed. Traditionally, the approach was determined by the direction of dislocation because of concern that an approach from the opposite direction
    would further disrupt the remaining blood supply to
    the femoral head.10 However, it has been shown that it
    is safe to approach the hip opposite the direction of dislocation when such an approach is warranted because
    of associated injuries (for example, an anterior approach for a posterior dislocation if there is an associated femoral head or neck fracture).11
    The critical time period from injury to reduction to
    prevent osteonecrosis is controversial. Based on studies
    showing lower rates of osteonecrosis in fractures reduced within 6 hours of injury, many surgeons use the
    6-hour period as a guide.12 The goal should be to
    achieve adequate sedation of the patient and to perform reduction as quickly as possible without putting
    the patient at risk for other life- or limb-threatening injuries. If osteonecrosis occurs, it will usually become
    apparent within the first year, but may not present until
    several years following injury.
    After reduction, many surgeons restrict weight bearing by their patients to prevent possible femoral head
    collapse if osteonecrosis develops. Because no study has
    shown that prolonged nonweight-bearing restrictions
    impact the rate of osteonecrosis or femoral head collapse, consideration should be given to allowing patients to bear weight as tolerated immediately following
    reduction.13

    Posterior Dislocations
    Figure 1

    AP radiograph of the pelvis showing a posterior


    dislocation with the loss of profile of the lesser
    trochanter and the smaller femoral head.

    The Thompson-Epstein and the Stewart-Milford classification systems (Table 1) have both been described in
    the literature,4,5 and each essentially grades posterior

    Table 1

    The Thompson-Epstein and the Stewart-Milford Classification Systems for Hip Dislocations
    Thompson-Epstein System
    Type I

    Dislocation with or without minor fracture

    Type II

    Posterior fracture-dislocation with a single, significant fragment

    Type III

    Dislocation in which the posterior wall contains comminuted fragments with or without a major fragment

    Type IV

    Dislocation with a large segment of posterior wall that extends into the acetabular floor

    Stewart-Milford System
    Type I

    Simple dislocation with no fracture or an insignificant fracture

    Type II

    Dislocation in a stable hip that has a significant single or comminuted element to the posterior wall

    Type III

    Dislocation with a grossly unstable hip due to loss of bony support

    Type IV

    Dislocation associated with femoral head fracture

    (Reproduced from Foulk DM, Mullis BH: Hip dislocation: Evaluation and management. J Am Acad Orthop Surg 2010;18:199-209.)

    400

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 31: Hip Trauma

    Anterior Dislocations
    Anterior hip dislocations account for less than 10% of
    hip dislocations and can be divided into three types
    (obturator, pubic, and iliac) based on the position of
    the femoral head as seen on the AP plain radiograph of
    the pelvis. Treatment is the same as for posterior dislocations, with reduction achieved by traction with abduction, and gentle internal and external rotation with
    slight flexion after adequate sedation is achieved.

    The Role of Hip Arthroscopy


    As advances have been made in hip arthroscopy, it has
    become a viable alternative to formal arthrotomies to
    remove loose bodies present within the hip.8,9,19,20 Because the hip capsule has already been torn by the dislocation, hip arthroscopy is generally easier to perform
    in this setting because less force is needed to achieve
    distraction of the hip joint. Unfortunately, considerably
    more bleeding occurs during arthroscopy because it is
    typically done within several days of injury. Care must
    be taken to reduce surgical time to prevent complications from traction injuries or fluid extravasation because the hip capsule is torn.9

    Complications
    Because of the significantly increased risk of osteonecrosis and further articular injury, the most concerning
    complication is the missed or delayed diagnosis of a
    dislocation. The key to avoiding this complication is to
    obtain a good physical examination and to carefully
    review the AP plain radiograph of the pelvis. The risk
    of osteonecrosis following hip dislocation is 10% to
    34% and usually occurs within 2 years of injury; however, osteonecrosis has been reported as many as 8
    years following injury.4,21 Posttraumatic arthritis is the
    most common complication following hip dislocation,

    2011 American Academy of Orthopaedic Surgeons

    occurring in up to 20% of patients with simple dislocations and even higher rates in complex fracturedislocations.3,5,19,22 Sciatic nerve palsy is also common
    (15% occurrence rate) in posterior hip dislocations,
    with the peroneal division most affected.14 Partial
    nerve recovery may be expected in 60% to 70% of
    patients.

    Femoral Head Fractures


    Femoral head fractures are relatively rare injuries that
    may present in up to 15% of posterior hip dislocations.23 These fractures are usually associated with
    high-energy mechanisms such as motor vehicle collisions and are created by a shear mechanism as the femoral head is dislocated. The initial presentation is the
    same as that described for a posterior dislocation. The
    patient will typically present with an internally rotated,
    adducted, and flexed hip. Radiographic diagnosis is
    typically made by the plain AP radiograph of the pelvis.
    Because of the dislocation, emergent reduction is performed based on the principles described for posterior
    hip dislocations. Up to 10% of femoral head fracturedislocations will be irreducible and should be treated as
    emergencies with open reduction in the surgical suite.24
    For the irreducible dislocation, it is reasonable to obtain an emergent CT scan because this may help with
    surgical planning; however, the scan should only be
    done if it will not unduly delay surgery. Delayed treatment of irreducible fracture-dislocations has been associated with higher rates of osteonecrosis.24
    The most common classification used for femoral
    head fractures is still the Pipkin classification system
    (Figure 2). Pipkin type I fractures do not involve the
    weight-bearing portion of the femoral head. For this
    reason, if a concentric closed reduction can be achieved,
    nonsurgical management is acceptable. Pipkin type II
    fractures typically involve a large piece of the weightbearing portion of the femoral head and are typically
    treated with open reduction and internal fixation. An
    anterior (Smith-Peterson) or anterolateral (WatsonJones) approach provides the best visualization of the
    fracture. It has been shown that an anterior approach is
    safe following posterior dislocations and may allow
    shorter surgical time with less blood loss than a posterior approach for Pipkin type I and II fractures.11 Pipkin
    type III fractures represent a more challenging injury because there is an associated femoral neck fracture. Reduction and fixation of the femoral head and neck can
    most easily be performed through an anterior or anterolateral approach. Pipkin type IV fractures have a posterior wall acetabulum fracture associated with the
    femoral head fracture. A posterior approach with a digastric osteotomy may afford the best visualization for
    both injuries and also protects the medial femoral circumflex artery from injury, thus preserving the blood
    supply to the femoral head25,26 (Figure 3).
    Fixation of a femoral head fracture has been described using a variety of implants. Two or more 3.5or 2.7-mm lag screws are most commonly used with

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    hip dislocations as simple if there is no fracture, or as


    a more complex fracture-dislocation that is more
    likely to be unstable.14,15 Small, posterior wall acetabulum fractures are frequently associated with posterior
    hip dislocations. Multiple studies have suggested that
    posterior wall fractures involving less than 20% of the
    wall are stable and may not necessarily warrant an examination under anesthesia if there is only a minor posterior wall fracture.16,17 Posterior wall acetabulum fractures involving 20% to 50% of the wall are more likely
    to be unstable and warrant an examination under anesthesia. The examination is done by flexing the hip to
    90 with slight adduction and internal rotation while
    applying a posteriorly directed force; fluoroscopy is
    used to determine if the femoral head maintains a concentric reduction.18 If the hip is stable during examination under anesthesia and an open approach is not otherwise indicated because of a fracture of the posterior
    wall, femoral head, or femoral neck, hip arthroscopy is
    also a reasonable alternative with potentially less morbidity than a formal open approach. Posterior wall acetabulum fractures involving more than 50% of the
    wall require surgery.

    401

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 2

    Illustration of the classification for femoral head fractures. A, Infrafoveal fracture, Pipkin type I. B, Suprafoveal fracture, Pipkin type II. Infrafoveal (C) or suprafoveal (D) femoral head fracture associated with a femoral neck fracture, Pipkin type III. E, Femoral head fracture associated with an acetabulum fracture, Pipkin type IV. (Reproduced
    with permission from Swiontkowski MF: Intrascapular hip fractures, in Browner BD, Jupiter JB, Levine AM, Trafton
    PF, eds: Skeletal Trauma: Basic Science Management and Reconstruction, ed 2. Philadelphia, PA, WB Saunders,
    1992, p 1775.)

    the heads of the screws countersunk to avoid prominence, but other implants, such as headless screws or
    bioabsorbable screws, are also available. The outcomes
    and complications of femoral head fractures mimic
    those of their associated injuries (hip dislocations and
    femoral neck fractures). A higher rate of osteonecrosis
    has been associated with the Kocher-Langenbeck approach, and worse outcomes with the use of 3.0-mm
    cannulated screws with washers.27 There is a wide
    range (6% to 64%) in the reported incidence of heterotopic ossification.12,23 In isolated hip injuries, consideration should be given to administering nonsteroidal
    anti-inflammatory drugs or radiation therapy if there is
    concern for heterotopic ossification, especially if the
    patient has an associated head injury.28

    Hip Fractures
    There are more than 2 million osteoporosis-related hip
    fractures in the United States annually, with an associated cost of more than $25 billion.29 The annual inci402

    Orthopaedic Knowledge Update 10

    dence is projected to increase to more than 3 million by


    2025. Most patients with low-energy hip fractures are
    cared for at community hospitals. Patients treated by
    low-volume surgeons (fewer than 7 cases per year) and
    at low-volume hospitals (fewer than 57 cases per year)
    recently have been shown to have higher mortality
    rates, longer hospital stays, and higher complication
    rates.30 This is not an indictment against community
    hospitals or surgeons, but does highlight the fact that
    even low-energy hip fractures should be not be considered simple fractures that are easily managed.
    The adage, never get sick in July, recently has
    been disproved with respect to hip fractures. Although
    some people believe that patients are placed at risk at
    academic centers in July because resident physicians
    take on new roles, the surgical mortality rate is no different in July for multiple procedures, including hip
    fractures.31 Interestingly, there appears to be a higher
    rate of morbidity associated with hip fractures at academic centers following changes restricting the work
    hours of residents compared with historical controls
    before duty hours were limited.32

    2011 American Academy of Orthopaedic Surgeons

    Chapter 31: Hip Trauma

    4: Lower Extremity

    Figure 3

    Illustration of digastric osteotomy to allow better visualization of a femoral head fracture from a posterior approach. A, Initial cut of the osteotomy (1: gluteus medius; 2: piriformis; 3: obturator internus and gemelli; 4:
    quadratus femoris; 5: deep branch of the medial circumflex femoral artery). B, Z-shaped capsular incision used for
    arthrotomy. C and D, Surgical dislocation with lag screw fixation of fracture. (Reproduced with permission from
    Henle P, Kloen P, Siebenrock KA: Femoral head injuries: Which treatment strategy can be recommended? Injury
    2007;38(4):478-488. http://www.sciencedirect.com/science/journal/00201383.)

    Femoral Neck Fractures

    Classification
    The type of femoral neck fracture is best determined with
    a traction, internal rotation, AP plain radiograph of the
    hip. The Garden classification is the most commonly
    used system for fractures in elderly patients, but could
    be further simplified to nondisplaced (Garden type I and
    II) and displaced (Garden type III and IV) fractures for
    treatment purposes33,34 (Figure 4). The anatomic classification of basicervical, transcervical, and subcapital is
    also routinely used for low-energy fractures.
    The Pauwels classification is more commonly used
    in describing high-energy fractures in young patients
    because this classification system is based on the angle
    of the fracture relative to a horizontal line (Figure 5).
    Type I fractures are less than 30, type II are 30 to 50,
    and type III fractures at greater than 50 are the most
    unstable fractures given the vertical orientation of the

    2011 American Academy of Orthopaedic Surgeons

    fracture line. Of note, the Pauwels classification system


    does not take into account fracture comminution,
    which is frequently present in high-energy fractures.

    Treatment
    Treatment principles differ for elderly patients with
    low-energy femoral neck fractures compared with
    younger patients with high-energy femoral neck fractures. Generally, elderly patients require appropriate
    medical risk stratification and management before surgery. Because delayed surgery has been shown to be an
    independent risk factor for mortality and other complications, every effort should be made to perform surgery
    within 2 to 4 days of the injury.35-38 Young patients
    with high-energy fractures are generally considered to
    require more urgent treatment because of concern for
    vascular embarrassment of the femoral head with delayed surgery; however, excessive time should not be
    spent in the surgical suite when a patient in extremis
    with multiple injuries requires resuscitation.

    Orthopaedic Knowledge Update 10

    403

    Section 4: Lower Extremity

    4: Lower Extremity

    show if a fracture is present and the fracture propagation. Typically, a stress fracture involving only the compression (inferior) aspect of the neck is treated nonsurgically by limiting weight bearing for several weeks
    until symptoms improve. If the fracture extends
    throughout the entire length of the femoral neck or involves the tension (superior) side, surgery is usually recommended to prevent displacement.
    In a young patient with a high-energy, displaced,
    femoral neck fracture, surgery is usually performed urgently unless the patient cannot tolerate surgery because of physiologic derangement or traumatic brain
    injury. An anatomic reduction must be obtained, which
    may require an open approach. This can be performed
    through either an anterior (Smith-Peterson) or anterolateral (Watson-Jones) surgical approach with direct visualization of the anterior neck. Cannulated screws
    may provide inadequate fixation for these fractures,
    which often have a high angle (Pauwels type III) and
    comminution because of the high-energy mechanism of
    injury.43-45 A fixed-angle device such as a blade plate or
    cephalomedullary nail, or even newer implants such as
    a locked proximal femoral plate, provide more resistance to displacement.
    Figure 4

    Illustration of the Garden classification of femoral


    neck fractures. Type I: incomplete valgus impacted fracture. Type II: complete but nondisplaced fracture. Type III: displaced femoral neck
    fracture with varus malalignment. Type IV: displaced femoral neck fracture with trabeculae of
    the femoral head aligned with trabeculae of the
    acetabulum. (Reproduced with permission from
    Swiontkowski MF: Intrascapular hip fractures, in
    Browner BD, Jupiter JB, Levine AM, Trafton PF,
    eds: Skeletal Trauma: Basic Science Management
    and Reconstruction, ed 2. Philadelphia, PA, WB
    Saunders, 1992, p 1775.)

    Elderly patients with nondisplaced or valgus impacted fractures can typically be treated with percutaneous fixation with cannulated screws. Traditionally,
    the displaced fracture was treated with hemiarthroplasty and there was debate over whether the femoral
    stem should be cemented or cementless. Current literature supports the use of cemented over cementless
    stems because most of the evidence shows no difference
    in perioperative mortality but more pain and higher
    complication rates with the cementless stems.39 More
    recent debate has centered over the use of hemiarthroplasty versus total hip arthroplasty for displaced femoral neck fractures. There is now considerable evidence
    to support total hip arthroplasty over hemiarthroplasty
    for highly functional elderly patients; however, there
    may still be a role for cemented unipolar hemiarthroplasty in bedridden or poorly functioning patients with
    limited life expectancy.40-42
    In the young patient, an occult femoral neck fracture
    may occur without acute trauma in patients at risk for
    stress fracture such as amenorrheic women or marathon runners. Because these fractures typically are not
    seen on plain radiographs, a screening MRI may best
    404

    Orthopaedic Knowledge Update 10

    Intertrochanteric Femoral Fractures

    Classification
    Radiographic diagnosis of an intertrochanteric femoral
    fracture is best made with an AP pelvic or hip radiograph. In addition to a lateral radiograph of the hip,
    internal rotation views are helpful in accurately identifying the fracture pattern. There are multiple classification systems for intertrochanteric femoral fractures,
    and essentially all of these systems help distinguish
    whether the fracture is stable or unstable. This determination can be misleading because all intertrochanteric
    femoral fractures are potentially unstable without fixation, but the fracture pattern is useful in choosing between different types of implants. The more stable fracture patterns are simple fracture patterns that run along
    the intertrochanteric ridge. Fractures that involve the
    lateral wall of the greater trochanter or that extend below the lesser trochanter with loss of the posteromedial
    buttress of the calcar are more unstable patterns. Reverse obliquity or low transverse pertrochanteric femoral fractures also represent more unstable patterns (Figure 6).

    Treatment
    Stable (or simple) intertrochanteric femoral fractures
    are best treated with a sliding hip screw. Although there
    are multiple other devices available, such as proximal
    femoral locking plates and cephalomedullary nails,
    there is no evidence that these more expensive devices
    provide added benefits for the patient, and there is
    overwhelming evidence that there is a higher complication rate with cephalomedullary nails.46-50 A simple
    two-hole sliding hip screw has been shown to be bio-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 31: Hip Trauma

    Illustration of the Pauwels classification for femoral neck fractures. A, Type I: the fracture angle is less than 30 from
    horizontal. B, Type II: the fracture angle is 30 to 50. C, Type III: the fracture angle is greater than 50. (Adapted
    with permission from Orthopaedic Trauma Association Classification, Database and Outcomes Committee: Fracture
    and Dislocation Classification Compendium, 2007. J Orthop Trauma 2007;21(suppl 10):S1-S163.)

    4: Lower Extremity

    Figure 5

    mechanically stable for this fracture pattern, provides


    good clinical outcomes, and can be placed percutaneously.51,52
    Fixation of unstable intertrochanteric femoral fractures is more controversial. There is a trend toward using cephalomedullary nails for these fractures among
    young practitioners.53 The reason for this is unclear, but
    it has been postulated that this trend may reflect differences in reimbursement, the effect of marketing, or
    changes in training. There is evidence that supports the
    use of cephalomedullary nails in unstable fracture
    patterns.49,54-56 Improved designs of newer-generation
    cephalomedullary nails and advances in techniques may
    have reduced the higher complication rate with these
    devices.57 It is important to recognize fracture patterns
    that have a higher failure rate with traditional sliding
    hip screws, including fractures involving the lateral
    wall, reverse obliquity fractures, and low transverse
    peritrochanteric fractures. These fracture patterns
    should not be treated with a sliding hip screw; a cephalomedullary nail appears to be a better choice than a
    fixed-angle device for these fractures.50

    Subtrochanteric Femoral Fractures

    Classification
    As with most fractures, there are multiple classification
    systems available to describe subtrochanteric femoral
    fractures. Most of these systems define the subtrochanteric fracture as a femoral fracture in which the major
    fracture line is within 5 cm of the lesser trochanter. As
    the fracture extends more proximally, the fracture is
    more difficult to control because of the deforming
    forces (flexion, abduction, and external rotation) on
    the proximal fragment and the greater distance of the
    fracture line from the isthmus of the femur.

    2011 American Academy of Orthopaedic Surgeons

    Figure 6

    AO/OTA classification of pertrochanteric femoral


    fractures. A1: relatively stable intertrochanteric
    femoral fracture; A2: relatively more unstable
    intertrochanteric femoral fracture because the
    fracture extends to lateral wall. A3: completely
    unstable pertrochanteric femoral fracture representing reverse obliquity or low transverse patterns. (Adapted with permission from Orthopaedic Trauma Association Classification, Database
    and Outcomes Committee: Fracture and Dislocation Classification Compendium, 2007. J Orthop
    Trauma 2007;21(suppl 10):S1-S163.)

    Orthopaedic Knowledge Update 10

    405

    Section 4: Lower Extremity

    Treatment

    4: Lower Extremity

    Although fixed-angle devices have been described as


    treatment options for subtrochanteric femoral fractures,58,59 most surgeons recommend the use of an intramedullary nail over an extramedullary device.60 Although there has been a trend toward using the greater
    trochanter as a starting point for antegrade nailing for
    femoral fractures, the traditional piriformis fossa starting point still has a role, especially for subtrochanteric
    femoral fractures, because the piriformis fossa is coaxial with the rest of the femur, making it easier to
    achieve normal alignment. The disadvantage of using
    the trochanter as a starting point for nailing is that
    there can be a tendency to ream too laterally on the trochanter, which would lead to a varus deformity.61 It is
    imperative to achieve an anatomic reduction before
    reaming a subtrochanteric femoral fracture. Many
    times this cannot be achieved by closed or percutaneous means, which may necessitate an open (or miniopen) reduction of the fracture to maintain alignment.
    It has been shown that judicious use of a cerclage wire
    placed to maintain the reduction is acceptable.62 It
    should be noted that this technique should only be used
    if closed or percutaneous reduction fails; great care
    should be taken to avoid stripping the periosteum or
    overtightening the cable, which would lead to biologic
    insult to the periosteum.

    have a fragility fracture in their lifetime. Involvement of


    orthopaedic surgeons in the identification, treatment,
    and referral of patients with osteoporosis has been
    shown to significantly reduce the risk of future fractures.66 Active treatment of osteoporotic patients by the
    orthopaedic surgeon is more effective than referring patients to primary care clinics for treatment.67 Treatment
    can be initiated while the patient is still an inpatient
    during his or her initial admission for the osteoporotic
    hip fracture. Although a multidisciplinary team is a
    good model for treating patients with osteoporosis, the
    orthopaedic surgeon should initiate therapy even if
    such a team has not been established at the physicians
    treatment facility. Prescribing calcium, vitamin D, and
    bisphosphonate therapy can significantly reduce the
    risk of a future hip fracture.68,69 The American Orthopaedic Associations Own the Bone initiative offers
    orthopaedic surgeons tools to improve their communication with both patients who have had a hip fracture
    and their primary care physicians.70

    Annotated References
    1.

    ip fractures among older adults. Centers for Disease


    Control and Prevention Web site. http://www.cdc.gov/
    ncipc/factsheets/adulthipfx.htm. Accessed June 10,
    2008.
    This online publication by the Centers for Disease Control and Prevention provides basic details regarding hip
    fractures in the United States.

    2.

    Bergen G, Chen L, Warner M, Fingerhut L: Injury in the


    United States: 2007 chartbook. Hyattsville, MD, National Center for Health Statistics, 2008. http://
    www.cdc.gov/nchs/data/misc/injury2007.pdf. Accessed
    July 1, 2010.
    This US government online publication provides recent
    statistics regarding injuries in the United States.

    3.

    Epstein HC: Traumatic dislocations of the hip. Clin Orthop Relat Res 1973;92:116-142.

    4.

    Foulk DM, Mullis BH: Hip dislocation: Evaluation and


    management. J Am Acad Orthop Surg 2010;18(4):199209.
    This review article focuses on recognition and management of traumatic hip dislocation and the role of newer
    technology such as hip arthroscopy in management.

    5.

    Upadhyay SS, Moulton A: The long-term results of


    traumatic posterior dislocation of the hip. J Bone Joint
    Surg Br 1981;63B(4):548-551.

    6.

    Dreinhfer KE, Schwarzkopf SR, Haas NP, Tscherne H:


    Isolated traumatic dislocation of the hip: Long-term results in 50 patients. J Bone Joint Surg Br 1994;76(1):
    6-12.

    7.

    Schmidt GL, Sciulli R, Altman GT: Knee injury in patients experiencing a high-energy traumatic ipsilateral

    Pathologic Fractures
    Metastatic lesions of the proximal femur are common.
    It is necessary to proceed cautiously if the patient has a
    history of malignancy; it cannot be assumed that a
    pathologic lesion is a metastasis because it may represent a primary bone tumor. If there is concern that a lesion is a primary bone tumor, the patient is best referred to a musculoskeletal oncologist at a tertiary care
    center because of the high rate of errors (20%) that occur with biopsies obtained and analyzed at community
    medical centers.63,64 Indications for surgery include pain
    with radiographic evidence of a lytic lesion in the proximal femur. Lesions of the femoral neck or femoral
    neck fractures are best treated with arthroplasty. Lesions or fractures in the intertrochanteric or subtrochanteric femur should be treated with a long cephalomedullary nail because of the possibility of skip
    lesions and future fracture if an extramedullary device
    is used. If there is significant lysis of the intertrochanteric region, a calcar-replacing prosthesis is also a reasonable treatment option.

    Osteoporosis Evaluation and Treatment After


    Hip Fracture
    Despite advances in medicine, the mortality rate following hip fracture in elderly patients is still 25% in the
    first year following injury, and may be higher in men
    than in women.65 Ten million Americans have osteoporosis; one third of men and one half of women will
    406

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 31: Hip Trauma

    hip dislocation. J Bone Joint Surg Am 2005;87(6):12001204.


    8.

    Mullis BH, Dahners LE: Hip arthroscopy to remove


    loose bodies after traumatic dislocation. J Orthop
    Trauma 2006;20(1):22-26.

    9.

    Yamamoto Y, Ide T, Ono T, Hamada Y: Usefulness of


    arthroscopic surgery in hip trauma cases. Arthroscopy
    2003;19(3):269-273.
    Epstein HC: Posterior fracture-dislocations of the hip:
    Long-term follow-up. J Bone Joint Surg Am 1974;56(6):
    1103-1127.

    11.

    Swiontkowski MF, Thorpe M, Seiler JG, Hansen ST:


    Operative management of displaced femoral head fractures: Case-matched comparison of anterior versus posterior approaches for Pipkin I and Pipkin II fractures.
    J Orthop Trauma 1992;6(4):437-442.

    12.

    Hougaard K, Thomsen PB: Coxarthrosis following traumatic posterior dislocation of the hip. J Bone Joint Surg
    Am 1987;69(5):679-683.

    13.

    Sahin V, Karakas ES, Aksu S, Atlihan D, Turk CY,


    Halici M: Traumatic dislocation and fracturedislocation of the hip: A long-term follow-up study.
    J Trauma 2003;54(3):520-529.

    14.

    Stewart MJ, Milford LW: Fracture-dislocation of the


    hip: An end-result study. J Bone Joint Surg Am 1954;
    36(A:2):315-342.

    15.

    Thompson VP, Epstein HC: Traumatic dislocation of


    the hip: A survey of two hundred and four cases covering a period of twenty-one years. J Bone Joint Surg Am
    1951;33(3):746-778, passim.

    16.

    Keith JE Jr, Brashear HR Jr, Guilford WB: Stability of


    posterior fracture-dislocations of the hip: Quantitative
    assessment using computed tomography. J Bone Joint
    Surg Am 1988;70(5):711-714.

    17.

    Moed BR, Ajibade DA, Israel H: Computed tomography as a predictor of hip stability status in posterior
    wall fractures of the acetabulum. J Orthop Trauma
    2009;23(1):7-15.
    The authors report on their retrospective study showing
    that if the largest area of a posterior wall acetabulum
    fracture measures less than 20%, the hip is likely to be
    stable under fluoroscopic examination. Level of evidence: IV.

    18.

    Tornetta P III: Non-operative management of acetabular


    fractures: The use of dynamic stress views. J Bone Joint
    Surg Br 1999;81(1):67-70.

    19.

    Byrd JW, Jones KS: Diagnostic accuracy of clinical assessment, magnetic resonance imaging, magnetic resonance arthrography, and intra-articular injection in hip
    arthroscopy patients. Am J Sports Med 2004;32(7):
    1668-1674.

    2011 American Academy of Orthopaedic Surgeons

    Philippon MJ, Kuppersmith DA, Wolff AB, Briggs KK:


    Arthroscopic findings following traumatic hip dislocation in 14 professional athletes. Arthroscopy 2009;
    25(2):169-174.
    This small retrospective series describes the results of
    hip arthroscopy for professional athletes with a simple
    (no fracture) hip dislocation. Level of evidence: IV.

    21.

    Cash DJ, Nolan JF: Avascular necrosis of the femoral


    head 8 years after posterior hip dislocation. Injury
    2007;38(7):865-867.
    This is a case report of a patient who had a simple posterior dislocation reduced within 3 hours of injury but
    did not develop osteonecrosis until 8 years after injury.
    Level of evidence: IV.

    22.

    Upadhyay SS, Moulton A, Srikrishnamurthy K: An


    analysis of the late effects of traumatic posterior dislocation of the hip without fractures. J Bone Joint Surg Br
    1983;65(2):150-152.

    23.

    Droll KP, Broekhuyse H, OBrien P: Fracture of the


    femoral head. J Am Acad Orthop Surg 2007;15(12):
    716-727.
    This review article discusses diagnosis and treatment of
    femoral head fractures.

    24.

    Mehta S, Routt ML Jr: Irreducible fracture-dislocations


    of the femoral head without posterior wall acetabular
    fractures. J Orthop Trauma 2008;22(10):686-692.
    The authors report on a retrospective study reviewing
    seven patients with femoral head fracture-dislocations
    without an associated posterior wall fracture treated
    with open reduction and internal fixation using an anterior approach. The authors found just fewer than 10%
    of femoral head fractures at their institution (fracturedislocations without posterior wall fracture) were of this
    variety and cautioned against attempts at closed reduction for this type of injury. They also noted those that
    were not treated as a surgical emergency were likely to
    develop osteonecrosis. Level of evidence: IV.

    25.

    Henle P, Kloen P, Siebenrock KA: Femoral head injuries: Which treatment strategy can be recommended?
    Injury 2007;38(4):478-488.
    This restrospective review of 12 patients with femoral
    head fractures treated with a digastrics osteotomy (with
    illustrations and description of the technique) showed
    good or excellent results in over 80% of patients. Level
    of evidence: IV.

    26.

    Solberg BD, Moon CN, Franco DP: Use of a trochanteric flip osteotomy improves outcomes in Pipkin IV
    fractures. Clin Orthop Relat Res 2009;467(4):929-933.
    This retrospective review of 12 patients with a combined
    femoral head and acetabulum fracture treated with a trochanteric flip osteotomy showed 10 of 12 patients had a
    good or excellent result. Level of evidence: IV.

    27.

    Stannard JP, Harris HW, Volgas DA, Alonso JE: Functional outcome of patients with femoral head fractures
    associated with hip dislocations. Clin Orthop Relat Res
    2000;377:44-56.

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    10.

    20.

    407

    Section 4: Lower Extremity

    28.

    29.

    4: Lower Extremity

    30.

    31.

    32.

    408

    Webb LX, Bosse MJ, Mayo KA, Lange RH, Miller ME,
    Swiontkowski MF: Results in patients with craniocerebral trauma and an operatively managed acetabular
    fracture. J Orthop Trauma 1990;4(4):376-382.

    of the garden classification on proposed operative treatment. Clin Orthop Relat Res 2003;409:232-240.
    35.

    Hommel A, Ulander K, Bjorkelund KB, Norrman PO,


    Wingstrand H, Thorngren KG: Influence of optimised
    treatment of people with hip fracture on time to operation, length of hospital stay, reoperations and mortality
    within 1 year. Injury 2008;39(10):1164-1174.
    This retrospective study showed that surgical delay in
    treating hip fractures significantly increases mortality
    rates in some patients. Level of evidence: IV.

    36.

    Moran CG, Wenn RT, Sikand M, Taylor AM: Early


    mortality after hip fracture: Is delay before surgery important? J Bone Joint Surg Am 2005;87(3):483-489.

    37.

    Al-Ani AN, Samuelsson B, Tidermark J, et al: Early operation on patients with a hip fracture improved the
    ability to return to independent living: A prospective
    study of 850 patients. J Bone Joint Surg Am 2008;
    90(7):1436-1442.
    This large prospective study showed that early fixation
    of hip fractures in elderly patients was significantly associated with a higher likelihood of return to independent living. Level of evidence: II.

    38.

    Zuckerman JD, Skovron ML, Koval KJ, Aharonoff G,


    Frankel VH: Postoperative complications and mortality
    associated with operative delay in older patients who
    have a fracture of the hip. J Bone Joint Surg Am 1995;
    77(10):1551-1556.

    39.

    Englesbe MJ, Fan Z, Baser O, Birkmeyer JD: Mortality


    in medicare patients undergoing surgery in July in
    teaching hospitals. Ann Surg 2009;249(6):871-876.
    This retrospective review of more than 300,000 patients
    having surgery for multiple conditions including hip
    fractures and others outside the field of orthopaedics
    showed no increased mortality in teaching hospitals in
    July (or any other month) relative to nonacademic hospitals. Level of evidence: III.

    Miyamoto RG, Kaplan KM, Levine BR, Egol KA,


    Zuckerman JD: Surgical management of hip fractures:
    An evidence-based review of the literature. I: Femoral
    neck fractures. J Am Acad Orthop Surg 2008;16(10):
    596-607.
    This article discusses the evidence supporting surgical
    treatment of hip fractures and outlining the evidence
    supporting different techniques and selection of implants.

    40.

    Browne JA, Cook C, Olson SA, Bolognesi MP: Resident


    duty-hour reform associated with increased morbidity
    following hip fracture. J Bone Joint Surg Am 2009;
    91(9):2079-2085.
    The 80-hour workweek restrictions were made in July
    2003. This retrospective review of more than 48,000
    patients in the United States (those treated during 20012002 compared to 2004-2005) showed an increased
    rate of perioperative pneumonia, hematoma, transfusion, renal complications, nonroutine discharge, costs,
    and length of stay at teaching hospitals following the required changes to the resident work hours. There was
    no change seen with mortality. Level of evidence: III.

    Blomfeldt R, Trnkvist H, Eriksson K, Sderqvist A,


    Ponzer S, Tidermark J: A randomised controlled trial
    comparing bipolar hemiarthroplasty with total hip replacement for displaced intracapsular fractures of the
    femoral neck in elderly patients. J Bone Joint Surg Br
    2007;89(2):160-165.
    This prospective randomized study of elderly patients
    with a displaced femoral neck fracture who were randomized to receive hemiarthroplasty versus total hip arthroplasty showed patients treated with total hip arthroplasty had higher function scores with no increased risk
    of complications as early as 1 year postoperatively.
    Level of evidence: I.

    41.

    Goh SK, Samuel M, Su DH, Chan ES, Yeo SJ: Metaanalysis comparing total hip arthroplasty with hemiarthroplasty in the treatment of displaced neck of femur
    fracture. J Arthroplasty 2009;24(3):400-406.
    The authors report on their meta-analysis of randomized controlled trials comparing total hip arthroplasty to
    hemiarthroplasty. Patients treated with total hip arthro-

    Burge R, Dawson-Hughes B, Solomon DH, Wong JB,


    King A, Tosteson A: Incidence and economic burden of
    osteoporosis-related fractures in the United States,
    2005-2025. J Bone Miner Res 2007;22(3):465-475.
    This study estimates the incidence of osteoporosisrelated fractures in the United States in 2005 at 2 million fractures with a cost of $17 billion. The authors
    project both the cost and incidence of osteoporosisrelated fractures to increase by 50% by the year 2025.
    Level of evidence: IV.
    Browne JA, Pietrobon R, Olson SA: Hip fracture outcomes: Does surgeon or hospital volume really matter?
    J Trauma 2009;66(3):809-814.
    This review of just fewer than 100,000 hip fractures
    treated with surgery in the United States found that lowvolume surgeons (those who operated on fewer than 7
    hip fractures per year) had a higher mortality rate and
    higher rate of transfusions, pneumonia, and decubitus
    ulcers than high-volume surgeons (those who performed
    more than 15 hip surgeries for fractures per year). The
    review also found low-volume hospitals (those who performed fewer than 57 surgeries for hip fracture per
    year) were associated with higher rates of postoperative
    infection, pneumonia, transfusion, and nonroutine discharge, but were not associated with higher mortality.
    Both low-volume surgeons and low-volume hospitals
    had a longer length of stay for patients with hip fracture
    requiring surgery. Level of evidence: III.

    33.

    Beimers L, Kreder HJ, Berry GK, et al: Subcapital hip


    fractures: The Garden classification should be replaced,
    not collapsed. Can J Surg 2002;45(6):411-414.

    34.

    Oakes DA, Jackson KR, Davies MR, et al: The impact

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 31: Hip Trauma

    plasty had better function, less pain, and fewer repeat


    surgeries than those treated with hemiarthroplasty.
    Level of evidence: I.
    42.

    44.

    45.

    46.

    47.

    Aminian A, Gao F, Fedoriw WW, Zhang LQ, Kalainov


    DM, Merk BR: Vertically oriented femoral neck fractures: Mechanical analysis of four fixation techniques.
    J Orthop Trauma 2007;21(8):544-548.
    This biomechanical study of vertically unstable femoral
    neck fractures created in cadavers evaluated four treatment methods. Strongest fixation to weakest fixation
    was achieved with the following: a proximal femoral
    locking plate, a dynamic condylar screw, a dynamic hip
    screw, and cannulated screws.
    Liporace F, Gaines R, Collinge C, Haidukewych GJ: Results of internal fixation of Pauwels type-3 vertical femoral neck fractures. J Bone Joint Surg Am 2008;90(8):
    1654-1659.
    The authors present their findings in this retrospective
    review of vertical femoral neck fractures treated with a
    fixed-angled device versus cannulated screws. No difference in outcomes was found, although there was a trend
    toward a higher nonunion rate in the group treated with
    cannulated screw fixation. Level of evidence: IV.
    Zlowodzki M, Brink O, Switzer J, et al: The effect of
    shortening and varus collapse of the femoral neck on
    function after fixation of intracapsular fracture of the
    hip: A multi-centre cohort study. J Bone Joint Surg Br
    2008;90(11):1487-1494.
    This retrospective review of patients with displaced femoral neck fractures treated with cannulated screws
    showed that patients with varus collapse or shortening
    of the femoral neck had worse outcomes than those in
    whom reduction and length were maintained. Level of
    evidence: IV.
    Adams CI, Robinson CM, Court-Brown CM, McQueen
    MM: Prospective randomized controlled trial of an intramedullary nail versus dynamic screw and plate for intertrochanteric fractures of the femur. J Orthop Trauma
    2001;15(6):394-400.
    Crawford CH, Malkani AL, Cordray S, Roberts CS, Sligar W: The trochanteric nail versus the sliding hip screw
    for intertrochanteric hip fractures: A review of 93 cases.
    J Trauma 2006;60(2):325-328, discussion 328-329.

    2011 American Academy of Orthopaedic Surgeons

    Aros B, Tosteson AN, Gottlieb DJ, Koval KJ: Is a sliding


    hip screw or im nail the preferred implant for intertrochanteric fracture fixation? Clin Orthop Relat Res
    2008;466(11):2827-2832.
    This case-control study reported longer length of hospital stay and higher costs associated with intramedullary
    nail versus sliding hip screw fixation for intertrochanteric femoral fractures. Level of evidence: III.

    49.

    Haidukewych GJ: Intertrochanteric fractures: Ten tips


    to improve results. J Bone Joint Surg Am 2009;91(3):
    712-719.
    This article provides technical tips and tricks on how to
    stay out of trouble when fixing intertrochanteric fractures. Level of evidence: V.

    50.

    Parker MJ, Handoll HH: Gamma and other cephalocondylic intramedullary nails versus extramedullary implants for extracapsular hip fractures in adults. Cochrane Database Syst Rev 2008;3:CD000093.
    The authors report on their case-control study comparing the Gamma nail to sliding hip screws for extracapsular hip fractures in adults. Higher reoperation and
    complication rates were found with Gamma nails. Level
    of evidence: III.

    51.

    Bolhofner BR, Russo PR, Carmen B: Results of intertrochanteric femur fractures treated with a 135-degree sliding screw with a two-hole side plate. J Orthop Trauma
    1999;13(1):5-8.

    52.

    McLoughlin SW, Wheeler DL, Rider J, Bolhofner B:


    Biomechanical evaluation of the dynamic hip screw
    with two- and four-hole side plates. J Orthop Trauma
    2000;14(5):318-323.

    53.

    Anglen JO, Weinstein JN; American Board of Orthopaedic Surgery Research Committee: Nail or plate fixation of intertrochanteric hip fractures: Changing pattern
    of practice. A review of the American Board of Orthopaedic Surgery Database. J Bone Joint Surg Am 2008;
    90(4):700-707.
    A review of records of orthopaedic surgeons taking part
    II of the Board certification of the American Board of
    Orthopaedic Surgery showed an increasing use of cephalomedullary nail fixation for intertrochanteric femoral
    fractures. Level of evidence: IV.

    54.

    Hardy DC, Descamps PY, Krallis P, et al: Use of an intramedullary hip-screw compared with a compression
    hip-screw with a plate for intertrochanteric femoral
    fractures: A prospective, randomized study of one hundred patients. J Bone Joint Surg Am 1998;80(5):618630.

    55.

    Kuzyk PR, Lobo J, Whelan D, Zdero R, McKee MD,


    Schemitsch EH: Biomechanical evaluation of extramedullary versus intramedullary fixation for reverse obliquity intertrochanteric fractures. J Orthop Trauma 2009;
    23(1):31-38.
    A biomechanical study of reverse obliquity intertrochanteric femoral fractures showed that an intramedullary
    hip screw performed better than a 95 or 135 hip screw

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    43.

    Macaulay W, Nellans KW, Garvin KL, Iorio R, Healy


    WL, Rosenwasser MP; Other members of the DFACTO
    Consortium: Prospective randomized clinical trial comparing hemiarthroplasty to total hip arthroplasty in the
    treatment of displaced femoral neck fractures: Winner
    of the Dorr Award. J Arthroplasty 2008;23(6, Suppl 1):
    2-8.
    In this prospective randomized study of patients treated
    with total hip arthroplasty versus hemiarthroplasty, the
    authors report that patients treated with total hip arthroplasty had better functional outcomes and less pain
    without a significantly increased risk of complication
    compared with patients treated with hemiarthroplasty.
    Level of evidence: I.

    48.

    409

    Section 4: Lower Extremity

    in a gap model. No differences in failure rates were seen


    when no gap existed at the fracture site.
    56.

    Ruecker AH, Rupprecht M, Gruber M, et al: The treatment of intertrochanteric fractures: Results using an intramedullary nail with integrated cephalocervical screws
    and linear compression. J Orthop Trauma 2009;23(1):
    22-30.
    This is a retrospective review of 48 patients treated with
    an InterTan (Smith and Nephew) cephalomedullary nail
    at a single institution. Level of evidence: IV.

    4: Lower Extremity

    57.

    62.

    Bhandari M, Schemitsch E, Jnsson A, Zlowodzki M,


    Haidukewych GJ: Gamma nails revisited: Gamma nails
    versus compression hip screws in the management of intertrochanteric fractures of the hip. A meta-analysis.
    J Orthop Trauma 2009;23(6):460-464.
    A meta-analysis of randomized trials comparing sliding
    hip screws to cephalomedullary nails for intertrochanteric femoral fractures showed the complications initially experienced with first-generation Gamma nails
    have improved over time. Recent trials suggest narrowing or a comparable complication rate with cephalomedullary nails of more recent design compared with
    compression hip screws. Level of evidence: I.

    58.

    Madsen JE, Naess L, Aune AK, Alho A, Ekeland A,


    Strmse K: Dynamic hip screw with trochanteric stabilizing plate in the treatment of unstable proximal femoral fractures: A comparative study with the Gamma nail
    and compression hip screw. J Orthop Trauma 1998;
    12(4):241-248.

    59.

    Lee PC, Hsieh PH, Yu SW, Shiao CW, Kao HK, Wu


    CC: Biologic plating versus intramedullary nailing for
    comminuted subtrochanteric fractures in young adults:
    A prospective, randomized study of 66 cases. J Trauma
    2007;63(6):1283-1291.

    In this retrospective review, subtrochanteric femoral


    fractures were treated with a limited open reduction if
    closed reduction could not be obtained. The reduction
    was held with a loosely applied cerclage cable. Acceptable union rates were achieved. Level of evidence: IV.
    63.

    Mankin HJ, Lange TA, Spanier SS: The hazards of biopsy in patients with malignant primary bone and softtissue tumors. J Bone Joint Surg Am 1982;64(8):11211127.

    64.

    Mankin HJ, Mankin CJ, Simon MA; Members of the


    Musculoskeletal Tumor Society: The hazards of the biopsy, revisited. J Bone Joint Surg Am 1996;78(5):656663.

    65.

    Yonezawa T, Yamazaki K, Atsumi T, Obara S: Influence


    of the timing of surgery on mortality and activity of hip
    fracture in elderly patients. J Orthop Sci 2009;14(5):
    566-573.
    This retrospective study of more than 500 patients
    found increased mobility in those treated less than 24
    hours, but higher mortality in a subset of sick patients
    treated less than 24 hours. The authors recommend otherwise healthy patients should have surgery within 24
    hours but patients who have a medical condition which
    can be improved prior to surgery should be delayed.
    Level of evidence: III.

    66.

    Kuzyk PR, Bhandari M, McKee MD, Russell TA,


    Schemitsch EH: Intramedullary versus extramedullary
    fixation for subtrochanteric femur fractures. J Orthop
    Trauma 2009;23(6):465-470.

    67.

    This review of the literature showed grade B evidence


    that there is less operative time and a lower risk for loss
    of fixation when using intramedullary implants versus
    extramedullary implants for subtrochanteric femoral
    fractures.
    61.

    Ostrum RF, Anglen JO, Archdeacon MT, Cannada LK,


    Herscovici D Jr: Prevention of complications after treatment of femoral shaft and distal femoral fractures. Instr
    Course Lect 2009;58:21-25.
    This article provides tips and tricks on how to stay out
    of trouble when treating femoral shaft and distal femoral fractures. Level of evidence: V.

    410

    Orthopaedic Knowledge Update 10

    Dell R, Greene D, Schelkun SR, Williams K: Osteoporosis disease management: The role of the orthopaedic
    surgeon. J Bone Joint Surg Am 2008;90(Suppl 4):188194.
    This study outlines how a dedicated program to identify
    and treat patients with osteoporosis was successful in a
    Kaiser HMO in California and estimates the reduction
    in hip fractures due to the program was 37%. The paper
    also discusses the role an orthopaedist can play in treating patients with osteoporosis.

    The authors of this prospective, randomized, nonblinded study reported no higher failure rate in subtrochanteric femoral fractures treated with a dynamic condylar screw compared with a reconstruction nail;
    however, the hip screw was associated with more pain.
    Level of evidence: II.
    60.

    Afsari A, Liporace F, Lindvall E, Infante A Jr, Sagi HC,


    Haidukewych GJ: Clamp-assisted reduction of high subtrochanteric fractures of the femur. J Bone Joint Surg
    Am 2009;91(8):1913-1918.

    Miki RA, Oetgen ME, Kirk J, Insogna KL, Lindskog


    DM: Orthopaedic management improves the rate of
    early osteoporosis treatment after hip fracture: A randomized clinical trial. J Bone Joint Surg Am 2008;
    90(11):2346-2353.
    This randomized prospective study showed there was a
    significantly higher rate of pharmacologic treatment for
    osteoporosis when the treatment was initiated by the orthopaedist with referral to a specialized orthopaedic osteoporosis clinic rather than recommendation to the patient to follow up with primary care for osteoporosis
    treatment. Level of evidence: I.

    68.

    Black DM, Cummings SR, Karpf DB, et al; Fracture Intervention Trial Research Group: Randomised trial of
    effect of alendronate on risk of fracture in women with
    existing vertebral fractures. Lancet 1996;348(9041):
    1535-1541.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 31: Hip Trauma

    69.

    Harrington JT, Ste-Marie LG, Brandi ML, et al: Risedronate rapidly reduces the risk for nonvertebral fractures in women with postmenopausal osteoporosis. Calcif Tissue Int 2004;74(2):129-135.

    70.

    Tosi LL, Gliklich R, Kannan K, Koval KJ: The American Orthopaedic Associations own the bone initiative to prevent secondary fractures. J Bone Joint Surg
    Am 2008;90(1):163-173.

    This article reviews the American Orthopaedic Associations Own the Bone program and shows how it has
    significantly improved communication between orthopaedic surgeons, primary care, and patients. Level of evidence: II.

    4: Lower Extremity

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    411

    Chapter 32

    Hip and Pelvic Reconstruction and


    Arthroplasty
    Rafael J. Sierra, MD

    Craig J. Della Valle, MD

    Arthritis of the Hip


    Osteoarthritis
    Arthritis and other rheumatologic conditions are the
    leading cause of disability among adults in the United
    States. In 2001 the estimated prevalence of arthritis
    among US adults was 33%, representing approximately
    70 million adults. The prevalence increases with age.
    Women had a higher prevalence than men, and nonHispanic whites and non-Hispanic blacks had a higher
    prevalence than Hispanics and people of other racial or
    ethnic backgrounds. The prevalence of self-reported,
    doctor-diagnosed arthritis is projected to increase to
    nearly 67 million by 2030.1
    Inflammatory Arthritis
    Rheumatoid arthritis (RA) affects 1.3 million adults
    older than 35 years of age in the United States.1,2 In
    2005, juvenile arthritis affected 294,000 children,
    spondyloarthritis affected 0.6 million to 2.4 million
    adults, systemic lupus erythematosus affected 161,000
    to 322,000 adults, systemic sclerosis affected 49,000
    adults, and primary Sjgrens syndrome affected 0.4
    million to 3.1 million adults.

    Dr. Sierra or an immediate family member serves as a


    paid consultant to or is an employee of Biomet; has received research or institutional support from DePuy, A
    Johnson & Johnson Company, Zimmer, and Stryker; and
    serves as a board member, owner, officer, or committee
    member of the Midamerica Orthopedic Society and
    Maurice Mueller Foundation. Dr. Della Valle or an immediate family member serves as a board member, owner,
    officer, or committee member of the American Association of Hip and Knee Surgeons and the Arthritis Foundation; serves as a paid consultant to or is an employee
    of Biomet, Kinamed, Smith & Nephew, and Zimmer; has
    received research or institutional support from Zimmer;
    and has received nonincome support (such as equipment
    or services), commercially derived honoraria, or other
    non-researchrelated funding (such as paid travel) from
    Stryker.

    2011 American Academy of Orthopaedic Surgeons

    4: Lower Extremity

    Epidemiology

    Posttraumatic Arthritis
    The incidence of posttraumatic arthritis has been very
    difficult to calculate, but approximately 12% of overall
    prevalence of symptomatic osteoarthritis (OA) may be
    attributed to posttraumatic arthritis of the hip, knee, or
    ankle. This corresponds to approximately 5.6 million
    individuals in the United States.

    Clinical Evaluation
    History
    The diagnosis of hip OA is usually straightforward and
    can be based on an appropriate history and physical
    examination. The pain associated with hip arthritis is
    commonly of insidious onset, unless there had been recent severe trauma. Pain is usually located in the groin
    and may be referred to the knee through a branch of
    the obturator nerve. The referral pattern for hip pathology is variable, and patients may have pain referred to
    the buttock and thigh. A patient may hold the hip with
    the hand, in a form of a C, so-called C-sign, that is
    commonly seen in patients with hip pathology. Pain
    that radiates past the knee, down the posterior thigh,
    and is associated with numbness or tingling is unlikely
    to be of hip origin. Articular pain is most commonly associated with groin pain and can be associated with diagnoses such as femoroacetabular impingement (FAI),
    hip dysplasia, osteonecrosis, OA, or femoral neck fractures. Buttock pain can be associated with posterior
    FAI, posterior acetabular wear, and OA, and piriformis
    or gluteus muscle problems.
    Physical Examination
    The examination of the arthritic hip is fairly simple and
    should focus on gait, measuring leg lengths, hip range
    of motion, provocative maneuvers and palpation, and a
    thorough neurovascular examination. Gait could be
    antalgic or related to limb-length discrepancy or muscle
    weakness (for example, Trendelenburg lurch). Pelvic
    obliquity and potential spine problems should be evaluated. The patients foot progression angle should be
    annotated. Range of motion of the hip is usually painful, especially flexion and internal rotation, which are
    commonly the directions in which motion is first lost
    with hip arthritis. Provocative maneuvers such as an
    active straight leg with the patient supine (Stinchfield)

    Orthopaedic Knowledge Update 10

    413

    Section 4: Lower Extremity

    can be positive. Pain is elucidated by an increase in contact pressures within the acetabulum. The anterior impingement test may be positive in patients with anterior
    FAI, hip dysplasia with labral pathology, or OA. The
    posterior impingement test is positive in patients with
    posterior FAI and in those with posterior acetabular
    OA, and anterior apprehension is seen in patients with
    hip dysplasia, as a feeling that the hip were going to
    subluxate anteriorly from the acetabulum.

    errant gait mechanics associated with the abnormal hip


    morphology. Many other conditions can produce
    symptoms in or around the hip. Differential diagnoses
    should include an era of pathologies such as sacroiliitis,
    degenerative disk disease, abductor muscle tears and
    sprains, femoral head osteonecrosis, hip OA, psoas tendinitis, labral pathology, pubic ramus fractures, stress
    fracture of the proximal femur, or trochanteric bursitis.

    Clinical Evaluation
    Radiographic Evaluation

    4: Lower Extremity

    Plain Radiographs
    Plain radiographs are usually all that are needed for diagnosis of hip OA. The pattern of OA may vary. Most
    patients develop superolateral narrowing, which would
    then progress to global narrowing of the hip joint. A
    subgroup of patients, most commonly females, with
    underlying coxa profunda may develop a more medial
    pattern of OA with preservation of the superior and
    lateral joint space; this finding is commonly missed during evaluation.
    Computed Tomography
    CT is rarely required for the diagnosis of hip arthritis,
    but could be helpful in identifying the structural abnormality associated with precursor hip pathology, such as
    femoroacetabular impingement.
    Magnetic Resonance Imaging
    MRI with or without contrast is also useful in the diagnosis of early OA and in studying labral pathology associated with the underlying hip arthritis. Newer biochemical imaging techniques, such as the delayed
    gadolinium-enhanced MRI of cartilage (dGEMRIC),
    possibly assist in the early detection of articular cartilage damage because of the ability to detect the biochemical change of tissue that precedes tissue loss.
    These techniques are currently under study.3

    Femoroacetabular Impingement
    FAI has been defined as a prearthritic mechanism that
    occurs when the proximal femur abuts the acetabulum
    with range of motion.4,5 Unrecognized and continued
    FAI can lead to cartilage degeneration and OA.5
    Three types of FAI have been observed; cam, pincer,
    and combined. Femoral-side problems caused by abnormally shaped proximal femurs, which include hips
    affected by slipped capital femoral epiphysis (SCFE),
    femoral retroversion, and posttraumatic deformities,
    lead to cam impingement. Acetabular structural abnormalities caused by retroversion and coxa profunda or
    protrusio lead to pincer impingement. Up to 80% of
    hips may have a combined type of impingement with
    both femoral and acetabular structural abnormalities.6
    Most patients who present with this condition are
    young and active and report groin pain in the affected
    hip during activity. Some patients report gluteal or trochanteric pain most commonly as the result of the ab414

    Orthopaedic Knowledge Update 10

    Patients with post-SCFE deformities may ambulate


    with an externally rotated extremity and an open foot
    progression angle (greater than 10). Hip range of motion is usually limited in patients with FAI, especially in
    flexion at 90 and internal rotation (<5). Some female
    patients, however, may have greater than 20 to 25 of
    internal rotation at 90; therefore, lack of internal rotation is not a universal finding. The anterior impingement test is usually positive in patients with rim and
    labral pathology. The posterior impingement sign may
    also be positive and may be seen in patients with posterior acetabular pathology and in patients with a
    coup-contrecoup lesion, a sign that both anterior
    and posterior acetabular damage has occurred, because
    of recurrent anterior impingement (Figure 1).

    Radiographic Evaluation
    Plain Radiographs
    Plain radiographs of the pelvis and hip are more commonly used for diagnosis of structural abnormalities
    about the hip. A cross-table lateral, frog-lateral, or
    Dunn view is commonly used for observing the proximal femoral deformity. It is now commonly accepted
    that a well-centered AP pelvic view is obtained when
    there is symmetry of the iliac wings and of the obturator foramina, and the coccyx is at a point in the midline
    within a distance of 0 to 2 cm above the symphysis pubis. With a well-centered radiograph, the borders of the
    acetabulum can be inspected for the absence of retroversion, coxa profunda, or protrusio (Figure 2). The radiographs should be examined for congruency of the
    femoral head and acetabulum, asphericity of the femoral head, and contour of the femoral head and neck
    junction. Asphericity of the femoral head or lateral
    head extension can be seen in patients with postPerthes or post-SCFE deformities (Figure 2, Table 1).
    The grade of OA should be classified according to the
    criteria described by Tnnis (Table 2).
    On the acetabular side, retroversion of the acetabulum should be diagnosed using the crossover sign or the
    ischial spine sign. Posterior wall coverage should be assessed using the posterior wall sign. A posterior wall
    sign indicates lack of posterior coverage; appropriate
    surgical treatment should be chosen (Table 1, Figure 3).
    Radiographic technique and assessment have been discussed in the literature.7
    Computed Tomography
    Conventional and three-dimensional CT scan of the hip
    is useful for assessing hip structural abnormalities and

    2011 American Academy of Orthopaedic Surgeons

    Chapter 32: Hip and Pelvic Reconstruction and Arthroplasty

    4: Lower Extremity

    Figure 2

    AP radiograph of the pelvis of a 27-year-old man


    with advanced cam-type FAI. The patient has
    asphericity of the femoral head depicted by extension of the lateral aspect of the femoral
    head outside the red circle.

    Table 1

    Figure 1

    AP (A) and lateral (B) radiographs of the pelvis


    of a 33-year-old woman with mostly pincer type
    FAI, with coxa profunda, involving sourcil. The
    lateral cross table radiograph depicts the typical
    coup-contrecoup lesion with narrowing of the
    posterior acetabular cartilage.

    serves as a good tool for preoperative planning in patients undergoing hip arthroscopy and possible reconstructive procedures.
    MRI-Arthrogram
    Axial, coronal oblique, sagittal oblique, and radial sequences should be obtained. The radial sequence is a
    proton densityweighted sequence orthogonal to the
    femoral head and neck junction, and is a reconstruction
    of the true axial slice orthogonal to the acetabular
    plane and the sagittal oblique slice parallel to the acetabular plane.
    Arthro-MRI is commonly used to diagnose labral
    pathology, articular cartilage degeneration, the presence or not of intraosseous ganglion formation, and
    femoral head and neck junction abnormalities. Adding
    a small field view to the arthro-MRI may increase sensitivity to diagnose labral tears as high as 92%. A ruptured labrum often shows increased signal intensity on
    T2-weighted images that extends to the articular surface (Figure 4). Acetabular cartilage degeneration can
    also be seen with arthro-MRI, but is less reliable than
    when assessing labral pathology. If on MRI the femoral

    2011 American Academy of Orthopaedic Surgeons

    Definitions of Radiographic Measurements


    Obtained in Patients With Structural
    Abnormalities Related to FAI
    Coxa profunda

    When the floor of the fossa acetabuli


    touches the ilioischial line.

    Protrusio
    acetabulum

    When the femoral head overlaps the


    ilioischial spine medially.

    Aspheric head

    When the epiphysis of the head


    protrudes laterally out of the circle
    around the head.

    Pistol grip

    Lateral contour of the femoral head


    extends into a convex shape to the
    base of the neck.

    Double contour
    sign

    Ossification of the rim caused by bone


    apposition resulting in a double
    projection of the anterior and
    posterior walls.

    head has migrated into the anterior-superior cartilage


    defect and the femoral head has lost its stable position,
    then joint-preserving surgery is usually contraindicated.
    The angle has been described on axial MRI views to
    depict the grade of femoral head and neck junction abnormalities. A mean angle of 74 was seen in patients
    with FAI compared to 42 in control groups.8

    Treatment Options
    Surgical Dislocation
    Surgical hip dislocation is currently considered the gold
    standard for management of FAI, with good to excel-

    Orthopaedic Knowledge Update 10

    415

    Section 4: Lower Extremity

    Table 2

    Classification of OA as Described by Tnnis


    Grade 0

    No signs of OA

    Grade 1

    Increased sclerosis of the head and acetabulum

    Grade 2

    Small cysts in the head or acetabulum, moderate


    joint space narrowing, moderate loss of head
    sphericity

    Grade 3

    Large cysts in head or acetabulum, severe joint


    space narrowing or obliteration, severe
    deformity of femoral head, evidence of
    necrosis

    4: Lower Extremity

    lent results reported in over 80% to 90% of


    patients.9-11 Indications for surgery include preserved
    articular cartilage, correctable structural abnormality,
    and reasonable expectations. Surgery is usually not recommended in patients in the fourth or fifth decade of
    life and in those with Tnnis grade 2 OA, or anterior
    translation of the femoral head into an anterior acetabular defect seen radiographically or on MRI, or a retroverted acetabulum with poor posterior coverage. A
    periacetabular osteotomy [PAO] would be a better
    treatment option for these patients. Surgery is absolutely not recommended for patients with grade 3 or
    higher OA, those with hip pain with an uncorrectable
    structural deformity, and the patient older than
    60 years in whom total hip arthroplasty (THA) would
    be a better option if cartilage damage is detected.
    The dislocation is performed with preservation of all
    external rotators and protection of the medial circumflex artery. The trochanter heals reliably and the operation allows direct visualization and protection of the
    superior femoral neck retinacular vessels at the time of
    surgery. The operation allows a 360 view of the acetabular and femoral heads for inspection, diagnosis,
    and treatment of abnormalities associated with FAI.
    Extra-articular components can also be corrected, such
    as a reorientation of the proximal femur with flexion,
    valgus intertrochanteric osteotomies, or correction of
    coxa vara. The trochanter can also be advanced if necessary through this same approach. Studies have shown
    that the best results are obtained in patients with early
    to no OA and when the labrum is preserved. Complications can be minimized by understanding the anatomy and with good surgical technique.
    Anterior Smith-Petersen or Heuter Approach
    This procedure could be used as the sole management
    of FAI or combined with arthroscopic management of
    the intra-articular pathology. Advantages include a
    smaller incision with minimal muscle damage and a
    fast recovery when compared to surgical hip dislocation done through a trochanteric osteotomy. A disadvantage of the procedure is that treatment of pathology
    is limited and is mainly aimed at the femoral side; although both sides can be treated, visualization is decreased in comparison with the surgical hip dislocation.
    416

    Orthopaedic Knowledge Update 10

    Figure 3

    AP radiograph of the hip of a 19-year-old man


    with isolated retroversion of the acetabulum.
    The red line depicts the posterior wall, and the
    white line depicts the anterior wall. The crossover between the anterior and posterior walls
    occurs more caudal than normal. The prominence of the ischial spine within the pelvic cavity also gives an idea of the significant retroversion encountered in this patient.

    To treat the acetabular side, the reflected head of the


    rectus may have to be taken down, and there are potential problems with traction of the superficial femoral
    cutaneous nerve. The results to date show that reasonable outcome can be achieved through this approach
    with an acceptable complication rate.12
    Arthroscopy
    The indications for hip arthroscopy in the setting of
    FAI are continually evolving. Central compartment arthroscopy allows management of labral pathology. Access to the peripheral compartment without traction allows treatment of mild to moderate cam FAI lesions of
    the anterior lateral femoral head and neck junction and
    can also be used to reattach the torn labrum. Limitations of hip arthroscopy are numerous. Hip arthroscopy is suitable in limited hands and has a long learning curve. It has a limited role in assessing posterior FAI
    pathology. The surgeon must have significant experience in hip arthroscopy to treat the acetabular rim with
    techniques that have been described for open surgery.
    Arthroscopy is also difficult to perform in patients with
    coxa profunda or protrusio, those with severe acetabular retroversion, or in the obese patient.
    There has been a growing body of literature reporting the results of hip arthroscopy in FAI. The consensus
    of recent literature is that satisfactory results can be obtained, and that the outcomes are comparable to those
    of the open technique, although patient selection may
    play an important role in the outcomes between these
    two groups.13-16

    2011 American Academy of Orthopaedic Surgeons

    Chapter 32: Hip and Pelvic Reconstruction and Arthroplasty

    Figure 4

    T2-weighted MRI with gadolinium shows an


    anterior-superior labral tear (arrow), seen as an
    increase in signal intensity that extends to the
    articular surface.

    Developmental Dysplasia of the Hip in the Adult

    4: Lower Extremity

    Figure 5

    A, The right side of an AP pelvic radiograph


    showing the radiographic measurements used
    for hip dysplasia. The dotted line denotes the
    anterior center edge angle. The solid white line
    denotes the Tnnis angle. The black line denotes the medial clear space. B, A false-profile
    view showing measurement of the anterior center edge angle.

    prehension test may also be positive as patients feel


    that the hip subluxates anteriorly. Abduction strength is
    usually not affected except in extreme grades of hip
    dysplasia such as in the dislocated hip.

    History
    Hip dysplasia is a structural hip disorder that can lead
    to degenerative arthritis in early adulthood if left untreated. Classic hip dysplasia has been well described in
    the literature and its pathologic features can vary substantially. It is common to see an increasing spectrum
    of abnormalities ranging from mild forms of dysplasia
    to severe cases in which the hip is completely dislocated
    from the acetabulum. In classic hip dysplasia, increased
    contact pressures on the small surface area between the
    acetabulum and femoral head can lead to degeneration
    of the superolateral cartilage, and early OA.

    Physical Examination
    Most patients with hip dysplasia are young and active
    and report groin pain during activity. Patients may also
    report pain over the trochanter. Patients usually do not
    specifically report loss of hip range of motion and actually may have increased range of motion. Patients
    with mild to moderate dysplasia report a knife-sharp
    pain in the groin and a sensation of catching or locking
    secondary to tearing of the labrum. Patients may ambulate with an antalgic gait; when weak abductors are
    present, they may have a Trendelenburg gait and a positive Trendelenburg test. Patients with classic dysplasia
    and increased femoral anteversion have more internal
    rotation than external rotation. With labral pathology
    an anterior impingement test will be positive. The ap-

    2011 American Academy of Orthopaedic Surgeons

    Radiographic Examination
    Plain radiographs of the pelvis and hip are commonly
    used for diagnosis of hip dysplasia. All pertinent information is usually obtained from the AP pelvic radiograph, but additional studies such as a Lequesne false
    profile view, a cross-table lateral view, hip abduction
    views, and MRI-arthrogram of the hip are commonly
    used ancillary tests. Pelvic radiographs should be standardized as described previously in the section on FAI.
    The most commonly used methods to describe the
    grade of hip dysplasia are the lateral center edge angle
    of Wiberg, the acetabular index of the weight-bearing
    surface of Tnnis, the femoral head extrusion index,
    and the acetabular depth to width index of Stulberg
    and Harris (Figure 5). In addition, the Shenton line can
    be used to assess superior subluxation of the hip. Lateral subluxation should be quantified by measuring
    from the lateral side of the teardrop to the medial edge
    of the femoral head (Table 3; Figure 5). One study
    demonstrated that these radiographic parameters reliably predicted the outcome of the untreated dysplastic
    hip after age 65 years. In this study no patient had developed severe arthritic changes in the hip or had a
    Wiberg center edge angle of less than 16, a Tnnis angle of more than 15, an acetabular depth to width index of less than 38%, or an uncovered femoral head of
    more than 31%.17
    An AP radiograph of the hip in maximal abduction

    Orthopaedic Knowledge Update 10

    417

    Section 4: Lower Extremity

    Table 3

    4: Lower Extremity

    Radiographic Measurements Obtained in


    Patients With Hip Dysplasia
    Lateral Center Edge Angle
    >25
    Between 20-25
    <20

    Normal
    Borderline
    Hip dysplasia

    Tnnis Angle
    0-10
    >10

    Normal
    Hip dysplasia

    Femoral Extrusion Index


    >25%

    Hip dysplasia

    False Profile View


    (Anterior Center Edge Angle)
    >25
    <20
    Between 20-25

    Normal
    Hip dysplasia
    Borderline

    is commonly obtained at the time of surgical planning.


    The ideal candidate for the pelvic rotational osteotomy
    shows that the hip reduces and the femoral head is adequately covered and congruent and the joint space is
    preserved. Although the absence of these criteria is not
    a contraindication to pelvic osteotomy, it may indicate
    that a femoral osteotomy may also be necessary or that
    the procedure should be considered a salvage operation
    as the outcome would be less predictable.
    Retroversion can also be seen in patients with hip
    dysplasia. It has been reported that up to one sixth of
    the hip dysplasias can have a retroverted acetabulum,
    and this has to be taken into account at the time of correction.18
    A CT scan is not routinely used for diagnosing hip
    dysplasia. An MRI with gadolinium as described in the
    section on FAI can be used to assess labral pathology
    and/or early cartilage degeneration. The acetabular
    labrum, which is usually large, aids differentiation in
    borderline hips with both FAI and dysplastic features.

    Treatment Options
    Nonarthroplasty
    Femoral osteotomy in itself is rarely used as sole management for acetabular hip dysplasia in the adult. The
    indications for concomitant femoral osteotomy in addition to a PAO are worth noting. Intertrochanteric osteotomy may be needed in approximately 10% of patients treated with PAO. There has been a significant
    association between a high extrusion index of the femoral head, abnormal femoral anteversion angles, a deformed femoral head, and radiographic signs of OA
    with the need for femoral osteotomy. Most importantly, a previous adduction osteotomy was highly predictive of the need for femoral osteotomy. Although
    these criteria can help in discerning which hips may
    need a femoral osteotomy preoperatively, consideration
    should be made at the time of the surgery if containment and congruency are not optimal after PAO.
    418

    Orthopaedic Knowledge Update 10

    Although there are multiple forms of acetabular osteotomy which are currently used for management of
    the patient with symptomatic hip dysplasia, PAO is the
    preferred pelvic osteotomy in many centers for treatment of the adult patient with hip dysplasia in the US.
    Surgical advantages include the ability to perform the
    osteotomy with a series of straight, relatively reproducible cuts through one incision preserving the abductors,
    the ability to permit a wide range of corrections medially, laterally, and anteriorly while maintaining adequate acetabular version, or the ability to perform isolated changes to acetabular version if needed, the need
    for minimal internal fixation and no external fixation
    as the posterior column is preserved, and the ability to
    perform a capsulotomy to assess the labrum and check
    for impingement without compromise to the acetabular
    fragment and blood supply. Patient-related advantages
    include the possibility of early mobilization and weight
    bearing because of the preserved posterior column and
    the ability to use the osteotomy in female patients who
    plan to become pregnant and deliver vaginally, as the
    pelvic ring and outlet are not changed after the correction.
    The ideal patient for the osteotomy is younger than
    40 years with little, if any, arthrosis (Tnnis grade 0 or
    1); has a poorly covered femoral head with a lateralized
    hip center of rotation, a congruent hip joint with a
    round acetabulum, and a round femoral head, and is
    not obese. Contraindications to the procedure include
    complete dislocation and/or high subluxation of the
    femoral head articulating with the secondary acetabulum with arthritic changes, poor hip range of motion
    (flexion <105 and abduction <30), and patient age
    younger than 12 years. Injury to the triradiate cartilage
    could result in acetabular retroversion.
    The results of PAO have been reported in several
    studies.14,19 The innovators of the osteotomy reported
    their long-term follow-up in 1999.19 At an average 11.3
    years after surgery, 58 of the 71 hips with the minimum
    follow-up of 10 years had a preserved hip joint. Thirteen hips had either a subsequent THA (12) or a hip fusion (1). Ninety percent of the patients who still had a
    preserved joint space at a minimum of 10 years had significant improvement in pain and functional scores. Including those hips in which treatment failed, 52 of 71
    hips (73%) had a score of good or excellent. The association between grade of OA and surgical outcome has
    been studied.20 At an average of 4 years of follow-up,
    patients with preoperative Tnnis grade 1 or 2 OA had
    mostly excellent or good results and those with grade 3
    OA had mostly poor results. Five of nine patients with
    grade 3 arthritis required further major surgery.
    Total Hip Arthroplasty
    The technique of THA in patients with hip dysplasia
    varies according to the structural deformity. On the pelvic side the native acetabulum is typically shallow and
    open anterolaterally in excess (excessive anteversion),
    or it can be completely deficient anteriorly and superiorly, commonly resulting in a lateralized hip center. On

    2011 American Academy of Orthopaedic Surgeons

    Chapter 32: Hip and Pelvic Reconstruction and Arthroplasty

    4: Lower Extremity

    Figure 6

    A, AP pelvic radiograph denoting a high dislocation with neoacetabulum formation. B, Radiograph obtained after
    THA. Acetabular autograft and subtrochanteric shortening osteotomy were required.

    the femoral side, the neck is usually short with excessive anteversion and an increased neck shaft angle. The
    head is usually small. The greater trochanter is displaced posteriorly and the femoral canal is narrow.
    Most commonly, however, the changes of the femur are
    minor and it is the acetabulum that is dysplastic and
    the disproportionate contact between the two structures that produces symptoms. The classification of
    Crowe has been routinely used to describe the grade of
    subluxation of the hip.21 Fifty percent subluxation is
    equal to translation of the medial head-neck junction
    superior to the interteardrop line by 10% of the pelvic
    height. Crowe I are hips with less than 50% subluxation, Crowe II are hips with 50% to 75% subluxation, Crowe III are hips with 75% to 100% subluxation, and Crowe IV are hips with more than 100%
    subluxation. For Crowe I hips, reconstruction of the
    anatomic hip center using an uncemented socket is usually the treatment of choice. Anterolateral structural
    autograft (femoral head) is used only if needed. The
    femoral component is either uncemented or cemented
    based on patient age, femoral anatomy, and surgeon
    philosophy. On the femoral side, the surgeon must try
    to avoid excessive anteversion of the stem. Distorted
    proximal anatomy suggests a role for modular stems or
    extensively coated stems that will obtain diaphyseal fixation and will allow for changes in femoral version. For
    Crowe II hips, the acetabulum is usually an uncemented socket in the anatomic or slightly high center;
    the goal is to optimize coverage with native bone and
    using autograft as needed. The femoral reconstruction
    is usually the same as for Crowe I hips. For Crowe III
    hips, the acetabulum reconstruction is the most difficult
    because of severe lateral deficiency; options include a
    high center with a small cup on native bone, or an anatomic hip center beneath a large autograft or metal
    augment. For Crowe IV, a completely dislocated hip,

    2011 American Academy of Orthopaedic Surgeons

    the true acetabulum usually has thicker bone, is shallow and dysplastic, and has a thin anterior wall with a
    posterior wall that is adequately thick; therefore, restoration of anatomic hip center of rotation would be
    ideal. Graft is usually not needed. Because the bone is
    usually soft, care should be taken at the time of preparation of the socket. Patients with high hip dislocations
    may require either a trochanteric osteotomy with proximal shortening or a subtrochanteric shortening osteotomy. A subtrochanteric shortening osteotomy maintains proximal femoral anatomy, allows for an
    uncemented femur, and avoids trochanteric problems
    (Figure 6). One must be aware of overlengthening the
    dysplastic extremity. A good rule of thumb is to prevent
    lengthening the extremity greater than 3.5 cm.

    Osteonecrosis of the Femoral Head

    Epidemiology and Risk Factors


    New cases of osteonecrosis of the femoral head are diagnosed at a rate of 10,000 to 20,000 per year, and the
    average age of these patients is 36 years.22 Treatment of
    early osteonecrosis of the femoral head remains controversial. Late-stage osteonecrosis is commonly treated
    with arthroplasty with good results. In some instances
    the inciting event leading to osteonecrosis is clearly
    known, such as when direct injury or trauma has occurred. In other instances, the inciting event is unknown
    and can only be associated with risk factors that could
    predispose to the disease process, which include steroid
    use, alcohol abuse, smoking, HIV, blood clotting disorders, organ transplantation, and radiation (Table 4).
    There have been recent associations with inherited coagulopathies and with genetic polymorphisms that are
    potentially treatable pathophysiologic conditions.

    Orthopaedic Knowledge Update 10

    419

    Section 4: Lower Extremity

    Table 4

    Table 5

    Risk Factors Associated With the Development


    of Osteonecrosis of the Femoral Head

    The Steinberg Classification for Staging


    Osteonecrosis of the Femoral Head

    Dysbaric (Caisson disease)

    Stage

    Gaucher disease

    Normal or nondiagnostic radiograph, bone scan,


    and MRI

    Ia

    Normal radiograph, abnormal bone scan and/or


    MRI

    IIa

    Abnormal radiograph showing cystic and


    sclerotic changes in the femoral head

    IIIa

    Subchondral collapse producing a crescent sign

    IVa

    Flattening of the femoral head

    Va

    Joint narrowing with or without acetabular


    involvement

    VI

    Advanced degenerative changes

    Sickle cell disease


    Pancreatitis
    Steroids
    Alcohol
    Vascular insult
    Subacute bacterial endocarditis
    Disseminated intravascular coagulation
    4: Lower Extremity

    Polycythemia rubra vera


    Systemic lupus erythematosus
    Polyarteritis nodosa
    RA

    The extent or grade of involvement should also be indicated as A, mild; B,


    moderate; or C, severe

    Giant cell arteritis


    Sarcoid metabolic diabetes
    Hyperuricemia
    Blood lipid disorders

    the so-called crescent sign is best demonstrated on the


    frog-lateral projection which represents subchondral
    fracture (Figure 7).

    Idiopathic

    Treatment Options
    It is currently believed that osteonecrosis is a multifactorial disease associated in some cases with a genetic
    predisposition and an exposure to one or more risk factors.
    After the insult occurs, bone death follows and the
    reparative process (creeping substitution) ensues. The
    reparative process weakens the subchondral bone, resulting in collapse.

    Radiographic Examination
    There is no single diagnostic test that is 100% reliable.
    Plain radiographs including an oblique view of the hip
    (frog-leg) are normal initially. A frog-lateral view, however, is the radiographic test to confirm subchondral
    collapse and to make decisions regarding patient management. MRI has been shown to be approximately
    98% sensitive and 98% specific. Bone scan in contrast
    is approximately 85% sensitive and 80% specific with
    an accuracy of about 85%.
    MRI can become positive within 24 hours of insult,
    and can document the insult at a mean of 3.6 months
    after initiation of steroid use.

    Classification
    Staging of the disease progression is important because
    options and outcomes of nonreplacement treatment are
    predicated on these data. The classification of Ficat and
    Arlet is the most commonly used; however, the Steinberg classification is the most complete with its six subgroups23 (Table 5). The classic radiographic finding of
    420

    Orthopaedic Knowledge Update 10

    The decision to proceed with one form of treatment


    modality should be based on patient symptoms and important radiographic findings that may portray outcome: evidence of precollapse or collapse involvement
    of the femoral head; the size of the necrotic lesion; the
    amount of femoral head depression; and acetabular involvement.
    Nonsurgical
    The natural history of the untreated osteonecrosis lesion is poor. Large lesions tend to progress while
    smaller (less than 10% involvement) may not.24,25 Nonsurgical intervention may be warranted in small, precollapse lesions that are asymptomatic and that may
    have the better natural history. Protected weight bearing has demonstrated a failure rate of greater than 80%
    at a mean of 34 months and is not recommended as
    sole treatment.26 Other nonsurgical interventions such
    as pulsed electromagnetic fields, hyperbaric oxygen,
    and extracorporeal shock wave therapy are not currently recommended. Pharmacologic treatment with
    lipid-lowering medications and/or bisphosphonates has
    shown some promising results in both animal models
    and early clinical series.27,28 Pharmacologic treatment
    may be the treatment of choice in patients with multifocal osteonecrosis and in those who are not good candidates for surgical intervention.
    Head-Sparing Procedures
    Core decompression has traditionally been the treatment of choice during stages of precollapse. The results, however, continue to be conflicting in the litera-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 32: Hip and Pelvic Reconstruction and Arthroplasty

    Arthroplasty
    Hemiarthroplasty is rarely indicated in patients with
    osteonecrosis of the femoral head. The disappointing
    results with an overall satisfactory rate of only 48% in
    31 patients with 38 bipolar endoprostheses has led to
    the abandonment of this procedure for management of
    the young patient with osteonecrosis. Hemiresurfacing
    is another option for management of the young patient
    with osteonecrosis of the femoral head without acetabular involvement. The results in the literature have been
    contradictory, with some institutions reporting excellent results and others reporting disappointing results
    with an overall hip survivorship of around 60% at
    short-term follow-up. Poor results of hemiresurfacing
    could be related to patient selection. Continued groin
    pain was the leading cause of conversion to total hip arthroplasty in one study.31
    The outcomes of total hip resurfacing for osteonecrosis are better than hemiresurfacing; however, the use
    of a metal-on-metal articulation in the young patient,
    especially female, is debatable. Newer data suggest that
    the results of total hip resurfacing are worse in patients
    with osteonecrosis than patients with OA.32 The literature reports approximately an 86% to 92% survivorship at mid-term follow-up in patients who have undergone total hip resurfacing for osteonecrosis.32 Total hip
    resurfacing should be performed in select patients with
    osteonecrosis, and evaluation of the lesion size, its loca-

    2011 American Academy of Orthopaedic Surgeons

    4: Lower Extremity

    ture. In a meta-analysis of outcomes of core


    decompression obtained from 24 published series before 1995, the best results were observed with core decompression in early stages. Eighty-four patients with
    Ficat stage 1 and 65% of patients with stage 2 had successful results.26 The success of core decompression was
    higher than nonsurgical management in another study
    reporting 22 studies that compared core decompression
    versus nonsurgical management.
    A recent study reports that vascularized fibular
    grafting can be performed even after subchondral collapse.29 In early experience with follow-up ranging
    from 8 months to 6 years, only 3 of 50 patients had
    progressed to the point of requiring hip joint arthroplasty. Femoral head collapse did occur in three patients. Longer-term results of vascularized fibular graft
    have shown consistent successful results with good
    functional recovery and relief of pain. The results obtained in this study have not been shared by others.
    Decompression of the femoral head and injection of
    mesenchymal stem cells into the necrotic lesion have
    gained some acceptance in the treatment of early osteonecrosis. A case series of 189 hips in 160 patients
    with ages ranging from 16 to 61 years old demonstrated slowing in the progression of osteonecrosis as
    well as a significant reduction in the need for total hip
    replacement.30 Only 18% of hips and 20% of patients
    required total hip replacement in the 5- to 10-year
    follow-up period. These results were best for early osteonecrosis, and in select patients based on etiology of
    osteonecrosis.

    Figure 7

    A, The crescent sign as depicted on the froglateral view (arrows). B, Intraoperative specimen
    of the same patient undergoing THA with evidence of subchondral collapse and a large necrotic segment.

    tion, and bone quality is mandatory. THA provides the


    most reliable pain relief and good early clinical results
    for patients with advanced stages of osteonecrosis. Failure of THA in the treatment of osteonecrosis is related
    to age and activity level, and could be further limited
    by predisposing conditions that led to osteonecrosis.
    Because of the concern about higher failure rates of
    cemented THA in patients with osteonecrosis, biologically fixed implants have become popular in this patient population. When uncemented femoral components with a favorable track record are used, a high
    rate of success has been reported in patients with
    osteonecrosis.33-35
    As in other young patient groups, the related problems of polyethylene wear and periprosthetic osteolysis
    have been reported in patients with osteonecrosis. The

    Orthopaedic Knowledge Update 10

    421

    Section 4: Lower Extremity

    4: Lower Extremity

    combination of good fixation achieved with uncemented sockets and newer bearing surfaces has the potential to markedly improve the durability of the acetabular component.
    If radiation necrosis has occurred, either a reinforcement ring or highly porous metal socket is recommended, with overall good results. Higher dislocation
    rates in patients with osteonecrosis may be related to
    factors associated with the diagnoses that led to osteonecrosis or to structural factors such as less capsular
    hypertrophy in the patients with osteonecrosis compared to other diagnoses.
    Patients with osteonecrosis and on immunosuppressive agents or those who are immunosuppressed because of their underlying disease probably are at high
    risk for prosthetic infection. These patients are at risk
    for numerous perioperative complications, such as
    sickle cell disease. Vaso-occlusive crises secondary to
    the stress of surgery may occur. This can be reduced
    with exchange transfusion before arthroplasty. Intraoperative bleeding in this group of patients is significant
    and a high reoperation rate has been seen in some studies.

    Primary THA

    Acetabular Reconstruction
    Most acetabular components inserted in North America are cementless devices, with 20-year data that show
    durable fixation with a low risk of failure from aseptic
    loosening.36 Optimal results seem to be associated with
    thinner walled, porous coated, titanium components.
    At longer-term follow-up, the prevalence of wearrelated complications such as catastrophic wear and osteolysis increases, particularly in patients younger than
    50 years, more active patients in whom standard polyethylene (non-highly cross-linked) was combined with a
    thinner liner (less than 7 mm),37 and/or larger femoral
    heads38 (which increase volumetric wear rates). As
    bearing surface technology improves along with better
    locking mechanisms for the liner to decrease backside
    wear, the prevalence of wear-related complications
    should decrease.39 Although several manufacturers are
    now selling highly porous metal acetabular components
    that offer the theoretical benefits of better initial pressfit fixation and improved bone ingrowth, there are no
    data to suggest any clinical benefit in primary THA
    from the use of these materials over traditional porous
    titanium ingrowth surfaces.
    Cemented acetabular components, although still
    used heavily outside of North America, have fallen out
    of favor secondary to a more demanding surgical technique, increased surgical time, lack of modularity, and
    a higher rate of aseptic loosening, particularly in
    younger, high-demand patient populations. They do,
    however, offer decreased implant costs, and in patients
    who are elderly and/or low demand, are an attractive
    option. They may also be useful for managing patients
    with poor acetabular bone quality (such as patients
    422

    Orthopaedic Knowledge Update 10

    with severe inflammatory arthritis) in whom the bony


    architecture may not be able to support a cementless
    device.

    Femoral Reconstruction
    Cemented Stems
    Although long-term data suggest that some cemented
    femoral component designs (particularly trapezoidalshaped stems that avoid sharp corners and have a
    smooth to matte finish) are associated with outstanding
    long-term survivorship,40 the usage of cemented femoral components has decreased dramatically over the
    past decade in North America. Cemented stems are still
    used extensively in Europe, with excellent reported survivorship in the European registries. Concerns over
    greater technical difficulty, increased surgical time, and
    more variable results have contributed to this trend.
    Cementless Stems
    Early-generation cementless stems that were noncircumferentially porous coated proximally were associated with high rates of failed ingrowth leading to
    early revision.36 If these stems did become ingrown, osteolysis developed later as the noncircumferential porous coating allowed for the egress of particles from the
    bearing surface to the femoral canal. Second-generation
    designs that incorporated proximal porous coating that
    was circumferential have fared much better,41 with high
    rates of osseointegration and low rates of distal osteolyis; however, loosening secondary to osteolysis has
    been reported. Third-generation designs, even when designed to gain fixation primarily in the metaphysis, often now incorporate a roughened, biologically active
    surface that allows for ongrowth in the midsection of
    the stem to increase fixation.
    Most cementless femoral components presently in
    use are made from titanium and gain their fixation primarily in the metaphysis. Stems may be metaphyseal
    filling or of a flat wedge taper design (Figure 8). Although outstanding survivorship has been reported
    with both designs at 10 years or more,41,42 flat wedge
    taper designs have the theoretical benefits of increased
    ability to adjust version intraoperatively and easier removal if required. However, as the forces are more concentrated over a smaller surface area, the risk of intraoperative and early postoperative periprosthetic
    fractures may be higher. The addition of hydroxyapatite (HA) to the surface of the prosthesis does not seem
    to affect clinical or radiographic outcomes.43
    Cylindrical, fully porous coated stems that are made
    from cobalt chromium and have a beaded surface are
    designed to gain fixation primarily in the diaphysis
    (Figure 8). Benefits of this design include a long track
    record of durable fixation beyond 20 years.44 In addition, once bone is ingrown, there are no reports of late
    loosening. The major disadvantages include difficulty if
    removal of a well-fixed stem is required and proximal
    stress-shielding (relative osteopenia of the proximal femur seen secondary to stress transfer distally), which
    seems to be primarily a radiographic finding and has

    2011 American Academy of Orthopaedic Surgeons

    Chapter 32: Hip and Pelvic Reconstruction and Arthroplasty

    Figure 8

    4: Lower Extremity

    not been clearly linked to adverse clinical outcomes.


    Modular femoral components, which allow for
    placement of a sleeve in the metaphysis for primary fixation and then independently allow for placement of
    the neck for anteversion, have been popular in some
    centers. Although reported results are excellent, these
    devices are generally reserved for treating patients with
    proximal femoral deformity or abnormal anteversion,
    such as patients with developmental hip dysplasia. In
    addition to increased surgical complexity and cost,
    some degree of corrosion occurs at the additional modular junction45 that can lead to osteolysis. More recently, several manufacturers have introduced more traditionally shaped femoral components that use
    modular neck segments in addition to modular femoral
    heads. Although these stems allow for the increased
    ability to adjust leg length, version, and offset (in the
    hopes of better restoration of hip mechanics and avoiding dislocation), the additional modular junctions increase the risk of corrosion (and thus potentially osteolysis), breakage at this junction can occur and cost is
    higher. No studies as of yet report a clinical benefit to
    this design.

    From left to right, flat wedge tapered stem,


    metaphyseal filling stem, and fully porous
    coated, parallel-sided, diaphyseal-engaging
    stem.

    Hip Resurfacing
    Metal-on-metal hip resurfacing has become more popular based on studies that show excellent durability,
    particularly in young active patients,46 and the recent
    Food and Drug Administration approval of two devices. One review of 1,000 cases showed survivorship
    of 92% at 8 years, with most failures occurring early in
    the series when indications and techniques were developing.47 Potential benefits of this approach include
    preservation of proximal femoral bone stock, better
    restoration of hip biomechanics (including a lower risk
    of limb length discrepancy), increased ability to engage
    in high-demand activities, and a lower risk of dislocation. The risk of fracture of the retained femoral neck
    and systemic and local effects of wear particles generated from the metal-on-metal bearing surface are cause
    for concern. Optimal results with a lower risk of complications have been reported for younger, larger, male
    patients with a diagnosis of OA48 (as opposed to osteonecrosis), although the effect of sex may be more related to patient size and bone quality. Notching of the
    femoral neck and varus positioning of the femoral component seem to be associated with the occurrence of
    femoral neck fractures.49 Prospective randomized trials
    have shown few differences between hip resurfacing
    and conventional, stemmed THA.50

    Revision THA

    Acetabular Reconstruction
    The most commonly used classification for acetabular
    defects is that described by Paprosky.51 This classification is based on evaluation of the AP pelvis radiograph
    and considers the quantity and quality of bone available for fixation of the revision component. It is impor-

    2011 American Academy of Orthopaedic Surgeons

    tant to recognize that the posterior column is the primary structure relied upon for fixation of a revision
    component.
    In a type I defect, the architecture of the acetabulum
    is essentially normal and reconstruction can proceed as
    for a primary THA. This defect is rare, and is typically
    only seen when revising a hemiarthroplasty with isolated loss of articular cartilage.
    In a type II defect, there is less than 3 cm of proximal migration of the component. A type IIa defect is associated with migration superomedially, whereas a type
    IIb defect is associated with superolateral migration
    and loss of the acetabular rim. A type IIc defect is associated with protrusion of the acetabular component
    medially, past the Kohler line (also known as the ilioischial line, which is drawn from the medial border of
    the ilium to the medial border of the ischium). Type II
    defects can normally be reconstructed using a cementless acetabular component with adjunctive screw fixation and morcellized cancellous bone grafting of contained defects.
    A type III defect is characterized primarily by migration of the acetabular component of >3 cm. This is important, as it indicates damage to the acetabular columns that compromises fixation of the revision
    acetabular component. The use of a standard, cementless hemispherical component may not be possible, as
    the defect is often oblong and with progressive reaming
    of the acetabulum, the surgeon runs out of space front
    to back while the defect has not been filled from top to
    bottom. A type IIIA defect (Figure 9) is often referred
    to as an up and out defect where damage occurs primarily to the remaining acetabular rim superiorly and
    anteriorly; however, the posterior column is usually still

    Orthopaedic Knowledge Update 10

    423

    Section 4: Lower Extremity

    4: Lower Extremity

    intact. A type IIIB defect (Figure 10) is associated with


    further reconstructive complexity and is often referred
    to as an up and in defect where there is a large defect
    of the medial wall (indicated by disruption of the
    Kohler line) and associated severe osteolysis of the
    ischium indicating further damage to the posterior column.
    A pelvic discontinuity refers to a separation of the
    superior and inferior halves of the hemipelvis.52 This
    condition can occur acutely, but is typically chronic and
    associated with severe bone loss that greatly complicates subsequent reconstruction. Radiographic indicators include a transverse fracture line, medial translation of the inferior hemipelvis and often an asymmetry
    of the obturator foramen as seen on the AP pelvis radiograph. The best reported results in the literature for
    reconstruction have included stabilization of the posterior column with a plate, adjunctive bone grafting, and
    the use of either a cementless cup with mulitiple screws
    for adjunctive fixation or a cage that spans from the ilium to the ischium.

    Figure 9

    Type IIIA acetabular defect with migration of


    more than 3 cm without migration medially.

    Hemispherical, Porous-Coated Acetabular Components


    The use of a hemispherical, cementless acetabular component with adjunctive screw fixation is appropriate
    for most acetabular revisions. The surgical technique is
    straightforward, and durable fixation has been shown
    at 20 years postoperatively.53
    Porous Metals
    Several manufacturers presently offer highly porous
    metals (two to three times more porous than standard
    ingrowth surfaces) that not only offer the promise of
    greater bone ingrowth but higher frictional interference
    that may augment initial component stability. Case series have shown good clinical results;54 however, comparative data on more traditional titanium ingrowth
    surfaces are lacking. An additional advantage of these
    materials is the availability of acetabular augments,
    which can be used in a manner similar to structural allograft for treating severe bony deficiency. Advantages
    of augments include decreased surgical time and complexity, while allowing for additional points for screw
    fixation and the potential for biologic ingrowth to occur without the risks of allograft resorption. The longer
    term results of this type of reconstruction are unknown.

    Figure 10

    424

    Type IIIB acetabular defect with migration of


    more than 3 cm, disruption of the Kohler line,
    and ischial osteolysis.

    Orthopaedic Knowledge Update 10

    Cages
    The use of cages has decreased dramatically in the past
    decade. Without a surface for biologic ingrowth, these
    devices are mechanical in nature and are associated
    with a high rate of subsequent breakage. Devices that
    do not span from the ilium to the ischium (reconstruction rings) are used infrequently by North American
    surgeons. The role of spanning devices seems limited to
    cases where biologic ingrowth is unlikely to occur (such
    as tumor or radiation necrosis of the pelvis) or as an
    adjunct to protect a cementless device (such as the cupcage construct) or a strutural allograft.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 32: Hip and Pelvic Reconstruction and Arthroplasty

    Femoral Reconstruction

    Cylindrical Fully Porous-Coated Stems


    These devices continue to be the workhorse for femoral
    revision surgery in North America. The surgical technique is relatively simple, and excellent initial component ingrowth and durable long-term fixation have
    been reported.56 They have been shown to be particularly reliable for managing femoral defects when at
    least 4 cm of press-fit is obtained between the implant
    and the isthmus of the femur.
    Modular Tapered Stems
    With the introduction of bibody, modular systems that
    allow for placement of the distal tapered portion of the
    stem first, followed by the use of proximal body seg-

    2011 American Academy of Orthopaedic Surgeons

    4: Lower Extremity

    The most commonly used classification of femoral defects is that described by Paprosky et al.55
    Type I defects are characterized by a supportive metaphysis and intact diaphysis and similar to a primary
    femur. They are unique in that there is intact cancellous
    bone present for fixation of the revision component with
    cement if desired. Revision can be performed as the surgeon would for a primary THA. This is typically only
    seen when revising a failed resurfacing or a cementless
    hemiarthroplasty without a porous ingrowth surface.
    In type II defects, the metaphysis is supportive with
    an intact diaphysis; however, the cancellous bone of the
    proximal femur is not present. Because the metaphysis
    is supportive, it can be relied on for fixation; however,
    the use of a stem that gains primary fixation in the diaphysis is common.
    In type III defects, the metaphysis is damaged and
    cannot be relied on for fixation; therefore, a stem that
    gains primary fixation in the diaphysis is used. If more
    than 4 cm of intact isthmus is available for distal fixation, the defect is classified as type IIIA (Figure 11),
    whereas if less than 4 cm is available it is classified as
    type IIIB. Type IIIA defects are most commonly reconstructed with a cylindrical, parallel-sided, fully porous
    coated stem. When less than 4 cm of isthmus is available for distal fixation, worse results have been reported with a fully porous coated device and thus a
    modular, titanium, tapered stem is typically used for
    type IIIB defects. Modular tapered stems are also used
    in the face of substantial femoral deformity (loose femoral components can cause the femur to remodel into
    varus and retroversion) and in cases where the diameter
    of the revision femoral component is larger than
    18 mm.
    In type IV defects, not only is the metaphysis unsupportive but there is no isthmus available for distal fixation and thus reconstruction is very difficult. If the
    tube of the femoral canal is intact, impaction grafting can be used. If it is not intact, a proximal femoral
    replacing prosthesis or a proximal femoral allograftprosthetic composite can be used. Modular tapered
    stems can be used in some situations; however, as there
    is no isthmus available, stable fixation may be difficult
    to achieve.

    Figure 11

    Type IIIA femoral defect. The metaphysis is nonsupportive; however, there is more than 4 cm
    of intact diaphysis for distal fixation.

    ments that can be used to independently reconstruct leg


    length, offset, and version, the popularity of these
    stems has increased. Although the bibody concept has
    improved upon the problem of stem subsidence, which
    was common with earlier nonmodular tapered stems,
    breakage at the modular junction has been reported
    and corrosion at this modular junction is a concern.
    More recent designs seem to have addressed the problems of breakage; however, increased implant cost and
    surgical complexity are disadvantages. These stems do
    work well with a very short isthmus for distal fixation
    (even when less than 4 cm), and the ability to adjust
    version to optimize stability is attractive. One retrospective study suggested better outcomes among patients who received a modular, tapered titanium stem
    than when a parallel-sided, cobalt-chromium, fully porous coated stem was used.57
    Impaction Grafting
    Although still commonly used in Europe, this technique
    is infrequently used in North America because it is time
    and resource intensive, and higher rates of complications (particularly intraoperative and early postoperative periprosthetic fracture and stem subsidence) have
    been reported.58
    Proximal Femoral Replacement
    Although proximal femoral replacement (with an allograft prosthesic composite or a proximal femoral re-

    Orthopaedic Knowledge Update 10

    425

    Section 4: Lower Extremity

    placement) may be the only solution in the most complex situations, surgeons should note that these
    techniques can be associated with a substantial risk of
    complications. In particular, instability is common as
    reattachment of the abductors to the allograft or prosthetic proximal femur can be unreliable. The use of a
    constrained acetabular liner should be considered.

    4: Lower Extremity

    Cemented Stems
    Cemented femoral revisions are performed infrequently
    because it can be difficult to obtain good cement interdigitation into viable cancellous bone in the revision femur with high rates of radiographic and repeat loosening requiring re-operation reported. The results of
    cementless revision femoral revision, particularly with
    stems that gain fixation primarily in the diaphysis, have
    been more consistent.

    Complications of THA

    Instability
    A recent study has shown that recurrent instability is
    the most common reason for revision THA.59 The risk
    of instability has been correlated with multiple factors,
    including surgeon experience, surgical approach (posterior approach higher risk than anterior or anterolateral
    approaches), and femoral head size. Larger femoral
    heads allow for increased range of motion before impingement, and component-to-component impingement is eliminated when they are larger than 36 mm.
    Large heads also eliminate the need for a skirt and increase the distance that the femoral head must travel
    (the so-called jump distance) for a dislocation to occur, although this still requires appropriate component
    position. The use of larger-diameter femoral heads has
    become more commonplace with the routine use of
    more wear-resistant bearing surfaces.
    When assessing the patient with recurrent instability,
    it is important to determine the cause of instability and
    also evaluate the patient for infection because not only
    may the two coexist, but infection may predispose to
    instability. A careful assessment of both femoral and
    acetabular component position is paramount with acceptable position being 15 of anteversion and 40 of
    abduction for the acetabular component (plus or minus
    10) and femoral component anteversion of 10 to 30.
    Although acetabular component abduction is easy to
    determine on an AP radiograph of the hip or pelvis, anteversion of the femoral and acetabular components
    can be more difficult to measure. A CT scan of the pelvis can be used to determine acetabular component version as this can be difficult to assess accurately intraoperatively. A CT scan of the proximal femur including a
    cut through the ipsilateral epicondylar axis of the knee
    can reliably measure femoral component anteversion,
    although most surgeons find this relatively easy to assess at the time of revision surgery.
    If component malposition is identified in a patient
    with recurrent instability, revision and component re426

    Orthopaedic Knowledge Update 10

    orientation should be performed because other revision


    techniques (such as isolated head/liner exchange or use
    of a constrained liner) are unlikely to be successful. A
    search for soft-tissue and bony impingement is also undertaken to further optimize stability, and a largediameter femoral head (typically larger than 36 mm) is
    used to decrease and potentially eliminate componentto-component impingement. Late instability has been
    associated with severe polyethylene wear and is typically treated with a modular head and liner exchange
    and a larger diameter femoral head.
    The most challenging patients to manage are those
    whose instability is associated with damage to the abductor musculature or their attachment via the greater
    trochanter. In these cases, large femoral heads have
    been shown not to be particularly effective and a constrained liner is usually required.60 Although devices
    such as a constrained liner are useful in the most complex of situations, it is important to recognize that
    these devices transmit strain to the bone-prosthesis interface and can lead to catastrophic failure and increased polyethylene wear. Finally, not all designs are
    the same, with variable rates of success reported in the
    literature.

    Infection
    All patients with a failed or painful THA should be
    screened for infection with an erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Studies
    have shown that these tests are very sensitive and that
    they are rarely normal in the face of infection.60 If the
    ESR and/or CRP are abnormal and the clinical suspicion for infection is high (such as less than 2 years after
    surgery or a history of prior infection or wound healing
    problems after the initial procedure), aspiration of the
    hip can be performed with fluoroscopic guidance; patients must refrain from antibiotics for a minimum of 2
    weeks before aspiration to decrease the risk of a falsely
    negative aspiration.
    A recent study found that the use of the synovial
    fluid white blood cell (WBC) count was the best perioperative test for identifying infection.60 Aspiration can
    be performed either preoperatively or intraoperatively
    (before entering the hip capsule). The test is inexpensive, objective, and ubiquitous. Optimal cutoff values
    for the synovial fluid WBC count were found to be
    3,000 /mm3 if the ESR and CRP were both elevated and
    9,000 /mm3 if the ESR or CRP (but not both) was elevated. The synovial fluid WBC differential was also
    found to be helpful, with an optimal cutoff point of
    80% polymorphonuclear cells. Intraoperative frozen
    sections have also been shown to be useful for diagnosing infection; however, the criteria for determining infection have been controversial and performance is dependent on a skilled pathologist and is subject to
    sampling error. Intraoperative Gram stains are not a
    useful test for identifying infection and while usually
    falsely negative, they can also be falsely positive and
    thus should not be routinely performed. For more information on the diagnosis of periprosthetic infection

    2011 American Academy of Orthopaedic Surgeons

    Chapter 32: Hip and Pelvic Reconstruction and Arthroplasty

    Table 6

    Annotated References

    Vancouver Classification for Periprosthetic


    Fractures of the Femur
    Type A

    Pertrochanteric fracture

    AL

    Fracture of the lesser trochanter

    AG

    Fracture of the greater trochanter

    Type B

    Fracture around the femoral component

    B1

    Femoral component well-fixed

    B2

    Femoral component loose

    B3

    Femoral component loose with severe loss of


    femoral bone stock

    Type C

    Fracture distal to the femoral component

    Helmick CG, Felson DT, Lawrence RC, et al; National


    Arthritis Data Workgroup: Estimates of the prevalence
    of arthritis and other rheumatic conditions in the United
    States: Part I. Arthritis Rheum 2008;58(1):15-25.
    The authors describe the prevalence of arthritis and
    other rheumatologic inflammatory conditions in the
    United States.

    2.

    Lawrence RC, Felson DT, Helmick CG, et al; National


    Arthritis Data Workgroup: Estimates of the prevalence
    of arthritis and other rheumatic conditions in the United
    States. Part II. Arthritis Rheum 2008;58(1):26-35.
    The authors described the prevalence of arthritis and
    other rheumatologic inflammatory conditions in the
    United States.

    3.

    Jessel RH, Zilkens C, Tiderius C, Dudda M, Mamisch


    TC, Kim YJ: Assessment of osteoarthritis in hips with
    femoroacetabular impingement using delayed gadolinium enhanced MRI of cartilage. J Magn Reson Imaging
    2009;30(5):1110-1115.
    The authors found that the results of osteoplasty for FAI
    depend on the amount of preexisting OA in the hip
    joint. dGEMRIC can be used in the diagnosis and staging of OA.

    4.

    Ganz R, Parvizi J, Beck M, Leunig M, Ntzli H, Siebenrock KA: Femoroacetabular impingement: A cause for
    osteoarthritis of the hip. Clin Orthop Relat Res 2003;
    417(417):112-120.

    5.

    Ganz R, Leunig M, Leunig-Ganz K, Harris WH: The


    etiology of osteoarthritis of the hip: An integrated mechanical concept. Clin Orthop Relat Res 2008;466(2):
    264-272.
    The authors describe eloquently how FAI may lead to
    OA in the native hip.

    6.

    Sierra RJ, Trousdale RT, Ganz R, Leunig M: Hip disease in the young, active patient: Evaluation and nonarthroplasty surgical options. J Am Acad Orthop Surg
    2008;16(12):689-703.
    This is a review article describing physical examination
    findings, radiographic features, and surgical management of FAI.

    7.

    Clohisy JC, Carlisle JC, Beaul PE, et al: A systematic


    approach to the plain radiographic evaluation of the
    young adult hip. J Bone Joint Surg Am 2008;90(suppl
    4):47-66.
    This is a description of the radiographic technique and
    evaluation of imaging findings in patients with FAI and
    hip dysplasia.

    8.

    Notzli HP, Wyss TF, Stoecklin CH, Schmid MR,


    Treiber K, Hodler J: The contour of the femoral headneck junction as a predictor for the risk of anterior impingement. J Bone Joint Surg Br 2002;84(4):556-560.

    9.

    Ganz R, Gill TJ, Gautier E, Ganz K, Krgel N, Berle-

    Periprosthetic Fracture
    The Vancouver classification is the most widely accepted for evaluation of periprosthetic fractures of the
    femur61 (Table 6). This classification considers the location of the fracture and most importantly, the stability
    of the component. B1 fractures with a stable femoral
    component are treated with internal fixation. Periprosthetic fractures associated with a loose femoral component (B2 or B3) require femoral component revision,
    most commonly with the use of a cementless stem that
    bypasses the fracture site and gains fixation in the diaphysis distal to the fracture; however, proximal femoral replacement may be required for B3 fractures. The
    most common error in management is misclassifying a
    Vancouver B2 fracture as a B1 and treating it with internal fixation.

    Deep Venous Thrombosis and Pulmonary


    Embolism
    This topic is covered in chapter 12. Please refer to the
    AAOS Clinical Practice Guidelines on Pulmonary Embolism, which can be accessed at www.aaos.org/
    research/guidelines/guide.asp.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    please see the AAOS clinical practice guideline, accessed at www.aaos.org/research/guidelines/guide.asp.


    The mainstays of treatment of a chronic infection include removal of the components, insertion of an
    antibiotic-loaded cement spacer, and systemic antibiotics for 6 weeks followed by reimplantation once the infection has been cleared. Dbridement and component
    retention has been shown to have a high rate of failure
    and seems only effective in the management of some
    early postoperative (infections occurring within the first
    4 to 6 weeks) and acute hematogenous infections, although the presence of staphylococcal species in both
    of these scenarios seems to portend a worse prognosis
    for success.

    1.

    427

    Section 4: Lower Extremity

    teotomy: The Bernese experience, in Sim H, ed: Instructional Course Lectures. Volume 50. Rosemont, IL,
    American Academy of Orthopaedic Surgeons, 2001, vol
    50, pp 239-245.

    4: Lower Extremity

    mann U: Surgical dislocation of the adult hip a technique with full access to the femoral head and acetabulum without the risk of avascular necrosis. J Bone Joint
    Surg Br 2001;83(8):1119-1124.
    10.

    Espinosa N, Rothenfluh DA, Beck M, Ganz R, Leunig


    M: Treatment of femoro-acetabular impingement: Preliminary results of labral refixation. J Bone Joint Surg
    Am 2006;88(5):925-935.

    20.

    Trousdale RT, Ekkernkamp A, Ganz R, Wallrichs SL:


    Periacetabular and intertrochanteric osteotomy for the
    treatment of osteoarthritis in dysplastic hips. J Bone
    Joint Surg Am 1995;77:73-85.

    11.

    Beck M, Leunig M, Parvizi J, Boutier V, Wyss D, Ganz


    R: Anterior femoroacetabular impingement: Part II.
    Midterm results of surgical treatment. Clin Orthop
    Relat Res 2004;418(418):67-73.

    21.

    Crowe JF, Mani VJ, Ranawat CS: Total hip replacement


    in congenital dislocation and dysplasia of the hip.
    J Bone Joint Surg Am 1979;61:15-23.

    22.
    12.

    Laude F, Sariali E, Nogier A: Femoroacetabular impingement treatment using arthroscopy and anterior approach. Clin Orthop Relat Res 2009;467(3):747-752.
    The authors describe the treatment of FAI using an anterior approach combined with hip arthroscopy. There
    was a high rate of labral refixation failure in this study.

    Lavernia CJ, Sierra RJ, Grieco FR: Osteonecrosis of the


    femoral head. J Am Acad Orthop Surg 1999;7(4):250261.

    23.

    Steinberg ME, Hayken GD, Steinberg DR: A quantitative system for staging avascular necrosis. J Bone Joint
    Surg Br 1995;77(1):34-41.

    24.

    Hernigou P, Habibi A, Bachir D, Galacteros F: The natural history of asymptomatic osteonecrosis of the femoral head in adults with sickle cell disease. J Bone Joint
    Surg Am 2006;88(12):2565-2572.

    25.

    Hernigou P, Poignard A, Nogier A, Manicom O: Fate of


    very small asymptomatic stage-I osteonecrotic lesions of
    the hip. J Bone Joint Surg Am 2004;86(12):2589-2593.

    26.

    Mont MA, Carbone JJ, Fairbank AC: Core decompression versus nonoperative management for osteonecrosis
    of the hip. Clin Orthop Relat Res 1996;324(324):169178.

    27.

    Ramachandran M, Ward K, Brown RR, Munns CF,


    Cowell CT, Little DG: Intravenous bisphosphonate
    therapy for traumatic osteonecrosis of the femoral head
    in adolescents. J Orthop Surg 2008;13(5):463-468.
    The authors evaluated the use of bisphosphonates in
    treating adolescents with osteonecrosis of the femoral
    head after trauma and found it to be a useful adjunct
    therapy.

    28.

    Iwakiri K, Oda Y, Kaneshiro Y, et al: Effect of simvastatin on steroid-induced osteonecrosis evidenced by the
    serum lipid level and hepatic cytochrome P4503A in a
    rabbit model. J Orthop Sci 2008;13(5):463-468.
    In a study to determine the efficacy of lipid-lowering
    agents in the prevention of steroid-induced osteonecrosis in a rabbit model, the authors found that simvastatin
    and pravastatin substantially reduced the incidence of
    osteonecrosis, with simvastatin being more effective.

    29.

    Korompilias AV, Lykissas MG, Beris AE, Urbaniak JR,


    Soucacos PN: Vascularised fibular graft in the management of femoral head osteonecrosis: Twenty years later.
    J Bone Joint Surg Br 2009;91(3):287-293.
    The authors discussed the advantages of vascularized
    fibular graft as a joint-preserving method in the treatment of femoral head osteonecrosis.

    13.

    Byrd JW, Jones KS: Arthroscopic femoroplasty in the


    management of cam-type femoroacetabular impingement. Clin Orthop Relat Res 2009;467(3):739-746.
    The authors describe the arthroscopic treatment of cam
    FAI lesions with overall excellent results.

    14.

    Ganz R, Klaue K, Vinh TS, Mast JW: A new periacetabular osteotomy for the treatment of hip dysplasias:
    Technique and preliminary results. Clin Orthop Relat
    Res 1988;232(232):26-36.

    15.

    16.

    17.

    428

    Philippon MJ, Briggs KK, Yen YM, Kuppersmith DA:


    Outcomes following hip arthroscopy for femoroacetabular impingement with associated chondrolabral dysfunction: Minimum two-year follow-up. J Bone Joint
    Surg Br 2009;91(1):16-23.
    The authors describe the arthroscopic management of
    FAI for both the acetabular and femoral sides. At a
    mean follow-up of 2.3 years, the results were satisfactory in most patients.
    Sthelin L, Sthelin T, Jolles BM, Herzog RF: Arthroscopic offset restoration in femoroacetabular cam
    impingement: Accuracy and early clinical outcome. Arthroscopy 2008;24(1):51-57, e1.
    The authors report on 22 patients with symptomatic
    cam type femoroacetabular impingement treated with
    arthroscopic dbridement and femoral osteochondroplasty. The results at 6 months were satisfactory with
    improvements in clinical scores.
    Murphy SB, Ganz R, Mller ME: The prognosis in untreated dysplasia of the hip: A study of radiographic
    factors that predict the outcome. J Bone Joint Surg Am
    1995;77(7):985-989.

    18.

    Li PL, Ganz R: Morphologic features of congenital acetabular dysplasia: One in six is retroverted. Clin Orthop Relat Res 2003;416:245-253.

    19.

    Siebenrock KA, Leunig M, Ganz R: Periacetabular os-

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 32: Hip and Pelvic Reconstruction and Arthroplasty

    Hernigou P, Beaujean F: Treatment of osteonecrosis


    with autologous bone marrow grafting. Clin Orthop
    Relat Res 2002;405:14-23.

    31.

    Cuckler JM, Moore KD, Estrada L: Outcome of hemiresurfacing in osteonecrosis of the femoral head. Clin Orthop Relat Res 2004;429(429):146-150.

    32.

    Revell MP, McBryde CW, Bhatnagar S, Pynsent PB,


    Treacy RB: Metal-on-metal hip resurfacing in osteonecrosis of the femoral head. J Bone Joint Surg Am 2006;
    88(suppl 3):98-103.

    33.

    Fye MA, Huo MH, Zatorski LE, Keggi KJ: Total hip arthroplasty performed without cement in patients with
    femoral head osteonecrosis who are less than 50 years
    old. J Arthroplasty 1998;13(8):876-881.

    34.

    Hungerford MW, Hungerford DS, Jones LC: Outcome


    of uncemented primary femoral stems for treatment of
    femoral head osteonecrosis. Orthop Clin North Am
    2009;40(2):283-289.
    The authors report the results of uncemented primary
    total hip arthroplasty in patients with osteonecrosis
    with excellent results using an uncemented stem.

    35.

    36.

    Steinberg ME, Lai M, Garino JP, Ong A, Wong KL: A


    comparison between total hip replacement for osteonecrosis and degenerative joint disease. Orthopedics 2008;
    31(4):360.
    The authors studied 203 total hip replacements for osteonecrosis and compared them with 300 done for degenerative joint disease. Total hip replacement was
    found to be a good treatment for patients with advanced osteonecrosis.
    Della Valle CJ, Mesko NW, Quigley L, Rosenberg AG,
    Jacobs JJ, Galante JO: Primary total hip arthroplasty
    with a porous-coated acetabular component: A concise
    follow-up, at a minimum of twenty years, of previous
    reports. J Bone Joint Surg Am 2009;91(5):1130-1135.
    At a minimum of 20 years, survivorship of the acetabular component was 96%. A modular polyethylene liner
    exchange was required or recommended in 19% of surviving hips. Level of evidence: IV.

    37.

    Della Valle CJ, Berger RA, Shott S, et al: Primary total


    hip arthroplasty with a porous-coated acetabular component: A concise follow-up of a previous report.
    J Bone Joint Surg Am 2004;86(6):1217-1222.

    38.

    Livermore J, Ilstrup D, Morrey B: Effect of femoral


    head size on wear of the polyethylene acetabular component. J Bone Joint Surg Am 1990;72(4):518-528.

    39.

    Leung SB, Egawa H, Stepniewski A, Beykirch S, Engh


    CA Jr, Engh CA Sr: Incidence and volume of pelvic osteolysis at early follow-up with highly cross-linked and
    noncross-linked polyethylene. J Arthroplasty 2007;
    22(6, suppl 2)134-139.
    Patients implanted with a highly cross-linked liner had a
    lower incidence of pelvic osteolysis than those implanted with a standard polyethylene liner that was not

    2011 American Academy of Orthopaedic Surgeons

    cross-linked as determined by pelvic CT scanning. Level


    of evidence: I.
    40.

    Callaghan JJ, Liu SS, Firestone DE, et al: Total hip arthroplasty with cement and use of a collared mattefinish femoral component: Nineteen to twenty-year
    follow-up. J Bone Joint Surg Am 2008;90(2):299-306.
    At a minimum of 19 years, the matte-finish cemented
    femoral component had 85% survivorship with revision
    for aseptic loosening as the end point. Level of evidence:
    IV.

    41.

    Lombardi AV Jr, Berend KR, Mallory TH, Skeels MD,


    Adams JB: Survivorship of 2000 tapered titanium porous plasma-sprayed femoral components. Clin Orthop
    Relat Res 2009;467(1):146-154.
    Survivorship of the tapered, titanium, porous plasma
    sprayed femoral component was 95.5% at 20 years
    with failure for any reason and 99.3% at 20 years with
    failure for aseptic loosening as the end point. Level of
    evidence: IV.

    42.

    Teloken MA, Bissett G, Hozack WJ, Sharkey PF, Rothman RH: Ten to fifteen-year follow-up after total hip arthroplasty with a tapered cobalt-chromium femoral
    component (tri-lock) inserted without cement. J Bone
    Joint Surg Am 2002;84(12):2140-2144.

    43.

    Kim YH, Kim JS, Oh SH, Kim JM: Comparison of


    porous-coated titanium femoral stems with and without
    hydroxyapatite coating. J Bone Joint Surg Am 2003;
    85(9):1682-1688.

    44.

    Belmont PJ Jr, Powers CC, Beykirch SE, Hopper RH Jr,


    Engh CA Jr, Engh CA: Results of the anatomic medullary locking total hip arthroplasty at a minimum of
    twenty years: A concise follow-up of previous reports.
    J Bone Joint Surg Am 2008;90(7):1524-1530.
    At a mean of 22 years, survivorship of the diaphyseal
    engaging, fully porous coated cobalt-chromium stem
    was 97.8%. Failure of the cementless acetabular component used was correlated with the presence of osteolysis.
    Level of evidence: IV.

    45.

    Rodrigues DC, Urban RM, Jacobs JJ, Gilbert JL: In vivo


    severe corrosion and hydrogen embrittlement of retrieved modular body titanium alloy hip-implants.
    J Biomed Mater Res B Appl Biomater 2009;88(1):206219.
    In this retrieval analysis of three different designs of
    modular body femoral components, some degree of corrosion was seen at the modular junction of all components studied.

    46.

    Daniel J, Pynsent PB, McMinn DJ: Metal-on-metal resurfacing of the hip in patients under the age of 55 years
    with osteoarthritis. J Bone Joint Surg Br 2004;86(2):
    177-184.

    47.

    Amstutz HC, Le Duff MJ: Eleven years of experience


    with metal-on-metal hybrid hip resurfacing: A review of
    1000 conserve plus. J Arthroplasty 2008;23(6, suppl 1):
    36-43.

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    30.

    429

    Section 4: Lower Extremity

    In this report of 1,000 consecutive resurfacings performed by a single surgeon, survivorship was 92% at 8
    years, with most failures occurring early in the series. It
    is important to note that in general this series is a challenging group of young patients with abnormal femoral
    anatomy. Level of evidence: IV.

    4: Lower Extremity

    48.

    430

    Buergi ML, Walter WL: Hip resurfacing arthroplasty:


    The Australian experience. J Arthroplasty 2007;22(7,
    suppl 3):61-65.
    In this report of the Australian hip registry, early revision rates for hip resurfacing were shown to be higher
    than a conventional THA for all groups of patients
    other than males younger than 55 years. Level of evidence: IV.

    49.

    Shimmin AJ, Back D: Femoral neck fractures following


    Birmingham hip resurfacing: A national review of 50
    cases. J Bone Joint Surg Br 2005;87(4):463-464.

    50.

    Lavigne M, Therrien M, Nantel J, Roy A, Prince F, Vendittoli PA: The John Charnley Award: The functional
    outcome of hip resurfacing and large-head THA is the
    same: A randomized, double-blind study. Clin Orthop
    Relat Res 2010;468:326-336.
    In this prospective, blinded, randomized clinical trial,
    the functional outcomes of hip resurfacing and conventional THA were found to be similar. Level of evidence:
    I.

    51.

    Paprosky WG, Perona PG, Lawrence JM: Acetabular


    defect classification and surgical reconstruction in revision arthroplasty: A 6-year follow-up evaluation. J Arthroplasty 1994;9(1):33-44.

    52.

    Berry DJ, Lewallen DG, Hanssen AD, Cabanela ME:


    Pelvic discontinuity in revision total hip arthroplasty.
    J Bone Joint Surg Am 1999;81(12):1692-1702.

    53.

    Park DK, Della Valle CJ, Quigley L, Moric M, Rosenberg AG, Galante JO: Revision of the acetabular component without cement: A concise follow-up, at twenty
    to twenty-four years, of a previous report. J Bone Joint
    Surg Am 2009;91(2):350-355.
    At a minimum of 20 years, revision of the acetabulum
    with a cementless acetabular component showed survivorship of 95%. The most common reasons for repeat
    revision were infection and recurrent dislocation. Level
    of evidence: IV.

    Orthopaedic Knowledge Update 10

    54.

    Nehme A, Lewallen DG, Hanssen AD: Modular porous


    metal augments for treatment of severe acetabular bone
    loss during revision hip arthroplasty. Clin Orthop Relat
    Res 2004;429:201-208.

    55.

    Della Valle CJ, Paprosky WG: The femur in revision total hip arthroplasty evaluation and classification. Clin
    Orthop Relat Res 2004;420:55-62.

    56.

    Weeden SH, Paprosky WG: Minimal 11-year follow-up


    of extensively porous-coated stems in femoral revision
    total hip arthroplasty. J Arthroplasty 2002;17(4, suppl
    1):134-137.

    57.

    Garbuz DS, Toms A, Masri BA, Duncan CP: Improved


    outcome in femoral revision arthroplasty with tapered
    fluted modular titanium stems. Clin Orthop Relat Res
    2006;453:199-202.

    58.

    Meding JB, Ritter MA, Keating EM, Faris PM: Impaction bone-grafting before insertion of a femoral stem
    with cement in revision total hip arthroplasty: A minimum two-year follow-up study. J Bone Joint Surg Am
    1997;79(12):1834-1841.

    59.

    Bozic KJ, Kurtz SM, Lau E, Ong K, Vail TP, Berry DJ:
    The epidemiology of revision total hip arthroplasty in
    the United States. J Bone Joint Surg Am 2009;91(1):
    128-133.
    A review of 51,345 revision THAs from the nationwide
    inpatient sample database showed that instability and
    prosthetic loosening were the most common causes of
    revision THA. Level of evidence: II.

    60.

    Kung PL, Ries MD: Effect of femoral head size and abductors on dislocation after revision THA. Clin Orthop
    Relat Res 2007;465:170-174.
    This retrospective review of 230 patients undergoing revision THA showed that a 36-mm femoral head was associated with a significantly lower risk of dislocation
    than a 28-mm femoral head; however, the dislocation
    rate remained high if the abductor muscles were not intact. Level of evidence: IV.

    61.

    Masri BA, Meek RM, Duncan CP: Periprosthetic fractures evaluation and treatment. Clin Orthop Relat Res
    2004;420:80-95.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 33

    Femoral Fractures
    Jodi Siegel, MD

    Paul Tornetta III, MD

    Introduction

    Classification
    Femoral shaft fractures are often classified by location
    and geometry. The femoral shaft is often divided into
    thirds for descriptive purposes, with fractures reported
    in the proximal, middle, or distal portion of the shaft.
    Additionally, the fracture pattern is generally reported
    as transverse, short oblique, long spiral, or comminuted. The Winquist and Hansen classification more
    specifically quantifies the comminution of the fracture1
    (Table 1). This classification system helps to characterize axial stability; types I and II are axially stable and
    types III and IV are axially and rotationally unstable.

    Mechanisms of Injury and Fracture Management


    High-energy femoral shaft fractures occur from the
    usual trauma mechanisms: motor vehicle crashes, motorcycle crashes, pedestrian versus motor vehicle injuries, and falls from a height. Because patients often
    have other systemic injuries in addition to musculoskeletal injuries, a complete trauma examination must be
    performed.

    Dr. Siegel serves as a paid consultant to or is an employee of Smith & Nephew. Dr. Tornetta serves as a
    board member, owner, officer, or committee member of
    the American Orthopaedic Association, has received royalties from Smith & Nephew, serves as a paid consultant
    to or is an employee of Smith & Nephew, has received
    research or institutional support from Smith & Nephew,
    and has stock or stock options held in Exploramed.

    2011 American Academy of Orthopaedic Surgeons

    4: Lower Extremity

    Fractures of the femoral shaft occur in patients of all


    ages and result from a variety of mechanisms. These
    fractures tend to show a bimodal incidence, typically
    occurring as a result of high-energy trauma in younger
    patients or low-energy falls in elderly patients. The understanding of femoral shaft fractures and the effect of
    these fractures on patients has continued to grow over
    the past 60 years, allowing improvements in overall patient care and creating expectations of treatment success.

    The evaluation of patients with high-energy femoral


    shaft fractures must include a systematic assessment for
    associated injuries. Patients should be examined for
    head, chest, and abdominal injuries. Hemodynamic status must be monitored because clinically relevant blood
    loss can occur into the thigh.2 The neurovascular status
    of the limb must be assessed in addition to the integrity
    of the skin. Although vascular compromise in association with closed femoral shaft fractures caused by blunt
    trauma is uncommon, it must not go undiagnosed. Restoration of general fracture alignment can unkink vessels and allow a more accurate examination. If there is
    any difficulty in examining the distal pulse, anklebrachial index measurements should be obtained.
    Ankle-brachial values less than 0.9 are considered abnormal and may indicate clinically significant vascular
    compromise. A neurologic examination can be difficult
    because of the patients inability to cooperate; however,
    attempts must be made to achieve an accurate examination.
    Other musculoskeletal injuries are common. Bilateral femoral fractures occur in as many as 10% of patients and are associated with higher mortality and Injury Severity Scores.3,4 Associated femoral neck
    fractures should be evaluated. Dedicated hip radiographs and a fine-cut CT scan through the femoral
    neck are recommended.5 CT scans used to evaluate the
    abdomen and pelvis can be formatted to include fine
    cuts through the femoral neck to allow for a more thorough bony radiographic examination. Preoperative radiographs of the entire femur and dedicated radiographs of the hip and knee are necessary to look for

    Table 1

    Winquist and Hansen Classification of Femoral


    Shaft Fracture Comminution
    Grade

    Degree of Comminution

    No comminution

    Small butterfly fragment; 50% cortical contact

    II

    Large butterfly fragment; < 50% cortical contact

    III

    Larger butterfly fragment; minimal cortical


    abutment

    IV

    No cortical contact; segmentally comminuted

    Orthopaedic Knowledge Update 10

    431

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 1

    Radiographs showing unicortical beaking hypertrophy in a patient on prolonged bisphosphonate therapy. A, The injury is seen. B, Fixation
    with a cephalomedullary nail.

    additional fractures that can affect the treatment plan.


    The stability of the knee can be evaluated after the femur has been stabilized.
    Although elderly patients may present for treatment
    as a result of high-energy trauma, low-energy femoral
    fractures resulting from a fall from standing height are
    a common occurrence. Preexisting medical conditions
    complicate treatment in this patient cohort. The use of
    oral bisphosphonates for more than 4 years has recently been associated with simple transverse or short
    oblique femoral fractures in areas of diaphyseal cortical
    hypertrophy with a unicortical beak6-9 (Figure 1).
    Pathologic femoral fractures can also present after
    trauma. Careful examination of the radiographs in addition to a thorough history should be completed for
    every patient to allow for appropriate treatment.

    Treatment
    Nonsurgical treatment for femoral fractures is rarely
    used in adult patients. Traction as a form of definitive
    treatment has limited indications, such as in patients
    with significant medical comorbidities. Traction is applicable for the temporary stabilization of femoral fractures until definitive internal fixation can be performed
    because it can reestablish limb length, prevent further
    injury to the soft tissues, and provide comfort to the
    patient. Traction is also useful when infection requires
    removal of all internal fixation devices. Both distal fem432

    Orthopaedic Knowledge Update 10

    oral and proximal tibial skeletal traction can be used;


    however, proximal tibial traction is contraindicated in
    patients with knee dislocations.
    External fixation as definitive treatment also has
    limited indications but is used more often as a temporizing measure. It provides bony stability while allowing for the care of multiple-trauma patients. Its application can also be beneficial in cases of vascular injury
    when fracture stability is urgent. External fixation also
    has a role in severely contaminated wounds, especially
    when the intramedullary canal is heavily soiled and
    would benefit from repeat dbridements before definitive fixation.
    Closed, locked, intramedullary nailing remains the
    treatment of choice for adult femoral shaft fractures.
    Union rates are reported as high as 99% and surgical
    complication rates are low.1 Various techniques have
    been introduced, with support in the literature for the
    use of each technique.
    Damage control orthopaedics has been advocated to
    avoid a second hit in multiple-trauma patients by delaying definitive fracture repair in favor of temporizing
    the fracture with traction or external fixation in physiologically unstable patients. Exacerbation of a systemic
    inflammatory response in an already compromised patient and of fat emboli released into a traumatized pulmonary system may be avoided by less invasive, temporizing measures in unstable patients and patients in
    extremis.10 The borderline patient, especially with an
    associated chest injury, remains difficult to universally
    define11 (Table 2). Multiple studies report acceptable
    pulmonary outcomes with early fixation, but there is
    concern that selection bias exists in those studies
    against patients with the most severe chest injuries.12-14
    Although thoracic trauma does not preclude fixation
    with an intramedullary nail, the exact timing of optimal stabilization in these patients is still being
    debated.12,13,15-17
    Reamed intramedullary nailing is considered the
    gold standard of treatment.13 The canal is filled by the
    insertion of a large-diameter nail, which is associated
    with greater union rates compared with smaller diameter nails. In patients with chest trauma, several investigators have examined whether reaming further compromises pulmonary function.13,18,19 Initial reports
    expressed concern for worsening of pulmonary function with reaming, especially in the borderline patient.18
    More recent data report no difference (P = 0.42) in the
    incidence of acute respiratory distress syndrome using
    reamed nails (3 of 171 fractures) versus unreamed nails
    (2 of 151 fractures).13 Additionally, delayed fixation
    compared with early fixation (within 24 hours of injury) was associated with higher rates of pneumonia in
    patients both with (48% versus 15%, respectively; P =
    0.002) and without (38% versus 10%, respectively; P =
    0.07) chest trauma. Mortality rates and the length of
    mechanical ventilation also tended to be higher in the
    delayed fixation groups.19

    2011 American Academy of Orthopaedic Surgeons

    Chapter 33: Femoral Fractures

    Table 2

    Clinical Condition of Multiple-Trauma Patientsa


    Shock

    Coagulation

    Stable

    Borderline

    Unstable

    In Extremis

    Blood pressure

    100

    80-100

    < 90

    70

    Units blood over 2


    hours

    0-2

    2-8

    5-15

    > 15

    Lactate

    Normal

    ~2.5

    > 2.5

    Severe acidosis

    ATLS class

    II-III

    III-IV

    IV

    Platelets

    > 110,000

    90,000-110,000

    < 70,000-90,000

    < 70,000

    Factors II and IV

    90-100

    70-89

    50-70

    < 50

    Fibrinogen

    >1

    ~1

    <1

    DIC

    D-dimer

    Normal

    Abnormal

    Abnormal

    DIC

    C (F)

    < 33 (< 91.4)

    33-35 (91.4-95.0)

    30-32 (86.0-89.6)

    30 ( 86.0)

    350-400

    300-350

    200-300

    < 200

    1 or 2

    Moore abdomen

    II

    III

    III

    III

    AO pelvic fracture

    A (none)

    B or C

    External

    AIS I-II

    AIS II-III

    AIS III-IV

    Crush

    Soft-tissue injury Pao2/FiO2


    AIS chest

    4: Lower Extremity

    Temperature

    Parameter

    Three of four criteria must be met to classify for a certain grade.


    ATLS = Advanced Trauma Life Support; AIS = Abbreviated Injury Score; Moore = classification for abdominal trauma; AO = pelvic trauma classification system;
    DIC = disseminated intravascular coagulation.

    Antegrade Nailing
    Insertion of an intramedullary nail from the hip is considered by many surgeons to be the gold standard for
    femoral fracture fixation. The piriformis fossa, which is
    colinear with the long axis of the intramedullary canal,
    has long been the preferred starting point for an antegrade nail. Using this site as the entry portal decreases
    the chances of fracture malalignment and iatrogenic
    comminution, particularly in proximal third fractures.
    However, precision in locating the piriformis fossa is
    important because an entry portal directed too anteriorly is associated with increased hoop stresses and iatrogenic femoral neck fracture.20
    The greater trochanter is an attractive alternative to
    the piriformis fossa as an entry portal because of its
    more subcutaneous location. This entry portal facilitates access in patients with truncal obesity and may be
    preferred by a surgeon based on his or her experience.
    Nail designs have been altered to include a proximal
    lateral bend in an attempt to avoid varus malalignment
    with trochanteric entry.21 Recent comparisons of trochanteric entry nails to piriformis entry nails have
    shown similar outcomes.22,23 There was no difference in
    union (97% in trochanteric entry compared with 98%
    in piriformis entry), average surgical time (62 minutes
    versus 75 minutes, respectively; P = 0.08), number of infections (one in each group), or baseline and subsequent
    improvements in the Lower Extremity Measure score.
    Hip abductor weakness and a Trendelenburg gait are
    common after antegrade nailing regardless of the entry
    portal used. Early postoperative lateral trunk lean correlates with poorer long-term patient-reported func-

    2011 American Academy of Orthopaedic Surgeons

    tional outcomes.24 Even when there is no clinical evidence of a Trendelenburg gait, hip abductor muscles
    may still be significantly weak when compared with the
    uninjured extremity; this can lead to persistent mild to
    moderate pain.25

    Retrograde Nailing
    Proposed indications for retrograde nailing include patients with bilateral femoral fractures;26 ipsilateral pelvic, acetabular, or hip fractures; multiple trauma; ipsilateral tibial fractures; and those who are pregnant or
    obese. Recently, retrograde nailing in obese patients was
    found to be associated with less surgical time and less
    radiation exposure compared with antegrade nailing.27
    Many surgeons have expressed concerns for inserting
    femoral nails through the knee. The theoretical increased risk of joint sepsis, knee stiffness, or iatrogenic
    arthritis has not proven to be a problem. The effect on
    functional outcome of insertion site complications is
    unknown. In a randomized trial performed in the year
    2000, proximal thigh and hip pain was reported in 10
    of 46 patients (22%) treated with antegrade nailing.28
    Although knee pain and range of motion were similar in
    each group, 18 of 54 patients (33%) treated with retrograde nailing reported distal locking bolt pain. Lysholm
    knee scores and isokinetic knee measurements were
    similar between groups in a study of 71 patients randomized to either antegrade or retrograde nail.29 Union
    rates and malalignment complications with newer techniques are similar between antegrade and retrograde
    nailing.30

    Orthopaedic Knowledge Update 10

    433

    Section 4: Lower Extremity

    Plating
    Plate fixation of femoral shaft fractures is rarely used in
    adult patients secondary to the excellent union rates
    and limited complications associated with intramedullary nailing. Percutaneous techniques with indirect reduction methods and submuscular plating have decreased the morbidity of plate fixation. Nonetheless,
    periprosthetic fractures, fractures in patients with small
    intramedullary canals, and ipsilateral neck-shaft fractures may be more amenable to treatment with a plate.

    Special Situations

    Femoral Neck-Shaft Fractures


    4: Lower Extremity

    Ipsilateral femoral neck and femoral shaft fractures are


    believed to result from a longitudinal force directed
    through a flexed knee and hip. The incidence is reported to be as high as 10%, and as many as 30% of
    these injuries are not identified during the initial patient
    assessment.31-34 Although femoral neck fractures that
    occur with an ipsilateral shaft fracture are associated
    with less risk of osteonecrosis than isolated femoral
    neck fractures because of the dissipation of force to the
    shaft,35 the complications of nonunion of the femoral
    neck and osteonecrosis of the femoral head are time
    sensitive and more severe than those of femoral shaft
    fractures. Every effort should be used to prevent a delay in diagnosing femoral neck-shaft fractures. Because
    25% to 60% of these femoral neck fractures are nondisplaced at the time of presentation, diagnosis can be
    difficult without adequate imaging studies. Various
    protocols have been reported to decrease the incidence
    of missed femoral neck fractures. A preoperative thincut CT scan of the femoral neck and postoperative 15
    internal rotation AP image of the hip before waking the
    patient have been reported to reduce the delay in diagnosing an associated femoral neck fracture.5
    Multiple treatment options exist for stabilizing these
    ipsilateral injuries. Prioritizing reduction and fixation
    of the femoral neck fracture is advocated. The pattern
    of femoral neck fracture tends to be a Pauwels type III
    vertical fracture. (See chapter 31, figure 5, for an illustration showing the Pauwels classification system.) A
    recent study reported that open reduction with internal
    fixation of the femoral neck followed by retrograde
    nailing for the shaft fracture allowed accurate reduction and uneventful union of both fractures.36 The use
    of a cephalomedullary nail resulted in more malreductions of one of the fractures compared with the use of
    two devices. Thus, the current recommendation is using
    two devices for fixation, with accurate reduction of
    both fractures.

    Open Fractures
    Open femoral shaft fractures are much less common
    than open tibial shaft fractures because of the extensive
    soft-tissue envelope. Most open fractures are the result
    of high-energy trauma and are typically associated with
    significant soft-tissue injury and periosteal stripping.
    434

    Orthopaedic Knowledge Update 10

    These open fractures should be treated as soon as the


    patient is medically able and the appropriate resources
    are available. Wounds should be extended to dbride
    all devitalized soft tissue and bone. Unless the intramedullary canal is grossly contaminated, immediate
    intramedullary nailing is acceptable. Low infection and
    nonunion rates have been reported.1

    Gunshot Wounds
    Femoral shaft fractures caused by low-velocity gunshot
    wounds are technically believed to be open injuries but
    can be treated like closed fractures; local dbridement
    of the skin and subcutaneous tissues at the entry and
    exit sites without deep dbridement is adequate.37,38 Immediate, reamed, locked intramedullary nailing is associated with similar union and infection rates as those in
    closed femoral fractures.39,40 Higher-energy gunshot
    wounds, such as those caused by shotgun blasts and
    high-velocity guns, should be treated with standard
    open fracture care because of the increased amount of
    soft-tissue injury.41

    Bilateral Fractures
    Patients with bilateral fractures of the femur have a
    higher mortality rate and overall worse prognosis.
    There is an increased risk of adult respiratory distress
    syndrome. The mortality rate ranges from 5% to 25%,
    compared with 1.5% to 11% for patients with unilateral femoral fractures.3,4,26 This increase is related to the
    associated injuries and physiologic parameters as opposed to the fractures themselves.3 Treatment with bilateral reamed intramedullary nails is recommended.4,26

    Vascular Injury
    Femoral shaft fractures with vascular or neurologic injury are typically caused by penetrating trauma. Bony
    stability and prompt revascularization is the goal but
    the sequence of these events is controversial.42,43 The
    timing of the injury in relationship to presentation is vital because revascularization within 6 hours will decrease complications. External fixation is the simplest
    way to achieve immediate bony stability. In the absence
    of infected pin sites, external fixation can be converted
    safely to an intramedullary nail within 2 weeks without
    an increased risk of deep infection.44 An alternative
    treatment method is to use a temporary vascular shunt
    to reestablish blood flow and then perform definitive internal fixation and vascular repair.45 A shunt decreased
    total ischemia time in a group of patients with blunt
    popliteal injury treated with a temporary intraluminal
    arterial shunt compared with a group of patients treated
    without a shunt.45 The shunt group had less total ischemic time, which decreased the fasciotomy rate, the need
    for repeat operations, and the overall complication rate.

    Complications
    Although surgical complication rates with locked intramedullary nail treatment of femoral shaft fractures is

    2011 American Academy of Orthopaedic Surgeons

    Chapter 33: Femoral Fractures

    low, the rate of other minor complications, including


    hip and knee pain, hardware-related pain, and the presence of a limp, is as high as 40%.30

    Malunion

    Nonunion
    Regardless of the technique used, the nonunion rate of
    femoral shaft fractures after reamed, locked intramedullary nailing is less than 10%. When nonunion occurs,
    the first step in treatment should include a thorough
    evaluation for deep infection and metabolic abnormalities. Infection rates in closed fractures treated with intramedullary nails is 1%; open fracture infection rates
    are higher and correlate with the associated soft-tissue
    injury. In general, the most common metabolic or endocrine abnormality associated with fracture nonunion is
    vitamin D deficiency; correction of this abnormality
    has been reported to lead to union without further surgery with medical treatment alone.50 A recent, large,
    case-controlled study reported that risk factors for nonunion include tobacco use, the presence of an open
    fracture, and delayed weight bearing (defined as more
    than 6 weeks after surgery).51 Previous investigations
    identified nonsteroidal anti-inflammatory drug use and
    unreamed nail insertion as other risk factors.52,53 Dynamization as a treatment method has questionable
    support in the literature. Patients must be followed
    closely because of the risk of significant limb shortening. Success rates are variable, with one study reporting
    a decrease in the nonunion rate from 16% to 4% with
    early dynamization.54 The success rate of exchange
    nailing has been reported only in poorly controlled,
    small, retrospective studies, with failure rates approaching 50%.55 A recent study reported fracture
    union in 36 of 42 patients (86%) 4 months after exchange nailing.56 Plate fixation of nonunions, with or
    without bone grafting, has a more reliable union rate;

    2011 American Academy of Orthopaedic Surgeons

    Figure 2

    Illustration of a C-arm used to obtain a perfect


    lateral fluoroscopic image of the femoral neck
    of the uninjured femur. The C-arm is then rotated until the posterior condyles of the femur
    are aligned for a perfect lateral image of the
    distal femur. This angle (a) is the true anteversion; it can then be applied to the fractured femur before interlocking to prevent rotational
    malalignment. (Adapted with permission from
    Tornetta P III, Ritz G, Kantor A: Femoral torsion
    after interlocked nailing of unstable femoral
    fractures. J Trauma 1995;38:213-219.)

    4: Lower Extremity

    Malalignment of femoral shaft fractures can be prevented by obtaining an adequate reduction before reaming
    and nail insertion. Obtaining an accurate entry portal is
    also essential to preventing malalignment because lateralized starting portals with antegrade nailing cause
    varus malalignment.1,23,46,47 Fractures involving the isthmus rarely (2% of cases) result in unacceptable alignment (2%). Proximal (30%), distal (10%), and unstable
    (12%) shaft fractures are at higher risk for malunion.48
    Rotational alignment can be difficult to judge intraoperatively. Careful assessment and positioning can prevent unacceptable reductions. By using the intact, contralateral femur as the template, fluoroscopy can be
    used to judge rotational alignment based on the femoral
    neck anteversion, the position of the lesser trochanter,
    and the cortical thickness49 (Figure 2). The surgically
    treated limb should be compared clinically with the
    contralateral side for any malrotation or length discrepancies, and these should be corrected before leaving the
    operating theater. Prepping both lower extremities into
    the surgical field may facilitate this evaluation.

    however, protected weight bearing is required after surgery.

    Other Complications
    Painful hardware in association with femoral nailing is
    most commonly encountered with distal locking bolts
    and retrograde femoral nails.28 Because of the trapezoidal anatomy of the femoral condyles, if the length of
    the locking bolts is determined radiographically, the
    bolts will be proud and cause irritation. Additionally,
    nails that are left even 1 mm proud in the intercondylar
    notch can irritate the patellar cartilage, especially in
    knee flexion. Care must be taken when inserting the
    nails to use accurate fluoroscopic views to avoid these
    complications. A direct examination by palpation
    should be performed if there is concern for nail protrusion.
    Patient positioning and the surgical table used affect
    the risk of complications. Antegrade nailing on a fracture table with a peroneal post can cause pudendal
    nerve compression and neurapraxia. Symptoms resolve
    in most patients by 6 months. The magnitude of intraoperative traction is implicated more than the duration
    of traction.57 Genitoperineal skin necrosis can result
    from prolonged traction against the post. A recent report describes six patients who required surgical dbridement of partial-thickness necrosis involving the
    perineum and scrotum.58 The hemilithotomy position
    of the well leg can cause compartment syndrome, especially in instances of prolonged nailing or when there
    are contralateral leg injuries. Using a heel support instead of a calf sling to allow the calf to hang freely has
    been reported to significantly decrease the intramuscular pressures.59

    Orthopaedic Knowledge Update 10

    435

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 4

    Figure 3

    Lateral radiograph showing a typical deformity in


    a supracondylar femoral fracture.

    Fat embolism is often discussed as a complication of


    intramedullary nailing of femoral fractures in the patient with multiple traumatic injuries with an associated chest injury. Patients with pathologic fractures are
    also at risk. Severe embolization and large coagulative
    masses have been shown to occur with reaming of
    pathologic femurs.60 Venting of the femur may decrease
    the risk of fat embolism during prophylactic nailing of
    intact femurs.

    Axial CT scan showing a Hoffa fracture of the distal femoral condyle.

    pulled by a head of the gastrocnemius muscle. Open injuries typically occur anteriorly through the distal
    quadriceps, just proximal to the patella.
    Many musculoskeletal injuries can occur with an axial load along the femoral shaft. Radiographic assessment of the pelvis, acetabulum, hip, and femoral shaft
    must be included in the initial evaluation. If any concern exists for an intra-articular component to the fracture, a CT scan will assist in delineating the complexity
    of the fracture, aid in detecting a coronal place fracture
    (Figure 4), and allow maximal preparation for an anatomic reduction.61

    Classification
    Distal Femoral Fractures
    Fractures at the distal end of the femur can also be categorized into high-energy injuries in trauma patients
    and low-energy injuries in elderly patients. The highenergy fractures can include significant damage to the
    articular surface and can potentially result in long-term
    disability and posttraumatic arthritis.

    Mechanism of Injury
    Most distal femoral fractures are the result of an axial
    load on the knee. Motor vehicle crashes or falls from a
    height are typical injury mechanisms. In the elderly
    population, a fall from standing height onto a flexed
    knee is a common cause of distal femoral fractures.
    The resulting deformity is characteristic and caused
    by the anatomy in the region. The muscle pull of the
    quadriceps and hamstrings shortens the femur. The
    shaft is shortened and anterior. The gastrocnemius
    muscles pull the distal fragment posteriorly (Figure 3).
    The gastrocnemius, quadriceps, and hamstring muscle
    groups provide this deforming force. An intercondylar
    split can further displace, with each condyle being
    436

    Orthopaedic Knowledge Update 10

    The AO/Orthopaedic Trauma Association classification


    of distal femur fractures is often used. Type A fractures
    are extra-articular, supracondylar fractures. Type B
    fractures include partial articular, condylar fractures
    (either medial or lateral) in the sagittal plane or the socalled Hoffa fracture in the coronal plane (Figure 5).
    Intra-articular fractures with metadiaphyseal dissociation are classified as type C fractures.
    Supracondylar Fractures
    Supracondylar fractures are rarely treated nonsurgically. Indications for nonsurgical treatment include
    nondisplaced fractures and fractures in nonambulating
    patients or in those who are poor surgical candidates.
    Surgical treatment includes either intramedullary
    nail or plate fixation depending on the characteristics
    of the fracture. The more distal the fracture and the
    more extensive the intra-articular component, the less
    likely the fracture will be amenable to intramedullary
    nailing rather than fixation with plating.
    The basic principles of articular fixation apply in
    these fractures. Surgical goals are anatomic reduction
    and stable fixation of the joint surface followed by re-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 33: Femoral Fractures

    4: Lower Extremity

    Figure 5

    A, Radiograph of a Hoffa fracture (arrows) of the distal femoral condyle. B, Radiograph showing the fracture stabilized with lag screws.

    duction to the intact shaft while maintaining physiologic valgus. Modern plating techniques allow open reduction of the joint with direct visualization, passing a
    plate submuscularly while using indirect fracture reduction techniques, and then fixing the joint to the shaft
    percutaneously. Locked plating technology has almost
    completely replaced 95 condylar screws and blade
    plates in fixing these difficult fractures. Fixed-angle
    plates have eliminated the need for a medial buttress
    plate in all but the most comminuted fractures.
    Biologically sound percutaneous plating of distal
    femoral fractures with locked plates is associated with
    a union rate of approximately 93% at between 11 and
    14 weeks.62,63 Malreduction rates have decreased as surgeons have become more experienced with newer techniques but approaches 20% in some studies.64 Reported knee range of motion averages 105 to 110 of
    flexion.62,63
    Periprosthetic Fractures
    Periprosthetic supracondylar fractures about a stable
    total knee arthroplasty are similar to extra-articular
    fractures. If the arthroplasty implant allows, these fractures can be treated with either an intramedullary nail
    or a fixed-angle plate depending on the amount of bone
    remaining intact to the distal fragment. Posteriorstabilized total knee implants will not allow passage of
    an intramedullary implant unless the knee implant is
    cut. If an intramedullary nail is to be used with posterior cruciate-sparing implants, it is vital to determine
    the size of the intercondylar distance that would accept

    2011 American Academy of Orthopaedic Surgeons

    the nail. If the information is unavailable, a CT scan


    will allow radiographic measurement of the distance. A
    recent report on 15 patients with 16 supracondylar
    periprosthetic fractures treated with intramedullary
    nails reported 100% union at an average of 16 weeks
    with return to preinjury function in 11 of 13 patients.65
    Minimally invasive locked plating for periprosthetic
    supracondylar fractures also provides satisfactory results. The authors of a 2006 study reported union in 19
    of 22 patients (86%) and postoperative alignment within 5 of the contralateral limb in 20 of 22 patients.66
    Hoffa Fractures
    Coronal plane condylar fractures (Hoffa fractures)
    have been reported to occur in 38% of distal femoral
    fractures.61 These fractures are 2.8 times more likely in
    open fractures, with the lateral condyle more commonly involved. CT scans should be obtained preoperatively to reliably evaluate the distal femur for these
    fractures (Figure 4). Because nonsurgical treatment is
    associated with poor functional outcomes, surgical fixation is generally recommended. These fractures can be
    difficult to reduce and stabilize because of their size,
    shape, and location. Often the optimal location for
    placement of the lag screws is in the articular surface
    (Figure 5). Headless screws or countersunk screws can
    be used in those situations.
    Unicondylar Fractures
    Unicondylar fractures are articular and require anatomic reduction with stable fixation to avoid posttrau-

    Orthopaedic Knowledge Update 10

    437

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 6

    AP (A) and lateral (B) preoperative radiographs of a distal femoral condylar fracture. C, Axial CT scan of the fracture
    showing the intercondylar split. Postoperative AP (D) and lateral (E) radiographs showing the fracture stabilized
    with a buttress plate and lag screws.

    matic arthritis. Open reduction with lag screw fixation


    can maintain the fracture reduction in patients with
    good bone quality. Large varus and valgus shear
    stresses on the knee in the plane of these fractures can
    exceed the ability of lag screws to maintain the reduction; therefore, a buttress plate is recommended, especially if there is any question regarding bone quality
    (Figure 6).

    Complications
    Partial articular type B fractures are more likely to result in nonunion because of the shearing forces across
    the fracture and often are associated with inadequate
    438

    Orthopaedic Knowledge Update 10

    fixation. Nonunion of the metaphyseal portion of distal


    fractures, with or without intra-articular extension, is
    reported to be as high as 17% and is most common in
    open fractures with associated bone loss.67 Fortunately,
    the articular extension, if present, typically heals. Rigid
    stability with compression of the metaphyseal fracture
    site either with lag screws and a neutralization plate or
    with a compression plate is often all that is necessary to
    achieve union in fractures without a large defect. If
    there is a defect, then grafting is needed. The need for
    grafting is often overlooked when using locked plates
    for fixation of distal femoral fractures; however, this
    can lead to plate failure. If necessary, a medial plate or

    2011 American Academy of Orthopaedic Surgeons

    Chapter 33: Femoral Fractures

    nonalendronate patients (mean age, 80.3 years).

    intramedullary augmentation with a plate or fibula allograft may also be used.


    8.

    Annotated References
    Winquist RA, Hansen ST Jr, Clawson DK: Closed intramedullary nailing of femoral fractures. A report of
    five hundred and twenty cases. J Bone Joint Surg Am
    1984;66(4):529-539.

    2.

    ATLS Subcommittee, eds: Advanced Trauma Life Support for Doctors: Student Course Manual, ed 8. Chicago, IL, American College of Surgeons, 2008.

    3.

    Copeland CE, Mitchell KA, Brumback RJ, Gens DR,


    Burgess AR: Mortality in patients with bilateral femoral
    fractures. J Orthop Trauma 1998;12(5):315-319.

    4.

    Nork Se, Agel J, Russell GV, Mills WJ, Holt S, Routt


    ML Jr: Mortality after reamed intramedullary nailing of
    bilateral femur fractures. Clin Orthop Relat Res 2003;
    415(415):272-278.

    5.

    Tornetta P III, Kain MS, Creevy WR: Diagnosis of femoral neck fractures in patients with a femoral shaft fracture: Improvement with a standard protocol. J Bone
    Joint Surg Am 2007;89(1):39-43.
    The authors present a standardized protocol, including
    a preoperative fine-cut CT scan of the femoral necks
    and a dedicated postoperative 15 internal rotation hip
    radiograph to reduce the delay in diagnosing a femoral
    neck fracture in association with an ipsilateral femoral
    shaft fracture. A 91% reduction in the risk of a delayed
    diagnosis was reported.

    6.

    7.

    Lenart BA, Neviaser AS, Lyman S, et al: Association of


    low-energy femoral fractures with prolonged bisphosphonate use: A case control study. Osteoporos Int 2009;
    20(8):1353-1362.
    The authors present a retrospective case-control study
    comparing 41 postmenopausal women with low-energy
    subtrochanteric or femoral shaft fractures with women
    who sustained low-energy intertrochanteric or femoral
    neck fractures. Bisphosphonate use was higher in the
    subtrochanteric/shaft fracture group compared with the
    intertrochanteric/femoral neck fracture groups. Of the
    15 subtrochanteric/shaft fracture patients using bisphosphonates, 10 had the characteristic radiographic pattern termed simple with thick cortices.
    Goh SK, Yang KY, Koh JS, et al: Subtrochanteric insufficiency fractures in patients on alendronate therapy: A
    caution. J Bone Joint Surg Br 2007;89(3):349-353.
    This retrospective review, over a 10-month period, of 13
    women with low-energy subtrochanteric femoral fractures identified alendronate therapy in 9 of those
    women within the year before the fracture. Five of those
    patients reported prodromal pain compared with none
    of the patients in the nonalendronate group. Cortical
    hypertrophy was identified in six patients in the alendronate group. The patients in the alendronate group
    were younger (mean age, 66.9 years) compared with the

    2011 American Academy of Orthopaedic Surgeons

    The authors retrospectively reviewed patients admitted


    to their institution with a low-energy subtrochanteric femur fracture over a 20-month period. Seventeen patients with an average age of 66 years were identified.
    All patients had been on bisphosphonate therapy; 13
    patients reported prodromal pain before the fracture.
    All patients had characteristic radiographic findings of
    cortical thickening laterally and a transverse fracture
    line with a medial cortical spike.
    9.

    Neviaser AS, Lane JM, Lenart BA, Edobor-Osula F, Lorich DG: Low-energy femoral shaft fractures associated
    with alendronate use. J Orthop Trauma 2008;22(5):
    346-350.

    4: Lower Extremity

    1.

    Kwek EB, Goh SK, Koh JS, Png MA, Howe TS: An
    emerging pattern of subtrochanteric stress fractures: A
    long-term complication of alendronate therapy? Injury
    2008;39(2):224-231.

    The authors describe a characteristic low-energy femur


    fracture pattern in elderly patients (mean age, 75 years).
    The study included 70 patients, 25 of whom were being
    treated with alendronate therapy. A simple transverse
    fracture pattern with unicortical beaking in an area of
    cortical diaphyseal hypertrophy was discovered in 19 of
    the 25 patients (76%). The average duration of alendronate use in this group was 6.9 years.
    10.

    Pape HC, Hildebrand F, Pertschy S, et al: Changes in the


    management of femoral shaft fractures in polytrauma
    patients: From early total care to damage control orthopedic surgery. J Trauma 2002;53(3):452-461, discussion
    461-462.

    11.

    Pape HC, Giannoudis PV, Krettek C, Trentz O: Timing


    of fixation of major fractures in blunt polytrauma: Role
    of conventional indicators in clinical decision making.
    J Orthop Trauma 2005;19(8):551-562.

    12.

    Bosse MJ, MacKenzie EJ, Riemer BL, et al: Adult respiratory distress syndrome, pneumonia, and mortality following thoracic injury and a femoral fracture treated either with intramedullary nailing with reaming or with a
    plate: A comparative study. J Bone Joint Surg Am 1997;
    79(6):799-809.

    13.

    Canadian Orthopaedic Trauma Society: Reamed versus


    unreamed intramedullary nailing of the femur: Comparison of the rate of ARDS in multiple injured patients.
    J Orthop Trauma 2006;20(6):384-387.

    14.

    Pape HC, AurmKolk M, Paffrath T, Regel G, Sturm


    JA, Tscherne H: Primary intramedullary femur fixation
    in multiple trauma patients with associated lung contusiona cause of posttraumatic ARDS? J Trauma 1993;
    34(4):540-547, discussion 547-548.

    15.

    Bone LB, Johnson KD, Weigelt J, Scheinberg R: Early


    versus delayed stabilization of femoral fractures: A prospective randomized study. J Bone Joint Surg Am 1989;
    71(3):336-340.

    Orthopaedic Knowledge Update 10

    439

    Section 4: Lower Extremity

    Morshed S, Miclau T III, Bembom O, Cohen M, Knudson MM, Colford JM Jr: Delayed internal fixation of
    femoral shaft fracture reduces mortality among patients
    with multisystem trauma. J Bone Joint Surg Am 2009;
    91(1):3-13.
    The authors present a retrospective cohort study (level
    III) of the National Trauma Data Bank to evaluate the
    timing of internal fixation on mortality in patients with
    multisystem trauma and a femoral shaft fracture. A delay in internal fixation greater than 12 hours to allow
    for appropriate resuscitation reduced mortality by approximately 50%.

    17.

    Pape HC, Rixen D, Morley J, et al; EPOFF Study


    Group: Impact of the method of initial stabilization for
    femoral shaft fractures in patients with multiple injuries
    at risk for complications (borderline patients). Ann Surg
    2007;246(3):491-499, discussion 499-501.
    Ten European trauma centers randomized 165 multiply
    injured patients with femoral shaft fractures to immediate (< 24 hours) intramedullary nail fixation or external
    fixation, with later conversion to intramedullary nail
    fixation. The patients were evaluated for an increased
    incidence of acute lung injuries. After accounting for the
    differences in initial injury severity between the groups,
    the odds of developing an acute lung injury were 6.7
    times greater (P < 0.05) in the borderline patients
    treated with immediate intramedullary nailing compared with those treated with external fixation.

    4: Lower Extremity

    16.

    440

    18.

    Pape HC, Regel G, Dwenger A, et al: Influences of different methods of intramedullary femoral nailing on
    lung function in patients with multiple trauma.
    J Trauma 1993;35(5):709-716.

    19.

    Charash WE, Fabian TC, Croce MA: Delayed surgical


    fixation of femur fractures is a risk factor for pulmonary failure independent of thoracic trauma. J Trauma
    1994;37(4):667-672.

    20.

    Johnson KD, Tencer AF, Sherman MC: Biomechanical


    factors affecting fracture stability and femoral bursting
    in closed intramedullary nailing of femoral shaft fractures, with illustrative case presentations. J Orthop
    Trauma 1987;1(1):1-11.

    21.

    Ricci WM, Devinney S, Haidukewych G, Herscovici D,


    Sanders R: Trochanteric nail insertion for the treatment
    of femoral shaft fractures. J Orthop Trauma 2005;
    19(8):511-517.

    22.

    Ricci WM, Schwappach J, Tucker M, et al: Trochanteric


    versus piriformis entry portal for the treatment of femoral shaft fractures. J Orthop Trauma 2006;20(10):663667.

    23.

    Starr AJ, Hay MT, Reinert CM, Borer DS, Christensen


    KC: Cephalomedullary nails in the treatment of highenergy proximal femur fractures in young patients: A
    prospective, randomized comparison of trochanteric
    versus piriformis fossa entry portal. J Orthop Trauma
    2006;20(4):240-246.

    24.

    Archdeacon M, Ford KR, Wyrick J, et al: A prospective

    Orthopaedic Knowledge Update 10

    functional outcome and motion analysis evaluation of


    the hip abductors after femur fracture and antegrade
    nailing. J Orthop Trauma 2008;22(1):3-9.
    The authors report on eight patients with isolated femoral shaft fractures treated with an antegrade nail and
    evaluated with motion analysis, clinical examination,
    radiography, and patient-reported functional outcomes.
    Early lateral trunk lean was correlated to longer-term,
    poorer, self-reported functional outcomes. A significant
    improvement in the dysfunction index (21.3 15.0 versus 6.5 8.9; P = 0.08) was reported over time.
    25.

    Helmy N, Jando VT, Lu T, Chan H, OBrien PJ: Muscle


    function and functional outcome following standard antegrade reamed intramedullary nailing of isolated femoral shaft fractures. J Orthop Trauma 2008;22(1):10-15.
    The authors retrospectively reviewed 21 patients with
    isolated femoral shaft fractures treated with a reamed,
    piriformis entry intramedullary nail. Lower peak hip abductor torque was present compared with the contralateral side (89.6 Nm versus 106.4 Nm: P = 0.003) despite
    a normal gait pattern.

    26.

    Cannada LK, Taghizadeh S, Murali J, Obremskey WT,


    DeCook C, Bosse MJ: Retrograde intramedullary nailing in treatment of bilateral femur fractures. J Orthop
    Trauma 2008;22(8):530-534.
    The authors retrospectively report data on a cohort of
    111 patients with bilateral femoral fractures of whom
    89 were treated with retrograde reamed intramedullary
    nails within 48 hours of injury. Associated injuries were
    present in 85 of 89 patients (96%), including 35 of 89
    (39%) with thoracic injuries. The mortality rate was
    5.6% (5 of 89 patients).

    27.

    Tucker MC, Schwappach JR, Leighton RK, Coupe K,


    Ricci WM: Results of femoral intramedullary nailing in
    patients who are obese versus those who are not obese:
    A prospective multicenter comparison study. J Orthop
    Trauma 2007;21(8):523-529.
    In a prospective, multicenter study, the authors report
    longer surgical time (94 minutes versus 62 minutes; P <
    0.003) and increased radiation exposure (247 seconds
    versus 135 seconds; P < 0.03) for femoral intramedullary antegrade nailing in obese patients compared with
    nonobese patients. With respect to obese patients, retrograde nailing required less surgical time (67 minutes versus 94 minutes; P < 0.02) and less radiation exposure
    (76 seconds versus 247 seconds; P < 0.002) compared
    with antegrade nailing.

    28.

    Ostrum RF, Agarwal A, Lakatos R, Poka A: Prospective


    comparison of retrograde and antegrade femoral intramedullary nailing. J Orthop Trauma 2000;14(7):496501.

    29.

    Daglar B, Gungor E, Delialioglu OM, et al: Comparison


    of knee function after antegrade and retrograde intramedullary nailing for diaphyseal femoral fractures:
    Results of isokinetic evaluation. J Orthop Trauma
    2009;23(9):640-644.
    Seventy patients with 71 femoral shaft fractures were
    randomized by surgeon to treatment with either ante-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 33: Femoral Fractures

    37.

    Dickey RL, Barnes BC, Kearns RJ, Tullos HS: Efficacy


    of antibiotics in low-velocity gunshot fractures. J Orthop Trauma 1989;3(1):6-10.

    38.

    Wiss DA, Brien WW, Becker V Jr: Interlocking nailing


    for the treatment of femoral fractures due to gunshot
    wounds. J Bone Joint Surg Am 1991;73(4):598-606.

    30.

    Ricci WM, Bellabarba C, Evanoff B, Herscovici D, DiPasquale T, Sanders R: Retrograde versus antegrade
    nailing of femoral shaft fractures. J Orthop Trauma
    2001;15(3):161-169.

    39.

    Bergman M, Tornetta P, Kerina M, et al: Femur fractures caused by gunshots: Treatment by immediate
    reamed intramedullary nailing. J Trauma 1993;34(6):
    783-785.

    31.

    Cannada LK, Viehe T, Cates CA, et al; Southeastern


    Fracture Consortium: A retrospective review of highenergy femoral neck-shaft fractures. J Orthop Trauma
    2009;23(4):254-260.

    40.

    Nowotarski P, Brumback RJ: Immediate interlocking


    nailing of fractures of the femur caused by low- to midvelocity gunshots. J Orthop Trauma 1994;8(2):134141.

    41.

    Patzakis MJ, Harvey JP Jr, Ivler D: The role of antibiotics in the management of open fractures. J Bone Joint
    Surg Am 1974;56(3):532-541.

    42.

    McHentry TP, Holcomb JB, Aoki N, Lindsey RW: Fractures with major vascular injuries from gunshot
    wounds: Implications of surgical sequence. J Trauma
    2002;53(4):717-721.

    43.

    Starr AJ, Hunt JL, Reinert CM: Treatment of femur


    fracture with associated vascular injury. J Trauma 1996;
    40(1):17-21.

    44.

    Harwood PJ, Giannoudis PV, Probst C, Krettek C, Pape


    HC: The risk of local infective complications after damage control procedures for femoral shaft fracture. J Orthop Trauma 2006;20(3):181-189.

    45.

    Hossny A: Blunt popliteal artery injury with complete


    lower limb ischemia: Is routine use of temporary intraluminal arterial shunt justified? J Vasc Surg 2004;
    40(1):61-66.

    46.

    French BG, Tornetta P III: Use of an interlocked cephalomedullary nail for subtrochanteric fracture stabilization. Clin Orthop Relat Res 1998;348(348):95-100.

    47.

    Kempf I, Grosse A, Beck G: Closed locked intramedullary nailing. Its application to comminuted fractures of
    the femur. J Bone Joint Surg Am 1985;67(5):709-720.

    48.

    Ricci WM, Bellabarba C, Lewis R, et al: Angular malalignment after intramedullary nailing of femoral shaft
    fractures. J Orthop Trauma 2001;15(2):90-95.

    49.

    Tornetta P III, Ritz G, Kantor A: Femoral torsion after


    interlocked nailing of unstable femoral fractures.
    J Trauma 1995;38(2):213-219.

    50.

    Brinker MR, OConnor DP, Monla YT, Earthman TP:


    Metabolic and endocrine abnormalities in patients with
    nonunions. J Orthop Trauma 2007;21(8):557-570.
    The authors present their data on a subset of nonunion
    patients who were referred to an endocrinologist for an

    The authors reviewed data from eight level I trauma


    centers to report the incidence of missed femoral neck
    fractures in association with ipsilateral shaft fractures
    and to evaluate the timing of the diagnosis. In a database that included 2,897 femoral shaft fractures, there
    were 91 ipsilateral neck-shaft fractures. Sixty-seven of
    the neck fractures were discovered preoperatively; of the
    24 identified late, 11 fractures were discovered in the
    operating room, 10 were diagnosed during the hospital
    stay, and 3 were found at the follow-up visit. Sixteen of
    the 24 patients with a missed fracture had preoperative
    CT scans; 12 were read as negative for neck fracture
    and 4 showed fractures but the diagnosis was not made
    preoperatively.
    32.

    Wolinsky PR, Johnson KD: Ipsilateral femoral neck and


    shaft fractures. Clin Orthop Relat Res 1995;318:81-90.

    33.

    Alho A: Concurrent ipsilateral fractures of the hip and


    shaft of the femur: A systematic review of 722 cases.
    Ann Chir Gynaecol 1997;86(4):326-336.

    34.

    35.

    36.

    Riemer BL, Butterfield SL, Ray RL, Daffner RH: Clandestine femoral neck fractures with ipsilateral diaphyseal fractures. J Orthop Trauma 1993;7(5):443-449.
    Swiontkowski MF, Winquist RA, Hansen ST Jr: Fractures of the femoral neck in patients between the ages of
    twelve and forty-nine years. J Bone Joint Surg Am
    1984;66(6):837-846.
    Bedi A, Karunakar MA, Caron T, Sanders RW, Haidukewych GJ: Accuracy of reduction of ipsilateral femoral neck and shaft fracturesan analysis of various internal fixation strategies. J Orthop Trauma 2009;23(4):
    249-253.
    Accurate reductions and uneventful union with open reduction and fixation of femoral neck fractures followed
    by retrograde nailing were reported by the authors of
    this study. The use of cephalomedullary nails resulted in
    fracture malreduction of one fracture in 3 of 9 patients
    compared with no malreductions in 28 patients treated
    with two devices. Two patients who had good to excellent reductions and who were treated with two devices
    went on to femoral neck nonunion and required secondary procedures.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    grade or retrograde femoral nailing. Patients were followed for at least 1 year. Lysholm knee scores and isokinetic knee measurements were obtained at least 6
    months after fracture union, and 30 patients had a minimum follow-up of 24 months. These were no differences in Lysholm knee scores, isokinetic measurements,
    or time to union between the groups.

    441

    Section 4: Lower Extremity

    58.

    Coelho RF, Gomes CM, Sakaki MH, et al: Genitoperineal injuries associated with the use of an orthopedic table with a perineal posttraction. J Trauma 2008;
    65(4):820-823.
    The authors report on six patients, followed over a
    2-year period, with perineal and scrotal complications
    attributed to the use of intraoperative traction on a fracture table. Partial-thickness necrosis developed in all patients necessitating surgical dbridement. Infection developed in three patients. Five of six wounds healed by
    secondary intention and one was closed primarily.

    59.

    Meyer RS, White KK, Smith JM, Groppo ER, Mubarak


    SJ, Hargens AR: Intramuscular and blood pressures in
    legs positioned in the hemilithotomy position: Clarification of risk factors for well-leg acute compartment syndrome. J Bone Joint Surg Am 2002;84(10):1829-1835.

    60.

    Christie J, Robinson CM, Pell AC, McBirnie J, Burnett


    R: Transcardiac echocardiography during invasive intramedullary procedures. J Bone Joint Surg Br 1995;
    77(3):450-455.

    61.

    Canadian Orthopaedic Trauma Society: Nonunion following intramedullary nailing of the femur with and
    without reaming: Results of a multicenter randomized
    clinical trial. J Bone Joint Surg Am 2003;85(11):20932096.

    Nork SE, Segina DN, Aflatoon K, et al: The association


    between supracondylar-intercondylar distal femoral
    fractures and coronal plane fractures. J Bone Joint Surg
    Am 2005;87(3):564-569.

    62.

    Moed BR, Watson JT, Cramer KE, Karges DE, Teefey


    JS: Unreamed retrograde intramedullary nailing of fractures of the femoral shaft. J Orthop Trauma 1998;
    12(5):334-342.

    Weight M, Collinge C: Early results of the less invasive


    stabilization system for mechanically unstable fractures
    of the distal femur (AO/OTA types A2, A3, C2, and
    C3). J Orthop Trauma 2004;18(8):503-508.

    63.

    Kregor PJ, Stannard JA, Zlowodzki M, Cole PA: Treatment of distal femur fractures using the less invasive stabilization system: Surgical experience and early clinical
    results in 103 fractures. J Orthop Trauma 2004;18(8):
    509-520.

    64.

    Schandelmaier P, Partenheimer A, Koenemann B, Grn


    OA, Krettek C: Distal femoral fractures and LISS stabilization. Injury 2001;32(suppl 3):SC55-SC63.

    65.

    Chettiar K, Jackson MP, Brewin J, Dass D, ButlerManuel PA: Supracondylar periprosthetic femoral fractures following total knee arthroplasty: Treatment with
    a retrograde intramedullary nail. Int Orthop 2009;
    33(4):981-985.

    66.

    Ricci WM, Loftus T, Cox C, Borrelli J: Locked plates


    combined with minimally invasive insertion technique
    for the treatment of periprosthetic supracondylar femur
    fractures above a total knee arthroplasty. J Orthop
    Trauma 2006;20(3):190-196.

    67.

    Bellabarba C, Ricci WM, Bolhofner BR: Indirect reduction and plating of distal femoral nonunions. J Orthop
    Trauma 2002;16(5):287-296.

    underlying metabolic or endocrine abnormality. Vitamin


    D deficiency was the most common abnormality identified (25 of 37 patients). Eight patients who received
    treatment of the newly diagnosed metabolic or endocrine disorder went on to union without surgical intervention.

    4: Lower Extremity

    51.

    52.

    53.

    54.

    Giannoudis PV, MacDonald DA, Matthews SJ, Smith


    RM, Furlong AJ, De Boer P: Nonunion of the femoral
    diaphysis: The influence of reaming and non-steroidal
    anti-inflammatory drugs. J Bone Joint Surg Br 2000;
    82(5):655-658.

    55.

    Weresh MJ, Hakanson R, Stover MD, Sims SH, Kellam


    JF, Bosse MJ: Failure of exchange reamed intramedullary nails for ununited femoral shaft fractures. J Orthop
    Trauma 2000;14(5):335-338.

    56.

    Shroeder JE, Mosheiff R, Khoury A, Liebergall M, Weil


    YA: The outcome of closed, intramedullary exchange
    nailing with reamed insertion in the treatment of femoral shaft nonunions. J Orthop Trauma 2009;23(9):653657.
    Exchange nailing in 42 patients with femoral shaft nonunions, which were initially managed with an intramedullary nail, were retrospectively evaluated. Thirty-six of
    42 patients (86%) went on to union without further intervention. There were six failures (three aseptic and
    three septic), which all went on to union with further interventions. Treatment failures were associated with
    lack of immediate weight bearing, open fractures,
    atrophic/oligotrophic nonunions, and infection.

    57.

    442

    Taitsman LA, Lynch Jr, Agel J, Barei DP, Nork SE: Risk
    factors for femoral nonunion after femoral shaft fracture. J Trauma 2009;67(6):1389-1392.
    The authors evaluated risk factors for nonunion after
    femoral nailing in a case-controlled study based on cases
    in their trauma database. There were 1,126 femoral
    shaft fractures treated with intramedullary nails during
    the study period with 46 (4.1%) going on to nonunion.
    Independent variables and a regression model predictive
    of nonunion were open fracture, delay to weight bearing
    (> 6 weeks), and tobacco use.

    Brumback RJ, Ellison TS, Molligan H, Molligan DJ,


    Mahaffey S, Schmidhauser C: Pudendal nerve palsy
    complicating intramedullary nailing of the femur.
    J Bone Joint Surg Am 1992;74(10):1450-1455.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 34

    Fractures About the Knee


    Michael J. Gardner, MD

    Tibial Plateau Fractures

    Classification
    Several classification systems for tibial fractures have
    been proposed. Historically, the Schatzker classification
    has been used most frequently.1 In this system, types I,
    II, and III are lateral plateau pure split, split-depressed,
    and pure depressed fractures, respectively. These fractures commonly result from lower-energy injuries. Type
    I patterns occur in younger patients with good bone
    quality. Type II fractures are the most common, and account for up to 75% of all tibial plateau fractures. Type
    III fractures are extremely rare, occurring in patients
    with severe osteoporosis (Figure 1). Types IV, V, and VI
    are medial plateau, bicondylar plateau, and metaphyseal dissociation fractures, respectively. These three
    types of fractures most often occur following highenergy mechanisms. Unfortunately, many fracture patterns do not fall into one of these categories. Additional
    variables that influence treatment, such as the presence
    of a fracture-dislocation and coronal obliquity of the
    medial plateau fracture, are not accounted for with the
    Schatzker classification system (Figure 2). Nevertheless,
    the Schatzker system is useful in providing clinicians
    with general fracture descriptions.
    The Orthopaedic Trauma Association (OTA) classification was devised as a more comprehensive classification system. The proximal tibia is number 41, and A,
    B, or C denotes extra-articular, partial articular, or
    complete articular fractures, respectively. Each category
    has many additional subtypes. Because of the large

    Dr. Gardner or an immediate family member serves as a


    paid consultant to or is an employee of Synthes, Amgen,
    and DGIMed and has received research or institutional
    support from AO, Synthes, Smith & Nephew, Wright
    Medical Technologies, and the Foundation for Orthopaedic Trauma.

    2011 American Academy of Orthopaedic Surgeons

    Mechanisms of Injury
    The specific details of the injury mechanism are extremely important aspects of the evaluation and treatment planning process. The first consideration is whether
    the injury occurred from a low- or high-energy mechanism. Although this can be somewhat subjective, attempts
    should be made to quantify the energy involved. A fall
    from a standing height is a typical low-energy mechanism. Motorcycle or motor vehicle collisions often impart
    greater energy to the injury. The soft-tissue status reveals
    significant and clinically relevant information, particularly when fracture blisters, nonwrinkling skin, open lacerations, tense compartments, or ecchymosis is present.
    The fracture pattern itself often contributes to the personality of the injury. Fracture-dislocations, involvement of the medial tibial plateau, and metaphyseal comminution all indicate high-energy mechanisms. In
    general, the bony injury is static and the soft-tissue injury is dynamic and can evolve.

    4: Lower Extremity

    Tibial plateau fractures involve the proximal tibial articular surface. These injuries are extremely heterogeneous, ranging from minimally displaced fractures with
    mild soft-tissue injuries to highly comminuted fractures
    of both tibial condyles and the metaphysis, which are
    often associated with significant soft-tissue injury.
    Many injury- and patient-specific factors influence
    treatment decisions.

    number of fracture types delineated, the OTA classification is the most useful system for research purposes.2

    Evaluation
    Prior to evaluating the injured limb, a thorough trauma
    evaluation should be performed on the patient when
    warranted. Many tibial plateau fractures occur in multiply injured patients, and Advanced Trauma Life Support protocols must be initiated in this setting. After
    the airway and ventilation have been secured and hemodynamic stability has been assessed and managed,
    attention is turned to the extremity. Visual inspection
    focuses on soft-tissue swelling, open lacerations, and
    limb deformity. A complete neurologic examination is
    performed. Because of the close proximity of the common peroneal nerve to the fibular neck, this nerve is at
    particular risk for injury. Tibial plateau fractures can be
    associated with a knee dislocation, especially with medial tibial plateau fractures. Thus, a vascular examination is critical and should include distal pulse palpation, assessment of the color and temperature of the
    foot, and obtaining ankle-brachial indices. An anklebrachial index of less than 0.9 warrants more invasive
    vascular studies.3 Even though these are periarticular
    fractures, because of the low fascial compliance and
    abundant muscular tissue in the proximal tibia, a high
    index of suspicion should be maintained for compartment syndrome.

    Orthopaedic Knowledge Update 10

    443

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 1

    The Schatzker classification of tibial plateau fractures. Type I is a wedge (split) fracture of the lateral tibial plateau.
    Type II is a split-depression fracture of the lateral plateau. Type III is a pure central depression fracture of the lateral
    plateau without an associated split. Type IV is a fracture of the medial tibial plateau, usually involving the entire
    condyle. Type V is a bicondylar fracture, which typically consists of split fractures of both the medial and lateral plateaus without articular depression. Type VI is a tibial plateau fracture with an associated proximal shaft fracture.
    (Adapted from Koval KJ, Helfet DL: Tibial plateau fractures: Evaluation and treatment. J Am Acad Orthop Surg
    1995;3:86-94).

    Radiographic evaluation typically includes two or


    four radiographic views of the knee and the entire tibia.
    CT scans are also extremely helpful for delineating specific fracture lines and fragments. MRI may also provide adequate bony detail, and additionally shows
    structural injuries to soft tissues, such as meniscal tears,
    displacement, and ligament injuries.4 Both CT and MRI
    provide more information when obtained after closed
    reduction and external fixation; therefore, if provisional external fixation is necessary, these studies
    should be deferred until external fixation is performed.

    Treatment
    Indications
    Although tibial plateau fractures are intra-articular injuries, some fractures can effectively be treated nonsurgically. For fractures that are stable to varus and valgus
    stress, those that do not affect the coronal plane limb
    alignment, and those with minimal articular displacement, initial nonsurgical treatment is appropriate. Additionally, nonambulatory or medically unstable pa444

    Orthopaedic Knowledge Update 10

    tients should be considered for nonsurgical treatment.


    The necessity of anatomic articular reduction has been
    questioned because of a lack of data,5 and the knee
    joint may tolerate greater levels of incongruity because
    of the protective effects of the meniscus. Historically, a
    threshold for acceptable articular step-off of up to 10
    mm had been recommended.6-8 However, many of these
    early studies included older implant and fixation techniques with total meniscectomies; involved a long period of postoperative casting; and were based on nonvalidated, physician-based, outcome scores.
    Over the past several decades, the understanding of
    many aspects of these injuries has improved. The importance of early joint motion to minimize stiffness and
    improve the nutrition and health of the injured cartilage has been stressed. It is now clear that meniscal
    preservation is critical for long-term joint maintenance.7 Many patient-based outcomes scores have been
    developed and validated that accurately capture functional outcomes after injury and treatment. A recent
    large series of bicondylar tibial plateau fractures reported that a more accurate articular reconstruction

    2011 American Academy of Orthopaedic Surgeons

    Chapter 34: Fractures About the Knee

    4: Lower Extremity

    Figure 2

    AP (A) and lateral (B) radiographs showing a tibial plateau fracture with an associated dislocation of the knee joint,
    as well as a coronal plane fracture of the medial tibial plateau, neither of which are accounted for with current
    classification systems.

    improved functional outcomes.9 Laboratory data also


    indicate that with 1.5 mm of incongruity of the lateral
    tibial plateau, the contact stresses on the adjacent cartilage are approximately doubled.10 Currently, in most
    centers, a threshold of 2 mm of articular step-off is
    used for surgical indications and for intraoperative reductions.
    Urgent and Provisional Treatments
    Tibial plateau fractures with axial instability, metaphyseal comminution, associated dislocations, and substantial soft-tissue swelling are usually indicated for
    closed reduction and provisional spanning external fixation until soft-tissue swelling permits definitive treatment. This regimen achieves multiple goals, including
    bone stabilization, and realignment and healing of the
    soft-tissue injury, before definitive open reduction and
    internal fixation.11 It is important to achieve an accurate closed reduction, particularly length restoration, to
    achieve appropriate soft-tissue relationships. As a result, patient comfort is improved, useful postoperative
    imaging can be obtained, definitive open reduction is
    facilitated, and the overall complication rate is minimized. Typically, two Schanz half pins are placed in the
    femur, and two pins are placed in the tibia. These pins
    are connected with multiple clamps and bars in the region of the knee. Care should be taken to avoid placing
    the clamp directly over the knee to allow radiographic
    visualization. The tibial pins should be placed sufficiently distal to the knee joint to avoid interference
    with the definitive incisions and implants. Additionally,

    2011 American Academy of Orthopaedic Surgeons

    joint overdistraction may be detrimental to neurovascular structures.


    Compartment syndrome should be ruled out in all
    patients with a tibial plateau fracture. Leg compartment fullness associated with pain that is disproportionate to the injury severity, and increased pain with
    passive flexion and extension of the toes and ankle,
    should alert the clinician to the development of compartment syndrome. Direct compartment pressure measurements can then be used to confirm the diagnosis,
    and immediate decompressive fasciotomies should be
    performed through dual incisions or a single lateral incision.12 If a vascular lesion is suspected, consultation
    with a vascular surgeon is warranted.
    Definitive Surgical Treatment
    When the skin wrinkles and the fracture blisters have
    resolved and epithelialized, surgical intervention is
    planned. The goal of surgery is to restore bony anatomy, achieve bone and soft-tissue healing without complications, and impart adequate fixation stability to allow early knee motion to minimize stiffness. Most
    tibial plateau fractures involve the lateral plateau and
    are amenable to treatment through an anterolateral incision. A femoral distractor may be useful to distract
    the joint to allow space and visualization during elevation of depressed osteochondral fragments. A transverse submeniscal arthrotomy can be performed for direct articular visualization and instrument palpation.
    Displaced articular fragments may be accessed using elevators through fracture lines, or with tamps through

    Orthopaedic Knowledge Update 10

    445

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 3

    In these lateral fluoroscopic views, a bone tamp is inserted through a small window created with osteotomes (A)
    and is used to elevate the impacted articular fragment (B).

    separate bone windows created using osteotomes


    (Figure 3). The lateral plateau may also be externally
    rotated and displaced to improve access. Some fractures involving the medial tibial plateau are best treated
    with a separate posteromedial approach for direct reduction and fixation.13,14
    Subchondral screws placed through the lateral plate
    are anchored in strong medial bone, and nonlocking
    screws provide adequate fixation in most patients.
    Nonlocking screws allow for lag compression, which is
    important to maintain anatomic plateau width and for
    stabilization. The strongest subchondral support is
    achieved using multiple 3.5-mm cortical screws and
    small fragment fixation.15,16 In severely osteoporotic patients, locking screws may be considered after lag
    screws have been placed. The lateral plate in most fracture patterns needs to provide buttress or an antiglide
    function; therefore, in all OTA type B (partial articular)
    fractures, locking fixation is unnecessary, more costly,
    and may be counterproductive.
    Much attention has recently been focused on the
    morphology of the medial tibial plateau fracture fragments.17,18 Important fracture characteristics include the
    amount of articular surface comprised by the fragment
    and its coronal plane obliquity. Locking screws placed
    through a lateral plate, even if angled posteriorly, are
    not ideally suited to obtain stable fixation of medial
    coronal plane fractures (Figure 4). Both clinical and
    biomechanical studies have shown the low complication rate of a posteromedial approach, the low incidence of fixation failure, and the mechanical advantage
    with dual plating of these patterns.9,13,19,20
    446

    Orthopaedic Knowledge Update 10

    Conversely, some bicondylar patterns involve mainly


    metaphyseal fracture lines and result in a large medial
    plateau fragment that involves little or none of the articular surface. Although evidence is somewhat unclear,
    these patterns may be more amenable to stabilization
    using a lateral locking plate (Figure 5). Several studies
    have reported substantial rates of reduction loss using
    this technique, although no distinction between medial
    fracture patterns was made.21,22 A more recent study
    found no difference in reduction loss between lateral
    locked and dual plating but found a higher incidence of
    proximal tibial malalignment with lateral locked plating.23 Other authors have reported the efficacy of lateral locked plating for metaphyseal bicondylar fractures.24,25
    In many fractures, additional compressive support of
    the articular surface is provided using bone graft or biologic cement in the residual metaphyseal defect.26 A
    recent prospective, randomized, multicenter trial compared the use of calcium phosphate cement with autologous cancellous bone graft for subarticular defects.26
    A significantly higher rate of articular fragment subsidence occurred in the bone graft group. A metaanalysis of various fractures (including tibial plateau
    fractures) concluded that calcium phosphate cement to
    fill a defect leads to less fracture site pain compared
    with results in patients managed without defect grafting, and results in improved articular support compared with cancellous bone graft.27
    Aside from traditional open reduction and internal
    fixation, other methods have been used to definitively
    treat tibial plateau fractures. Circular thin-wire frames

    2011 American Academy of Orthopaedic Surgeons

    Chapter 34: Fractures About the Knee

    4: Lower Extremity

    Figure 4

    A, Radiograph showing a bicondylar tibial plateau fracture. B, On the lateral injury radiograph, the coronal plane
    nature of the medial tibial plateau fragment (arrow) is suggested. The axial (C) and sagittal (D) CT scans demonstrate the coronal obliquity of the medial plateau (arrows). This fragment is not amenable to lateral locked plate
    fixation. AP (E) and lateral (F) radiographs show a posterior buttress plate is applied through a supine posteromedial
    approach to buttress the medial plateau fragment.

    (with or without hybrid-type fixation) may be effective,


    particularly in patients with severe soft-tissue defects.28
    Arthroscopy can also be used to assist in articular visualization during reduction.29 In arthroscopically assisted techniques, no fluid or low pressure fluid should
    be used to minimize extravasation through the fracture
    into the leg compartments, which could potentially
    cause compartment syndrome.

    Outcomes
    Outcomes following tibial plateau fractures depend on
    patient characteristics and the extent of the bone and
    soft-tissue injuries. In a series of elderly patients, older
    age and the need for provisional spanning external fixation were predictors of worse functional outcomes.30

    2011 American Academy of Orthopaedic Surgeons

    A clinical analysis of 83 bicondylar tibial plateau fractures also reported that older patients and those with
    multiple injuries had worse outcomes.9 In this series,
    55% of patients had articular reductions within 2 mm;
    this correlated strongly with improved outcomes. In a
    Canadian study of patients with tibial plateau fractures
    treated with open reduction and internal fixation and
    followed for an average of 8.3 years, Medical Outcomes Study 36-Item Short Form scores were no different than in the normal population.31 However, only
    57% of patients older than 40 years returned to normal
    function. A large, long-term study of 109 patients with
    tibial plateau fractures treated with open reduction and
    internal fixation and followed for an average of 14
    years reported that overall results were excellent and
    were independent of age.32

    Orthopaedic Knowledge Update 10

    447

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 5

    AP (A) and lateral (B) radiographs showing a tibial plateau fracture. The articular component of the tibial plateau
    fracture was treated with open reduction and rigid lag screw compression. The medial plateau was a large extraarticular fragment, and the metaphyseal component was treated successfully with a lateral locked plate (C and D).

    Extensor Mechanism Injuries


    The extensor mechanism is considered the quadriceps,
    the patella, and the patellar tendon. Any of these structures can be traumatically disrupted, leading to incompetence of the extensor mechanism and the inability to
    actively extend the knee. Secure fixation of a fracture
    or tendon disruption is imperative for restoration of
    function.

    Patellar Fractures
    Patellar fractures typically occur following either direct
    impact, such as a dashboard injury, or from an indirect
    mechanism, such as eccentric quadriceps contraction
    with sudden knee flexion. Other less common causes
    include insufficiency fractures following graft harvesting for anterior cruciate ligament reconstruction and
    total knee arthroplasty. The patient history and physical examination typically lead to the diagnosis. Following a direct impact mechanism, a superficial abrasion
    or ecchymosis is often present along with a large
    hemarthrosis in the knee. Rupture of the medial and
    lateral retinacula are common, and the patient is unable to actively extend the knee. A straight leg raise
    leads to a substantial extensor lag, and often a defect is
    palpable. It is imperative to ensure any regional lacerations do not communicate with the joint or the fracture
    site; injection of normal saline will assist with this diagnosis.
    AP and lateral radiographs are obtained for fracture
    evaluation. The displacement is clearly seen on a true
    lateral radiograph. Common patterns include transverse noncomminuted, stellate, or avulsion fractures.
    Transverse fractures frequently occur in younger patients with healthy bone. Stellate fractures are multifragmentary and range from widely displaced to minimally displaced fractures. Superior and inferior pole
    avulsion fractures are functionally equivalent to quad448

    Orthopaedic Knowledge Update 10

    riceps and patellar tendon bonetendon junction disruptions, respectively. Elderly patients frequently have
    occult comminution and coronal plane splits, particularly of the inferior pole, and these should be actively
    sought as the presence of these fracture lines impacts
    fixation techniques.
    Fractures with minimal articular displacement and
    with an intact extensor mechanism can be managed
    with a trial of nonsurgical treatment. A period of
    weight bearing with the knee supported in extension
    with a cylinder cast, a locked knee brace, or a knee immobilizer is initiated for 4 to 6 weeks. For displaced
    fractures, or those with extensor mechanism dysfunction, surgical treatment is warranted. Supine positioning with a longitudinal midline incision allows full access for fracture reduction and fixation. Full-thickness
    flaps are raised medially and laterally for articular digital access through retinacular rents, and for retinacular
    repair following internal fixation. Most midaxial transverse fracture patterns have sufficient intact bone in the
    proximal and distal fracture fragments to permit longitudinal fixation. Many fixation constructs have been
    described. The historic workhorse of fixation constructs is the modified tension band, which involves
    longitudinal 0.062-inch Kirchner wires across the fracture, with a figure-of-8 wire passed deep to the ends of
    the longitudinal wires and joined and tensioned on the
    dorsal patellar surface. This construct acts as a tension
    band, converting dorsal distraction forces to articular
    compressive forces during knee motion. Other options
    include placing a cerclage wire circumferentially
    around the patella; independent minifragment lag
    screw fixation for individual fragments; or placing longitudinal cannulated screws, with the dorsal tension
    band wire passed through the screw cannulations.
    Biomechanical data indicate that wire fixation alone
    is inferior to tension band techniques.33 Modified tension band constructs using longitudinal cannulated

    2011 American Academy of Orthopaedic Surgeons

    Chapter 34: Fractures About the Knee

    4: Lower Extremity

    Figure 6

    A through C, Radiographs demonstrating treatment of an inferior pole patellar fracture. A, The fracture is clearly
    seen (A). The patellar tendon was repaired through drill holes in the superior patellar fragment (B). The inferior
    pole bone fragments were not excised, allowing for bone-to-bone healing at 10 weeks (C).

    screws combined with anterior tension band wires


    function better than using wires alone.34,35 Consideration should also be given to using a braided cable instead of a monofilament wire for the anterior tension
    band.36 When comminution exists, the addition of a
    cerclage wire can add to fixation stability.37
    Inferior pole patellar fractures, or those with highly
    comminuted inferior fragments, are often treated with
    partial patellectomy and advancement with repair to
    the patellar tendon. Three longitudinal drill holes are
    made through the superior pole. Several braided nonabsorbable sutures are then placed as locking stitches
    along the patellar tendon, leaving the free ends proximally. The suture ends are then passed through the drill
    holes and tied over the superior pole. Because the patellar tendon originates from the dorsal half of the patella,
    the drill holes should be made dorsally to avoid a patellar extension deformity. Alternatively, when using
    this technique, the comminuted fragments need not be
    completely excised to allow for bone-to-bone healing at
    the injury site (Figure 6).
    The incidence of patellar fracture fixation failure using current techniques is significant.38 Fixation failure,
    symptomatic implants, anterior knee pain, and revision
    surgery have frequently been reported. One study reported that 22% of 49 patellar fractures treated with
    modified tension band wiring and early motion showed
    displacement in the early postoperative period.39 Longterm functional outcomes have not been reliably excellent, although most clinical series have not used validated outcome scales.40-45 In a review of 68 patients
    with patellar fractures, only 72% were satisfied with
    the result.42 Thirty-seven percent of patients had broken implants and 15% required revision procedures.
    Bstrom reported that more than 50% of patients have
    long-term symptoms following a displaced patellar
    fracture, more than 33% have functional impairment,
    and 21% require additional surgery.46 In more recent

    2011 American Academy of Orthopaedic Surgeons

    studies, 34 of 203 fractures (17%) had fair or poor results,47 9 of 20 patients (45%) had moderate or poor
    results,48 and 12 of 68 elderly patients (18%) failed to
    return to their preinjury functional status.38,49

    Tendon Disruptions
    Traumatic disruptions of the quadriceps and patellar
    tendons occur by mechanisms similar to patellar fractures, although indirect, eccentric quadriceps contraction predominates. Quadriceps ruptures most commonly occur at the musculotendinous junction in older
    patients (typically older than 40 years).50 Patellar tendon ruptures are more often weekend warrior injuries, occurring in patients approximately 40 years of
    age. Physical examination is notable for ecchymosis
    and knee effusion, as well as a palpable defect and the
    inability to complete a straight leg raise. Because of the
    substantial contribution of the retinacula to extensor
    mechanism stability, the inability to perform a straight
    leg raise implies tears in the retinacula.51
    Lateral knee radiographs are valuable for diagnosing
    extensor mechanism tendon injuries based on the relationship of the patella to the tibial tubercle. The InsallSalvati ratio quantifies the relationship between the patellar height and the patellar tendon length (Figure 7).
    A difference of greater than 20% between these measurements indicates potential tendon disruption.52 The
    drawbacks of this threshold have been noted because of
    the high variability of patellar morphology; a difference
    of 100% has been suggested as a more accurate measurement for detecting acute injuries.53 MRI is useful
    for confirming lesions and can help delineate associated
    injuries.
    Treating acute tendon disruptions with direct suture
    repair leads to reliable tendon reapproximation, stability, and healing. Through a midline incision, a technique using large nonabsorbable sutures with locking

    Orthopaedic Knowledge Update 10

    449

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 7

    Lateral knee radiograph used to calculate the


    Insall-Salvati ratio. The ratio of patellar height
    (A) to patellar tendon length (B) should be approximately 1. A difference of at least 20% (for
    example, ratio A/B < 0.8 or > 1.2) indicates likely
    quadriceps or patellar tendon disruption,
    respectively.

    stitches longitudinally on either side of the tear, with at


    least four suture strands crossing the tendon, is preferable.54
    Following repair of a bony or tendinous extensor
    mechanism disruption, rehabilitation protocols must be
    carefully tailored to the individual patient and fracture
    characteristics. Early motion is desirable for cartilage
    health and for minimizing adhesion formation; however, it also increases the risk of fixation failure. Maintaining knee extension in an immobilizer brace or cylinder cast for the first 4 to 6 weeks allows early healing
    and may decrease repair failure rates.39 Weight bearing
    may be instituted during this time in compliant and
    able patients. Subsequently, supervised passive knee extension and gentle active-assisted flexion exercises are
    initiated; acceptable range of motion is usually attainable.

    2.

    Walton NP, Harish S, Roberts C, Blundell C: AO or


    Schatzker? How reliable is classification of tibial plateau fractures? Arch Orthop Trauma Surg 2003;123(8):
    396-398.

    3.

    Mills WJ, Barei DP, McNair P: The value of the anklebrachial index for diagnosing arterial injury after knee
    dislocation: a prospective study. J Trauma 2004;56(6):
    1261-1265.

    4.

    Gardner MJ, Yacoubian S, Geller D, et al: The incidence


    of soft tissue injury in operative tibial plateau fractures:
    A magnetic resonance imaging analysis of 103 patients.
    J Orthop Trauma 2005;19(2):79-84.

    5.

    Marsh JL, Buckwalter J, Gelberman R, et al: Articular


    fractures: Does an anatomic reduction really change the
    result? J Bone Joint Surg Am 2002;84-A(7):1259-1271.

    6.

    Lucht U, Pilgaard S: Fractures of the tibial condyles.


    Acta Orthop Scand 1971;42(4):366-376.

    7.

    Rasmussen PS: Tibial condylar fractures: Impairment of


    knee joint stability as an indication for surgical treatment. J Bone Joint Surg Am 1973;55(7):1331-1350.

    8.

    Lansinger O, Bergman B, Krner L, Andersson GB: Tibial condylar fractures: A twenty-year follow-up. J Bone
    Joint Surg Am 1986;68(1):13-19.

    9.

    Barei DP, Nork SE, Mills WJ, Coles CP, Henley MB,
    Benirschke SK: Functional outcomes of severe bicondylar tibial plateau fractures treated with dual incisions
    and medial and lateral plates. J Bone Joint Surg Am
    2006;88(8):1713-1721.

    10.

    Brown TD, Anderson DD, Nepola JV, Singerman RJ,


    Pedersen DR, Brand RA: Contact stress aberrations following imprecise reduction of simple tibial plateau fractures. J Orthop Res 1988;6(6):851-862.

    11.

    Egol KA, Tejwani NC, Capla EL, Wolinsky PL, Koval


    KJ: Staged management of high-energy proximal tibia
    fractures (OTA types 41): the results of a prospective,
    standardized protocol. J Orthop Trauma 2005;19(7):
    448-455, discussion 456.

    12.

    Maheshwari R, Taitsman LA, Barei DP: Single-incision


    fasciotomy for compartmental syndrome of the leg in
    patients with diaphyseal tibial fractures. J Orthop
    Trauma 2008;22(10):723-730.
    The authors present a detailed surgical technique and
    case series on using a single-incision, four-compartment
    fasciotomy for leg compartment releases. Of 58 leg fasciotomies performed, no patient required additional fasciotomies because of incomplete compartment releases.

    13.

    Barei DP, Nork SE, Mills WJ, Henley MB, Benirschke


    SK: Complications associated with internal fixation of
    high-energy bicondylar tibial plateau fractures utilizing
    a two-incision technique. J Orthop Trauma 2004;
    18(10):649-657.

    Annotated References
    1.

    450

    Schatzker J, McBroom R, Bruce D: The tibial plateau


    fracture: The Toronto experience 1968--1975. Clin Orthop Relat Res 1979;138:94-104.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 34: Fractures About the Knee

    14.

    Weil YA, Gardner MJ, Boraiah S, Helfet DL, Lorich


    DG: Posteromedial supine approach for reduction and
    fixation of medial and bicondylar tibial plateau fractures. J Orthop Trauma 2008;22(5):357-362.
    A case series and surgical technique of the posteromedial approach for tibial plateau fractures performed in
    the supine position is described. Twenty-seven fractures
    were analyzed. Fracture reductions were excellent overall, and a low complication rate was reported.

    Phisitkul P, McKinley TO, Nepola JV, Marsh JL: Complications of locking plate fixation in complex proximal
    tibia injuries. J Orthop Trauma 2007;21(2):83-91.
    Clinical series of lateral locked plates for treating proximal tibial bicondylar fractures is described. A high
    complication rate was reported, including an 8% loss of
    reduction.

    23.

    Jiang R, Luo CF, Wang MC, Yang TY, Zeng BF: A


    comparative study of Less Invasive Stabilization System
    (LISS) fixation and two-incision double plating for the
    treatment of bicondylar tibial plateau fractures. Knee
    2008;15(2):139-143.
    The authors of this clinical case series analyzed 84 bicondylar tibial plateau fractures treated with lateral
    locked plating or dual buttress plating. Although most
    outcomes were similar between groups, postoperative
    malalignment was greater in the group treated with lateral locked plating.

    15.

    Patil S, Mahon A, Green S, McMurtry I, Port A: A biomechanical study comparing a raft of 3.5 mm cortical
    screws with 6.5 mm cancellous screws in depressed tibial plateau fractures. Knee 2006;13(3):231-235.

    16.

    Karunakar MA, Egol KA, Peindl R, Harrow ME, Bosse


    MJ, Kellam JF: Split depression tibial plateau fractures:
    A biomechanical study. J Orthop Trauma 2002;16(3):
    172-177.

    17.

    Barei DP, OMara TJ, Taitsman LA, Dunbar RP, Nork


    SE: Frequency and fracture morphology of the posteromedial fragment in bicondylar tibial plateau fracture
    patterns. J Orthop Trauma 2008;22(3):176-182.
    The results of large clinical series of bicondylar tibial
    plateau fractures are presented with analyses of the
    anatomy of the posteromedial fracture fragment. A posteromedial fragment was present in 29% of all bicondylar fractures and in 74% of those with medial articular
    involvement.

    24.

    Egol KA, Su E, Tejwani NC, Sims SH, Kummer FJ,


    Koval KJ: Treatment of complex tibial plateau fractures
    using the less invasive stabilization system plate: clinical
    experience and a laboratory comparison with double
    plating. J Trauma 2004;57(2):340-346.

    25.

    Stannard JP, Wilson TC, Volgas DA, Alonso JE: The


    less invasive stabilization system in the treatment of
    complex fractures of the tibial plateau: short-term results. J Orthop Trauma 2004;18(8):552-558.

    18.

    Higgins TF, Kemper D, Klatt J: Incidence and morphology of the posteromedial fragment in bicondylar tibial
    plateau fractures. J Orthop Trauma 2009;23(1):45-51.
    An analysis of 111 bicondylar tibial plateau fractures, in
    which 59% included a posteromedial fragment, is presented. Most fractures had a sagittally oriented fracture
    line, indicating vertical instability and potentially requiring buttress plate fixation for adequate stabilization.

    26.

    19.

    Higgins TF, Klatt J, Bachus KN: Biomechanical analysis


    of bicondylar tibial plateau fixation: How does lateral
    locking plate fixation compare to dual plate fixation?
    J Orthop Trauma 2007;21(5):301-306.
    The authors describe a biomechanical cadaver study
    comparing lateral locked plating with dual plating for
    bicondylar tibial plateau fractures. After cyclic loading,
    significantly more medial fracture subsidence occurred
    in the group treated with lateral locked plating.

    Russell TA, Leighton RK; Alpha-BSM Tibial Plateau


    Fracture Study Group: Comparison of autogenous bone
    graft and endothermic calcium phosphate cement for
    defect augmentation in tibial plateau fractures: A multicenter, prospective, randomized study. J Bone Joint Surg
    Am 2008;90(10):2057-2061.
    In this clinical trial, 120 tibial plateau fractures were
    randomized to autograft versus calcium phosphate cement for defect grafting and subchondral support. Autografting led to a significantly greater articular subsidence compared with biologic cement.

    27.

    Bajammal SS, Zlowodzki M, Lelwica A, et al: The use


    of calcium phosphate bone cement in fracture treatment: A meta-analysis of randomized trials. J Bone
    Joint Surg Am 2008;90(6):1186-1196.
    The authors describe a meta-analysis of the evidence for
    using calcium phosphate cement to fill a defect during
    fracture fixation. Clinical evidence suggests that calcium
    phosphate leads to less fracture site pain and less loss of
    reduction compared with other traditional methods.

    28.

    Canadian Orthopaedic Trauma Society: Open reduction


    and internal fixation compared with circular fixator application for bicondylar tibial plateau fractures: Results
    of a multicenter, prospective, randomized clinical trial.
    J Bone Joint Surg Am 2006;88(12):2613-2623.

    29.

    Chan YS, Chiu CH, Lo YP, et al: Arthroscopy-assisted


    surgery for tibial plateau fractures: 2- to 10-year
    follow-up results. Arthroscopy 2008;24(7):760-768.
    In a case series of 54 tibial plateau fractures treated with

    20.

    21.

    Eggli S, Hartel MJ, Kohl S, Haupt U, Exadaktylos AK,


    Rder C: Unstable bicondylar tibial plateau fractures: A
    clinical investigation. J Orthop Trauma 2008;22(10):
    673-679.
    A small clinical series of bicondylar tibial plateau fractures using direct open reduction and plate fixation both
    medially and laterally is described. This treatment led to
    excellent fracture reduction and stabilization, low complications, and good functional outcomes.
    Gosling T, Schandelmaier P, Muller M, Hankemeier S,
    Wagner M, Krettek C: Single lateral locked screw plating of bicondylar tibial plateau fractures. Clin Orthop
    Relat Res 2005;439:207-214.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    22.

    451

    Section 4: Lower Extremity

    an arthroscopy assisted technique with a mean


    follow-up of 7 years, no nonunions, no complications
    related to arthroscopy, and good overall outcomes were
    reported.
    30.

    31.

    4: Lower Extremity

    32.

    452

    Su EP, Westrich GH, Rana AJ, Kapoor K, Helfet DL:


    Operative treatment of tibial plateau fractures in patients older than 55 years. Clin Orthop Relat Res 2004;
    421:240-248.
    Stevens DG, Beharry R, McKee MD, Waddell JP,
    Schemitsch EH: The long-term functional outcome of
    operatively treated tibial plateau fractures. J Orthop
    Trauma 2001;15(5):312-320.
    Rademakers MV, Kerkhoffs GM, Sierevelt IN, Raaymakers EL, Marti RK: Operative treatment of 109 tibial
    plateau fractures: Five- to 27-year follow-up results.
    J Orthop Trauma 2007;21(1):5-10.
    The results of a long-term outcome study of more than
    100 tibial plateau fractures followed for an average of
    14 years is described. Unicondylar fractures had better
    outcomes compared with bicondylar fractures. Malalignment was a predictor of radiographic arthritis.
    Overall, results were excellent.

    33.

    Benjamin J, Bried J, Dohm M, McMurtry M: Biomechanical evaluation of various forms of fixation of


    transverse patellar fractures. J Orthop Trauma 1987;
    1(3):219-222.

    34.

    Carpenter JE, Kasman RA, Patel N, Lee ML, Goldstein


    SA: Biomechanical evaluation of current patella fracture
    fixation techniques. J Orthop Trauma 1997;11(5):351356.

    41.

    Levack B, Flannagan JP, Hobbs S: Results of surgical


    treatment of patellar fractures. J Bone Joint Surg Br
    1985;67(3):416-419.

    42.

    Hung LK, Chan KM, Chow YN, Leung PC: Fractured


    patella: Operative treatment using the tension band
    principle. Injury 1985;16(5):343-347.

    43.

    Gosal HS, Singh P, Field RE: Clinical experience of patellar fracture fixation using metal wire or nonabsorbable polyestera study of 37 cases. Injury 2001;
    32(2):129-135.

    44.

    Wu CC, Tai CL, Chen WJ: Patellar tension band wiring:


    A revised technique. Arch Orthop Trauma Surg 2001;
    121(1-2):12-16.

    45.

    Bstman O, Kiviluoto O, Santavirta S, Nirhamo J, Wilppula E: Fractures of the patella treated by operation.
    Arch Orthop Trauma Surg 1983;102(2):78-81.

    46.

    Bostrm A: Fracture of the patella: A study of 422 patellar fractures. Acta Orthop Scand Suppl 1972;143:180.

    47.

    Mehdi M, Husson JL, Polard JL, Ouahmed A, Poncer


    R, Lombard J: [Treatment results of fractures of the patella using pre-patellar tension wiring: Analysis of a series of 203 cases]. Acta Orthop Belg 1999;65(2):188196.

    48.

    Ozdemir H, Ozenci M, Dabak K, Aydin AT: [Outcome


    of surgical treatment for patellar fractures]. Ulus
    Travma Derg 2001;7(1):56-59.

    49.

    Shabat S, Mann G, Kish B, Stern A, Sagiv P, Nyska M:


    Functional results after patellar fractures in elderly patients. Arch Gerontol Geriatr 2003;37(1):93-98.

    50.

    Clayton RA, Court-Brown CM: The epidemiology of


    musculoskeletal tendinous and ligamentous injuries. Injury 2008;39(12):1338-1344.
    A demographic analysis of a large series of patients who
    sustained a variety of soft-tissue injuries is presented.

    35.

    Burvant JG, Thomas KA, Alexander R, Harris MB:


    Evaluation of methods of internal fixation of transverse
    patella fractures: A biomechanical study. J Orthop
    Trauma 1994;8(2):147-153.

    36.

    Scilaris TA, Grantham JL, Prayson MJ, Marshall MP,


    Hamilton JJ, Williams JL: Biomechanical comparison of
    fixation methods in transverse patella fractures. J Orthop Trauma 1998;12(5):356-359.

    37.

    Curtis MJ: Internal fixation for fractures of the patella.


    A comparison of two methods. J Bone Joint Surg Br
    1990;72(2):280-282.

    51.

    38.

    Gardner MJ, Griffith MH, Lawrence BD, Lorich DG:


    Complete exposure of the articular surface for fixation
    of patellar fractures. J Orthop Trauma 2005;19(2):118123.

    Powers CM, Chen YJ, Farrokhi S, Lee TQ: Role of peripatellar retinaculum in transmission of forces within the
    extensor mechanism. J Bone Joint Surg Am 2006;88(9):
    2042-2048.

    52.

    Insall J, Salvati E: Patella position in the normal knee


    joint. Radiology 1971;101(1):101-104.

    53.

    Grelsamer RP, Meadows S: The modified Insall-Salvati


    ratio for assessment of patellar height. Clin Orthop
    Relat Res 1992;282:170-176.

    54.

    Konrath GA, Chen D, Lock T, et al: Outcomes following repair of quadriceps tendon ruptures. J Orthop
    Trauma 1998;12(4):273-279.

    39.

    Smith ST, Cramer KE, Karges DE, Watson JT, Moed


    BR: Early complications in the operative treatment of
    patella fractures. J Orthop Trauma 1997;11(3):183187.

    40.

    Bstman O, Kiviluoto O, Nirhamo J: Comminuted displaced fractures of the patella. Injury 1981;13(3):196202.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 35

    Soft-Tissue Injuries About the Knee


    Scott G. Kaar, MD

    Michael J. Stuart, MD

    Bruce A. Levy, MD

    Anterior Cruciate Ligament Injuries

    Neither Dr. Kaar nor any immediate family member has


    received anything of value from or owns stock in a commercial company or institution related directly or indirectly to the subject of this chapter. Dr. Stuart or an immediate family member serves as a paid consultant to
    Arthrex and Fios; has received research or institutional
    support from Stryker; and serves as a board member,
    owner, officer, or committee member of the American
    Academy of Orthopaedic Surgeons and the American
    Orthopaedic Society for Sports Medicine. Dr. Levy or an
    immediate family member has received royalties from
    VOT Solutions and serves as a paid consultant to Arthrex.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    Anterior cruciate ligament (ACL) injuries commonly


    occur from a noncontact, twisting, or landing event
    during sports activities. Video analysis has shown that
    athletes tear their ACL with the foot flat, the knee in
    relative abduction, and the hip in relative flexion.1
    Participation in high-risk activities is the main predisposing factor for an ACL injury; another notable
    factor is female sex. Females are more likely to sustain
    an ACL tear than males with similar sports activity involvement. Possible explanations include neuromuscular control differences of the trunk and the lower extremities. Females land from a height with the knee in a
    position of relative extension and apparent increased
    valgus due to hip internal rotation. Other possible factors include the size of the ACL, dimensions of the intercondylar notch, and cyclic hormonal levels. According to a systematic review, the ACL is at greater risk for
    injury during the first half (preovulatory phase) of the
    menstrual cycle.2 There is also a possible genetic predisposition for female athletes to sustain ACL ruptures.
    Female athletes with a CC genotype of the COL5A1
    BstUI RFLP gene that encodes for the 1 chain of type
    V collagen have a decreased risk of ACL rupture.3
    The ACL has two bundles that are not distinct from
    one another but rather are confluences of the ligament
    that function at slightly different knee flexion angles.
    The anteromedial and posterolateral bundles are
    named for the location of their tibial insertions between
    the tibial spines. The femoral insertion of both bundles
    is distal to the lateral intercondylar ridge and the bundles are separated by the bifurcate ridge.4 The antero-

    medial bundle is taut in relative knee flexion whereas


    the posterolateral bundle is taut in knee extension. The
    anatomic location of the ACL bundle insertions has important implications for reconstruction techniques.
    The main function of the ACL is to prevent a pivot
    shift of the knee during activities that may cause injury.
    Instrumented knee evaluation of anterior tibial laxity
    can also be performed with a KT-1000 arthrometer or
    other similar device.5 These tools are commonly used in
    research data collection; however, most surgeons do
    not use them routinely. The ACL has much less of a
    role in knee stability during activities of daily living
    such as walking, running on a flat surface, and biking.
    Therefore, a patients activity level must be taken into
    account when deciding whether to reconstruct the
    ACL, especially in middle-aged and elderly patients.6,7
    An active patient with no arthritic changes in their 40s
    or 50s may be a candidate for an ACL reconstruction
    to treat symptoms of instability. On the other hand,
    that same patient who is not involved in athletics or
    any high-risk activities may be better treated nonsurgically.
    Lateral meniscus tears are more common following
    an acute ACL disruption and medial meniscus tears in
    the chronic ACL-deficient knee. Studies have shown
    that the risk of cartilage lesions and meniscus tears increases over time.8,9 Recurrent instability episodes
    caused by ACL insufficiency are associated with the development of arthritis. However, patients who have undergone ACL reconstruction also are prone to develop
    arthritic changes in the tibiofemoral joint and it is not
    clear whether or not reconstruction alters this degenerative process.10,11 Young patients, high-demand athletes, and patients who experience instability symptoms
    should be considered candidates for ACL reconstruction. Middle-aged or elderly patients who lead a more
    sedentary lifestyle, especially those with preexisting arthritic changes, are best treated nonsurgically.
    Primary repair of the ACL leads to high failure
    rates.12 The exact reason is unknown; however, it may
    be because of a poor blood supply to the ligament or
    inhibitory factors in the synovial fluid. Therefore, ACL
    reconstruction is the treatment of choice and may be
    performed with various techniques using different graft
    options. Arthroscopic surgery, either by drilling tunnels
    in the tibia or the femur through a transtibial or a medial portal technique, is common. The transtibial femoral tunnel drilling method was initially developed during conversion from a two-incision to a single-incision
    453

    Section 4: Lower Extremity

    Table 1

    4: Lower Extremity

    Evidence for Postoperative ACL Protocol


    Protocol

    Evidence (For or Against)

    Continuous passive
    motion

    No evidence for or against the use of a


    continuous passive motion device

    Bracing

    No difference in ACL failure rates or


    laxity26

    Regional pain
    management

    No benefit to femoral nerve block


    compared with single intra-articular
    bupivacaine injection27

    Open vs closed
    chain quadriceps
    rehabilitation
    exercises

    Closed chain exercises may produce


    less pain, decreased laxity, and better
    subjective outcomes, although
    improved and more comprehensive
    studies are needed28

    do not consistently favor one type over another.23,24 A


    10-year comparative study showed similar functional
    outcomes of four-strand hamstrings and patellar tendon grafts.25
    Recent advances in ACL reconstruction surgical
    techniques have mirrored improvements in postoperative rehabilitation protocols26-28 (Table 1). Most surgeons encourage early range of motion immediately after surgery, with added emphasis on closed chain
    quadriceps strengthening. Guidelines for return to athletics vary from surgeon to surgeon but usually involve
    a quantitative measure of quadriceps strength and functional status. The recommended return to full sports
    participation ranges from 4 to 9 months after surgery.29
    Currently there is evidence based on randomized controlled trials that postoperative bracing has no benefit
    with regard to re-tear rates.26

    Medial Collateral Ligament Injuries


    arthroscopic technique. Recently, there has been a focus
    on the ACL femoral insertion anatomy. There is evidence that transtibial femoral tunnel drilling does not
    allow anatomic placement of the femoral tunnel on the
    medial wall of the lateral femoral condyle. Also, the reconstructed ACL fibers have a relatively vertical orientation in comparison with the native ligament.13 Drilling the femoral tunnel through a medial portal allows
    for independent access to the anatomic femoral insertion. Also, the fiber orientation can more closely resemble that of the native ligament.14 One study demonstrated similar rotational stability in a comparision of
    patients who had a low femoral tunnel drilled through
    a medial portal with those who had a double-bundle
    reconstruction.15
    Recent attempts to duplicate native ACL anatomy
    have led to the development of double-bundle ACL reconstruction techniques. Laboratory data have suggested that a double-bundle reconstruction provides
    improved rotational stability.16,17 Patient outcome studies to date have not shown a consistent improvement in
    outcomes between single- and double-bundle techniques.18,19
    There are many different graft options for ACL reconstruction, but they mainly consist of quadrupled
    hamstring autograft, bone-patellar tendon-bone autograft, and a variety of allografts. Allografts allow for
    quicker surgical techniques without patient morbidity
    associated with graft harvest and a slightly more cosmetic incision. Disadvantages include a small risk of viral transmission (1 in 1.6 million), increased surgical
    costs, and slower graft incorporation that may translate
    into a higher rate of graft failure.20,21 Studies comparing
    autograft and allograft ACL reconstruction have a variety of outcomes, with some showing similar failure
    rates and others demonstrating a significantly higher
    percentage of failures in the allograft groups.22 With the
    variety of allograft types used and the heterogeneity of
    surgical techniques, it is unclear which graft type is
    best. Likewise, comparative studies of autograft choices
    454

    Orthopaedic Knowledge Update 10

    Recent cadaver work has led to a greater understanding


    of the anatomy of the medial collateral ligament (MCL)
    and posteromedial corner (PMC).30 The MCL consists
    of a superficial band that originates just proximal and
    posterior to the medial femoral epicondyle and attaches
    distally approximately 6 cm below the joint line at the
    midportion of the proximal tibia. The deep layer has
    both a meniscofemoral ligament and a meniscotibial
    ligament, both of which adhere to the peripheral meniscocapsular region. The posterior oblique ligament
    (POL) runs posterior to the superficial MCL and has
    multiple bands that attach to the posteromedial capsule, the semimembranosus, and the proximal tibia
    (Figure 1, A). A greater understanding of the specific
    anatomic locations of these structures has led to the development of newer anatomic reconstruction techniques.31
    Stability examination is performed by applying a
    valgus stress to the knee at 0 and 30 of flexion.
    Greater than 10 mm of valgus opening in full extension
    is consistent with injury to the ACL, PCL, MCL, and
    POL. A thorough clinical examination of both knees is
    critical to truly appreciate the amount of clinical laxity.
    Standard AP and supine lateral radiographs often
    give clues to an injury to the MCL/PMC. Subtle
    amounts of medial joint space opening, subtle tibiofemoral subluxation, and bony avulsions off the femur in
    particular can often be seen. At times, fluoroscopic bilateral stress examination may be necessary to truly appreciate the amount of laxity. MRI is the diagnostic imaging modality of choice. MRI is advantageous because
    of its ability to identify the injury, its specific tear pattern, and location. Additionally, all other associated injuries can be readily identified.
    Treatment of isolated MCL injuries is typically nonsurgical, with bracing for 6 weeks. Because most of the
    injuries occur at the proximal femoral attachment site,
    healing rates are predictable and usually lead to complete return to preinjury function. However, distal injuries, including the Stener lesion of the knee in which the

    2011 American Academy of Orthopaedic Surgeons

    Chapter 35: Soft-Tissue Injuries About the Knee

    4: Lower Extremity

    Figure 1

    Ligamentous and tendinous anatomy of the knee. A, Medial aspect. B, Lateral aspect. (Panel A reproduced with
    permission from Wijdicks CA, Griffith CJ, LaPrade RF, et al: Radiographic identification of the primary medial knee
    structures. J Bone Joint Surg Am 2009;91:521-529. Panel B reproduced with permission from LaPrade RF, Ly TV,
    Wentorf FA, Engebretsen L: The posterolateral attachments of the knee: A qualitative and quantitative morphologic analysis of the fibular collateral ligament, popliteus tendon, popliteofibular ligament, and lateral gastrocnemius tendon Am J Sports Med 2003;31:854-860.)

    superficial MCL fibers displace superficial to the pes


    anserine tendons, prevent anatomic healing. Those
    MCL injuries in the setting of a multiligament knee injury usually require surgery.
    The decision to repair or reconstruct the MCL/PMC
    in the multiligament-injured knee is a subject of debate.
    A recent systematic review of the literature32 found
    only eight papers in the English literature that met inclusion criteria and found no advantage of one technique over the other. The decision to repair is also dependent on the tissue quality; repair can usually be
    accomplished in the acute setting. Typically, suture anchors as well as suture/washer post constructs are used
    for repair. However, when the tissue is difficult to identify and mobilize, reconstruction appears to be a better
    choice. Several authors have reported excellent outcomes with MCL/PMC reconstructions in the rare instance of combined instability.33,34 A recent study reported on the anatomic reconstruction of the MCL/
    PMC with the use of hamstring autograft in patients
    with chronic MCL instability.34 This series included pa-

    2011 American Academy of Orthopaedic Surgeons

    tients treated with isolated reconstruction as well as


    combined ligament injuries; results were satisfactory in
    91%.

    Fibular Collateral Ligament and Posterolateral


    Corner Injuries
    The posterolateral corner (PLC) of the knee consists of
    static and dynamic stabilizers. The three main static
    stabilizers include the fibular collateral ligament (FCL),
    the popliteofibular ligament (PFL), and the posterolateral capsule. The popliteus tendon serves as both a dynamic and static stabilizer. The FCL is the primary restraint to varus stress. It attaches to the femur just
    proximal and posterior to the lateral epicondyle, and to
    the anterior third of the fibular head. The PFL arises
    from the musculotendinous junction of the popliteus
    and attaches to the posterior aspect of the fibular head
    and has both anterior and posterior divisions. The PFL
    acts as the main restraint to external rotation of the

    Orthopaedic Knowledge Update 10

    455

    Section 4: Lower Extremity

    Table 2

    Examination Techniques for PCL


    and FCL/PLC Injuriesa
    PCL injury (isolated)
    Posterior drawer at 90 of knee flexion
    (grade I/II)
    Posterior sag sign at 90 of knee
    flexion (grade I/II)
    Positive quadriceps active test
    FCL/PLC injury (isolated)
    Positive varus stress test at 30 knee
    flexion
    4: Lower Extremity

    Positive dial test at 30, negative at 90


    of knee flexion
    Positive external rotation posterior
    drawer test at 90 of knee flexion
    PCL and FCL/PLC injuries
    Posterior drawer at 90 of knee flexion
    (grade III)
    Posterior sag sign at 90 of knee
    flexion (grade III)
    Positive dial test at 30 and 90 of knee
    flexion
    a

    Grade I: < 5 mm translation; grade II: 5-10 mm translation; grade III: > 10 mm
    translation. Degree of laxity is measured in comparison to the unaffected
    contralateral knee.

    tibia. The popliteus tendon attaches on the anterior


    fifth of the popliteal sulcus on the femur approximately
    2 cm anterior and distal to the FCL femoral attachment
    site (Figure 1, B).
    Physical examination for ligamentous stability includes the varus stress test at 0 and 30 of flexion. Recently, a biomechanical cadaver study35 demonstrated
    that greater than 2.5 mm of side-to-side difference in
    varus at 30 of flexion was consistent with isolated injury to the FCL, whereas greater than 4 mm side-toside difference was consistent with an injury to both
    the FCL and remaining posterolateral corner structures.
    To assess for rotational stability of the posterolateral
    corner, the dial test is performed at 30 and 90 of knee
    flexion. An increase in external rotation of greater than
    10 to 15 side-to-side comparison at 30 of flexion is
    consistent with an injury to the PLC. If this side-to-side
    difference persists at 90 of flexion, then injuries are
    present to both PLC and posterior cruciate ligament
    (PCL). More specific physical examination tests, including the external rotation recurvatum test and the
    external rotation drawer test, can aid in the diagnosis
    of PLC injury. The external rotation recurvatum test is
    a side-to-side comparison with both legs in fully extended positions. The examiner picks up the limbs by
    the great toe, and the test is positive when the tibia falls
    into external rotation in the recurvatum position relative to the femur. The external rotation drawer test is
    456

    Orthopaedic Knowledge Update 10

    performed at 90 of flexion with the foot in an externally rotated position. A positive test is when the medial step-off becomes absent when a posterior drawer is
    applied to the tibia. Grading is similar to a standard
    posterior drawer test (Table 2).
    It is important to recognize that isolated injuries to
    the FCL/PLC are extremely rare, and in most instances,
    concomitant ACL and/or PCL injuries are present. A
    recent study of 20 cadaver knees examined by posterior
    drawer and stress radiography was performed.36 The
    knees were tested intact and retested after sequential
    testing of the PCL and PLC. Posterior stress radiography demonstrated an average posterior displacement of
    10 mm with sectioning of the PCL, and an increase of
    approximately 20 mm with sectioning of the PCL and
    PLC structures. The authors concluded that a grade III
    posterior drawer or a side-to-side difference on stress
    radiography of greater than 10 mm implied a combined
    injury to both the PCL and PLC.
    Because most FCL/PLC injuries occur in the setting
    of the multiligament-injured knee, surgical management is most often recommended. The decision to repair rather than reconstruct remains controversial. A
    recently presented series from the Mayo Clinic demonstrated a failure rate of 45% with repair compared to
    4% with reconstruction in 44 multiligament-injured
    knees.37 Although neither of these studies was randomized, the authors cautioned against repair alone of the
    FCL/PLC in the multiligament-injured knee.
    Numerous reconstruction techniques have been developed with varying degrees of success. The anatomic
    reconstruction involves a two-tailed reconstruction of
    the FCL, PFL, and popliteus tendon. Although no clinical data are available, this anatomic reconstruction has
    been shown to biomechanically replicate the stability of
    the native ligaments. Other variations of anatomic reconstructions have shown satisfactory outcomes. One
    study described a single soft-tissue graft reconstruction
    of the FCL and PLC in 16 knees.38 At 2-year follow-up,
    no patients required revision reconstruction. This series
    showed no significant differences in clinical and functional outcomes between two-ligament and multiligament PLC-based reconstructions. The authors describe
    the importance of the posterolateral capsular shift in
    addition to reconstruction of the ligaments.

    PCL Injuries
    The PCL consists of the anterolateral and posteromedial bundles. The PCL is a robust ligament, 30% larger
    than the ACL, and measures approximately 33 mm
    13 mm wide. The anterolateral bundle is the strongest
    bundle and is taut in flexion, whereas the posteromedial bundle is taut in extension. Most reconstruction
    techniques in the past have focused on reconstruction
    of the anterolateral bundle. Difficulties arise in identifying the isometric point of the anterolateral bundle on
    the femur, as the insertion is crescent-shaped. Recent
    cadaver studies have helped to elucidate the anatomic
    characteristics and specific insertion points of the PCL

    2011 American Academy of Orthopaedic Surgeons

    Chapter 35: Soft-Tissue Injuries About the Knee

    Measurement of systolic blood pressure in the


    dorsalis pedis artery using ultrasound. (Reproduced with permission from Levy BA, Fanelli GC,
    Whelan DB, et al: Controversies in the treatment of knee dislocations and multiligament
    reconstruction. J Am Acad Orthop Surg 2009;17:
    197-206.)

    bundles,39,40 and numerous double-bundle reconstruction techniques are now available.41,42


    The posterior drawer test, performed with the knee
    at 90 of flexion, is the primary tool for assessment of
    PCL stability. The normal tibial step-off is approximately 1 cm (10 mm). Degree of laxity graded as I, II,
    and III injuries are defined as 5 mm, 10 mm, and
    > 10 mm of posterior translation, respectively. When
    applying a posterior drawer, if the tibia moves posterior
    to sit flush with the femoral condyles, this would imply
    approximately 10 mm of posterior translation, consistent with a grade II injury. If the tibia moves posterior
    to the femoral condyles, this would imply a grade III injury (Table 2).
    Radiographic assessment, in particular a supine lateral view, is helpful in assessing posterior tibiofemoral
    subluxation. Radiographic or fluoroscopic posterior
    stress views with bilateral comparison are often helpful
    in diagnosing and grading the PCL injury. MRI is the
    imaging modality of choice, although it can lead to
    falsely positive results. Often, substantial signal change
    may be seen; however, clinical examination may be
    completely normal. Therefore, it is important to correlate physical findings, MRI findings, and stress views to
    confirm the presence and extent of a clinically relevant
    PCL injury.
    Recent biomechanical evidence suggests that a grade
    III posterior drawer is indicative of a combined PCL/
    PLC injury.36 This has important ramifications for management of the isolated PCL tear. For example, an isolated grade I or grade II PCL injury can be successfully
    treated with quadriceps rehabilitation and PCL brac-

    2011 American Academy of Orthopaedic Surgeons

    4: Lower Extremity

    Figure 2

    ing, if necessary. An isolated grade III PCL injury, now


    thought to be a combined ligament injury, may best be
    treated with surgical reconstruction of both PCL and
    PLC ligamentous structures. This underscores the importance of differentiating between grade II and grade
    III injuries. A special circumstance is PCL avulsion injuries of the tibia. These injuries in isolation can be successfully treated surgically with open reduction and internal fixation with satisfactory results.
    Reconstruction of the PCL can be approached by transtibial or tibial inlay techniques. Several biomechanical
    and clinical studies have failed to demonstrate an advantage of one technique over the other.43 Current controversy persists regarding single-bundle versus doublebundle techniques. One study demonstrated in a
    cadaver model that a single-bundle anterolateral graft
    best reproduced normal PCL force profiles and that the
    double-bundle graft did slightly reduce posterior laxity
    at 0 to 30 of flexion but at the expense of higher than
    normal graft forces on the posteromedial bundle.44 The
    long-term ramification of these excess graft forces is
    unknown. A more recent cadaver sectioning study demonstrated that in the setting of a combined PCL/PLC
    injury, the double-bundle technique offered better rotational control when only the PCL was reconstructed.45
    The authors concluded that because PLC reconstruction techniques tend to stretch out over time, there may
    be an advantage to the double-bundle PCL reconstruction technique in this particular injury combination.
    Clinically, no studies to date have demonstrated an
    advantage of the double-bundle technique over the
    single-bundle anterolateral reconstruction. Further prospective randomized trials will be necessary to answer
    this question.

    Multiligament Knee Injuries/Traumatic Knee


    Dislocation
    The dislocated knee is a limb-threatening injury, with a
    significant rate of neurovascular compromise. It is imperative to recognize that a knee dislocation has occurred; most of these injuries are seen after spontaneous reduction. Normal radiographs and substantial
    soft-tissue swelling with gross instability in a patient
    who presents to the emergency department should alert
    the physician to the possibility of a knee dislocation.
    Thorough vascular assessment is probably the most
    important first step in the management of these injuries. Recently, it has been demonstrated that serial
    physical examination alone is safe. However, it is also
    recognized that normal and symmetric pulses may be
    present with a complete popliteal artery occlusion secondary to collateral flow. Measurement of the anklebrachial index (ABI) is recommended for every patient
    who presents to the emergency department with a diagnosis or presumption of a knee dislocation. The ABI is
    a noninvasive screening tool that is easy to perform in
    the acute setting46 (Figure 2).
    The ABI has shown excellent sensitivity and specificity for detecting clinically relevant vascular injury with

    Orthopaedic Knowledge Update 10

    457

    Section 4: Lower Extremity

    Table 3

    4: Lower Extremity

    Modified Schenck Classification System for


    Multiligament Knee Injury

    Figure 3

    Algorithm for vascular assessment.

    a negative predictive value of 100% if the ABI is


    greater than 0.9. If patients have an abnormal ABI,
    then further vascular screening with arterial duplex ultrasound is warranted. If the ultrasound is equivocal or
    nondiagnostic, conventional arteriography or CT arteriography is recommended (Figure 3). The advantage of
    CT arteriography compared to conventional arteriography is that the contrast material is injected into the antecubital fossa as opposed to the groin and requires less
    than one fourth the radiation.47
    A thorough neurologic examination is also important because the risk of peroneal nerve injury is approximately 25%. Chronic peroneal nerve palsy, even
    after a successful multiligament knee reconstruction,
    can cause significant functional impairment. Conventional treatment consists of neurolysis, nerve grafting,
    and tibial tendon transfers, all with moderate success.
    A technique for direct nerve transfer from a healthy
    motor branch of the tibial nerve to the healthy distal
    portion of the injured peroneal nerve has been described,48 although no clinical data are currently available.
    The modified Schenck classification system for multiligament knee injury (Table 3) has achieved popularity as a means of more precisely communicating patterns of ligament injury. Although this system does not
    offer a scheme for decision making with regard to management, it helps standardize research results. In this
    system, a multiligament injury involving only one cruciate ligament is defined as a KD-I. A KD-II describes
    injury to both cruciate ligaments only. Injury to both
    cruciate ligaments and either of the collateral ligaments
    is a KD-III, whereas injury to both cruciate and both
    collateral ligaments is a KD-IV. A KD-V injury describes damage to two or more ligaments with periarticular fracture.
    Optimal treatment strategies for the acutely dislocated knee remain highly debated. There are a paucity
    of data in the literature to help guide treatment strate458

    Orthopaedic Knowledge Update 10

    Classification

    Pattern of Injury

    KD-I

    Multiligamentous injury with


    involvement of only one cruciate
    ligament

    KD-II

    Injury to ACL and PCL only

    KD-III

    Injury to ACL, PCL, and either PMC


    or PLC

    KD-IV

    Injury to ACL, PCL, PMC, and PLC

    KD-V

    Multiligamentous injury with


    periarticular fracture

    gies with regard to ligament repair/reconstruction. Current controversies include surgical versus nonsurgical
    management, early versus delayed surgery, graft selection, repair versus reconstruction of the collateral ligaments, and postoperative rehabilitation. Once a reduction is maintained, the knee must be held stable in the
    reduced position, often with a long leg splint or cast.
    Care must be taken to obtain new radiographs with the
    knee in the splint or cast to verify reduction. Rarely,
    when the knee is too unstable to maintain a reduction
    in a splint or if there is a vascular injury, a temporary
    spanning external fixator can be placed in the acute setting.
    A recent evidence-based systematic review was reported, specifically addressing three areas: surgical versus nonsurgical treatment, repair versus reconstruction
    of injured ligamentous structures, and early versus late
    surgery of damaged ligaments. This review demonstrated that early surgical treatment (usually defined as
    within the first 3 weeks following injury) of the
    multiligament-injured knee led to improved functional
    and clinical outcomes compared with nonsurgical management or delayed surgery.49
    Performing research studies with high levels of evidence for these complex injuries is extremely difficult,
    predominantly because of the heterogeneity of the
    study group and wide variation of injury patterns/
    combinations.

    Meniscus Tears
    The menisci are fibrocartilage structures interposed between the medial and lateral tibiofemoral joints. They
    are attached to the capsule at their periphery and to the
    tibia at their anterior and posterior horns. The lateral
    meniscus is more C-shaped and mobile than its medial
    counterpart. The menisci function to increase tibiofemoral surface contact area and therefore decrease joint
    forces. They perform a dampening mechanism for articular cartilage from excessive loads. Joint compressive

    2011 American Academy of Orthopaedic Surgeons

    Chapter 35: Soft-Tissue Injuries About the Knee

    2011 American Academy of Orthopaedic Surgeons

    Figure 4

    Inside-out technique for meniscal repair.

    4: Lower Extremity

    forces are dissipated by the meniscus when they are


    converted to outwardly directed radial oriented forces.
    The radial forces are ultimately borne by meniscus fibers oriented parallel to its macroscopic semicircular
    structure. Outward forces on the parallel meniscus fibers are resisted by perpendicularly oriented radial tie
    fibers. A meniscectomized knee demonstrates significantly higher joint forces and leads to progressive tibiofemoral compartment arthritis.
    The outer 25% to 30% of each meniscus has a sufficient blood supply suitable for healing (the red-red
    zone). The middle third of the meniscus is termed the
    red-white zone because it is at the junction of the vascular outer third and the avascular central third. This
    central zone, which has no healing potential, is termed
    the white-white zone. With age, the meniscus becomes
    further devascularized and it also loses water content.
    A meniscus tear can be classified based on shape,
    size, chronicity, vascularity, and whether the tear is degenerative or acutely traumatic. A patients age is also
    important because there is some evidence that meniscus
    repair healing rates decrease with older age. The shape
    of a tear can be longitudinal, radial, horizontal, flap, or
    bucket-handle (a large, unstable, longitudinal tear). Degenerative and chronic tears often have more complex
    shapes and are often located more centrally. These tears
    are usually irreparable because of the complex nature
    of their shape, their chronicity, their avascular location,
    and the older age of most patients. Tears of the root of
    the meniscus also can occur and cause a significant decrease in meniscus function, leading to higher tibiofemoral contact forces more often than a tear not involving
    the root. Cadaver studies have shown that a posterior
    horn medial meniscus root tear increased medial joint
    contact pressures equivalent to a total meniscectomy,
    and those values were restored to normal following repair.50,51
    The natural history of meniscus tear progression depending on treatment is not known. Also, it is clear
    that many tears may exist in asymptomatic patients. In
    a young symptomatic patient with an acute meniscus
    tear that is longitudinal in shape and displaceable, repairing the meniscus is clearly indicated. Also, a symptomatic meniscus root tear in a patient without degenerative changes should undergo repair. Nondisplaceable
    acute tears less than 1 cm in length and those that are
    seen during knee arthroscopy in patients without symptoms should not undergo repair.
    Symptomatic meniscus tears cause mechanical symptoms of catching and locking due to displacement of
    the tear between the femoral condyle and the tibial plateau, or within the intercondylar notch. These tears
    should be treated with partial meniscectomy or repair.
    Meniscus tears that are avascular, complex degenerative in shape, found in elderly patients, and that are
    otherwise irreparable should undergo partial meniscectomy to a stable rim. Normal meniscus should be left
    intact to preserve some force-dissipating function in the
    remaining tissue.
    Repairable meniscus tears are repaired with one of
    three techniques: outside-in, inside-out, and all-inside.

    The inside-out technique with vertical mattress nonabsorbable suture configuration is the gold standard for
    meniscus repair and is the strongest repair technique
    (Figure 4). However, with recent advances in arthroscopic repair instrumentation, all-inside techniques
    have become more popular. All-inside repair techniques
    now approach the strength of inside-out repairs and
    outcomes have been largely successful. Disadvantages
    of inside-out repair are related to the increased morbidity and neurologic injury risk of the medial or lateral
    meniscus approach required to retrieve and tie sutures
    over capsule. Although all-inside techniques decrease
    this morbidity, there is still a risk of neurovascular injury following capsular penetration of all-suture passing devices.52
    Healing rates of meniscus repairs are generally
    good.53,54 The main determinant of healing rates, in addition to the tear pattern, is the location of the tear
    within the vascularized zone. Meniscus repairs in the
    setting of a concurrent ACL reconstruction have higher
    healing rates.55 This may be due to intra-articular
    bleeding that occurs from the injury or with bone tunnel preparation.
    Postoperative rehabilitation following a meniscus repair often involves a period of no or limited weight
    bearing as well as limitation of deep knee flexion. This
    is an attempt to decrease the shear forces across the repaired meniscus while it heals. One advantage of a partial meniscectomy is that immediate weight-bearing is
    possible, and therefore postoperative recovery is easier.
    A young patient who has had a meniscectomy may
    develop symptoms related to his or her lack of meniscus function (recurrent tibiofemoral joint pain and an
    effusion). When there are minimal degenerative cartilage changes, the patient may be a candidate for meniscus allograft transplantation. The patients lower extremity alignment must be taken into account and a
    high tibial or distal femoral osteotomy may be indicated before or concurrent with the transplantation.
    Medial meniscus transplantation can be performed

    Orthopaedic Knowledge Update 10

    459

    Section 4: Lower Extremity

    4: Lower Extremity

    with either a single bone plug containing both the anterior and posterior roots or with independent bone
    plugs for each root. This procedure is possible because
    there is sufficient distance between the anterior and
    posterior horn meniscus roots. Because the lateral meniscus roots are very close together, a single plug is usually used on this side. Leaving the allograft bone attached to the meniscus root during the transplantation
    is critical to maintaining the grafts ability to withstand
    compressive forces. Outcomes of meniscus transplantation are generally good; however, the rate of meniscus
    extrusion is approximately 33% and usually occurs in
    the first year postoperatively.56 A 10-year follow-up of
    meniscus transplants found an improvement in subjective outcome scores; however, 55% of grafts had failed
    and most had radiographic progression of tibiofemoral
    degenerative changes.57

    Articular Cartilage Injury


    Articular cartilage is mainly composed of type II collagen. Its main function is to dissipate forces within the
    tibiofemoral and patellofemoral joints. Compression of
    articular cartilage leads to extrusion of water normally
    contained within the cartilage matrix loosely bound to
    negatively charged proteoglycan molecules. Damage to
    articular cartilage occurs with various arthritides, most
    commonly osteoarthritis. Focal defects can lead to
    higher forces in the surrounding intact cartilage and
    lead to its subsequent breakdown.
    Focal injury to knee articular cartilage can occur
    with any injury to the knee that leads to excessive compression or shear forces from momentary impact of
    two surfaces. This type of injury can be isolated or seen
    at the time of concurrent cruciate ligament injury. The
    natural history of a focal traumatic lesion is unclear. A
    loose body produced by a cartilage injury may enlarge
    and become a source of mechanical locking. Cartilage
    defects in any compartment of the knee can also produce mechanical symptoms in some cases, although
    they are often asymptomatic once the initial injury subsides. There is evidence that with overloading forces to
    surrounding intact articular cartilage, the natural history might involve progressive cartilage deterioration
    and arthritis. However, other studies, including those in
    patients with concurrent ACL injuries, suggest a relatively benign natural history of untreated cartilage lesions.58
    Indications for treatment of focal articular cartilage
    lesions include pain with mechanical symptoms or recurrent swelling. Initial nonsurgical management of patients without true mechanical locking includes range
    of motion and quadriceps strengthening exercise as
    well as treatment of the knee effusion. Those patients
    with mechanical symptoms or with symptoms that persist despite nonsurgical treatment are candidates for
    surgical intervention. In general, patients younger than
    50 years could be considered for cartilage repair
    whereas older patients are more likely candidates for
    an arthroplasty procedure.
    460

    Orthopaedic Knowledge Update 10

    Surgical options for cartilage repair include chondral


    dbridement, marrow-stimulating techniques such as
    microfracture and drilling, osteochondral transfer (autograft and allograft), and autologous chondrocyte implantation (ACI). These techniques have all been well
    studied, and it is unclear which is superior. The size of
    the lesion is important in determining what graft options are appropriate. Small lesions less than 1 to 2 cm2
    can be treated with any of these options. Larger lesions
    that are greater than 2 cm are likely too large for an autograft osteochondral transfer. When there is subchondral bone loss present, the bone void can be filled with
    the bone plug of an osteochondral transfer or grafting
    beneath an ACI procedure.
    Dbridement or a marrow-stimulating technique is a
    first-line treatment of most small and many mediumsized lesions.59 In recent randomized controlled trials
    comparing microfracture and ACI, there was no difference found in outcomes.60 There is some evidence that
    second-generation ACI techniques involving a hyaluronic acid scaffold may have better midterm results
    than microfracture.61 Patients with large lesions and
    those in whom simpler procedures have failed are candidates for osteochondral transfer or ACI.62-64 There is
    some evidence that removing the calcified cartilage
    layer during a previous microfracture adversely affects
    the outcomes of ACI later.
    Postoperative rehabilitation from cartilage repair in
    general emphasizes range of motion, often with a continuous passive motion machine and a period of no
    weight bearing, usually around 6 to 8 weeks. Weightbearing exercises and deep bending weight training exercises are introduced gradually.
    A patients coronal plane alignment is extremely important in treating cartilage lesions and has a significant effect on tibiofemoral contact pressures.65 The
    weight-bearing line as measured on a full-length standing AP lower extremity radiograph must not go
    through the affected compartment. If it does, then a realignment procedure, either a high tibial osteotomy or
    distal femoral osteotomy, is indicated concurrent with
    or before cartilage repair. If alignment is not corrected,
    the failure rate of cartilage procedures is higher.

    Patellar Instability
    Many factors contribute to patellofemoral stability and
    include both local and distant anatomic etiologies. Factors related to knee anatomy include the medial patellofemoral ligament (MPFL), which is the primary restraint to lateral patellar translation in the first 20 of
    knee flexion and guides the patella into the trochlear
    groove. The bony structures of the patella and trochlea
    account for most patellofemoral stability in deeper knee
    flexion. Soft-tissue restraints include the medial and lateral patellofemoral retinacula and the quadriceps
    muscle-tendon unit. Patella alta can also lead to instability before the patella engages the trochlear groove.
    Factors that contribute to patellofemoral stability include those that can increase the lateral moment of the

    2011 American Academy of Orthopaedic Surgeons

    Chapter 35: Soft-Tissue Injuries About the Knee

    2011 American Academy of Orthopaedic Surgeons

    Annotated References
    1.

    Boden BP, Torg JS, Knowles SB, Hewett TE: Video analysis of anterior cruciate ligament injury: Abnormalities
    in hip and ankle kinematics. Am J Sports Med 2009;
    37(2):252-259.
    This video analysis of ACL injuries found that landing
    ground contact with a flatfoot or heel first, knee abduction, and hip flexion may be risk factors for injury.

    2.

    Hewett TE, Zazulak BT, Myer GD: Effects of the menstrual cycle on anterior cruciate ligament injury risk: A
    systematic review. Am J Sports Med 2007;35(4):659668.
    This systematic review of the effect of the menstrual cycle and hormone levels found that female athletes may
    be more predisposed to ACL injuries during the preovulatory phase of the menstrual cycle.

    3.

    Posthumus M, September AV, OCuinneagain D, van


    der Merwe W, Schwellnus MP, Collins M: The
    COL5A1 gene is associated with increased risk of anterior cruciate ligament ruptures in female participants.
    Am J Sports Med 2009;37(11):2234-2240.
    This case-control study of 345 patients demonstrated an
    underrepresentation of the CC genotype of a COL5A1
    gene sequence in females with ACL ruptures, demonstrating for the first time a genetic predisposition for
    ACL rupture in female athletes.

    4.

    Ferretti M, Ekdahl M, Shen W, Fu FH: Osseous landmarks of the femoral attachment of the anterior cruciate
    ligament: An anatomic study. Arthroscopy 2007;23(11):
    1218-1225.
    This anatomic study found that the ACL femoral attachment has a unique topography with a constant presence of the lateral intercondylar ridge and often an osseous ridge between anteromedial and posterolateral
    femoral attachments, the lateral bifurcate ridge.

    5.

    Pugh L, Mascarenhas R, Arneja S, Chin PY, Leith JM:


    Current concepts in instrumented knee-laxity testing.
    Am J Sports Med 2009;37(1):199-210.
    This systematic review of the literature suggested that
    the KT-1000 knee arthrometer and the Rolimeter were
    most reliable for testing anterior laxity in the knee,
    whereas the Telos device was determined to best discern
    posterior laxity.

    6.

    Arbuthnot JE, Brink RB: The role of anterior cruciate


    ligament reconstruction in the older patients, 55 years
    or above. Knee Surg Sports Traumatol Arthrosc 2010;
    18(1):73-78.
    This case series of ACL reconstruction in 14 patients
    older than 55 years showed a significant improvement
    in postoperative clinical outcomes with decreased anterior laxity in all but one patient, demonstrating the
    safety of this procedure in this population.

    7.

    Khan RM, Prasad V, Gangone R, Kinmont JC: Anterior


    cruciate ligament reconstruction in patients over 40
    years using hamstring autograft. Knee Surg Sports Traumatol Arthrosc 2010;18(1):68-72.

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    patella, such as increased femoral anteversion, internal


    tibial torsion, core and hip abductor weakness, and pes
    planus. Static coronal plane alignment of the extensor
    mechanism, the Q angle, has considerable influence on
    patellar stability. Generalized ligamentous laxity can
    contribute to patellofemoral instability.
    Patellofemoral instability is lateral in most instances.
    Medial dislocations occur mainly from iatrogenic
    causes such as a failed prior procedure for lateral instability. Lateral instability may be due to a single traumatic event causing an MPFL tear or a combination of
    the aforementioned pathology that has lead to chronic
    recurrent instability with minor or even no trauma.
    Treatment of patellofemoral instability is complex
    and depends on the exact pathoanatomy present in
    each case. Each abnormal structure or pathology must
    be addressed to ensure successful treatment. In atraumatic instability, initial treatment usually consists of
    physical therapy and bracing. With a first-time traumatic patellar lateral dislocation there is some controversy regarding treatment. The benefit of acute surgical
    repair has not been definitively established although
    some studies recommend this approach.66-68 Significant
    loose bodies should be removed arthroscopically. Residual lateral tilting or subluxation of the patella may
    be considered an indication for early MPFL repair. In
    most cases, however, initial treatment consists of a period of immobilization to allow the MPFL to heal, followed by physical therapy to regain motion and
    strength, including quadriceps control and hip abductor strengthening. Later transition to a J-brace resists
    lateral patellar translation.
    Surgical management for most patients is reserved
    for recurrence of instability. Most procedures are categorized as proximal-distal and combined realignment.
    Proximal realignment procedures mainly repair or reconstruct the MPFL and may address the retinaculum
    and/or the vastus medialis. These procedures are done
    for deficient soft-tissue structures that cause the patella
    to not consistently engage the trochlear groove in early
    flexion. The radiographic MPFL femoral attachment
    site for its reconstruction has been defined.69 Other
    common procedures include lateral retinacular lengthening and vastus medialis advancement. Distal realignment procedures are performed when there is an increased Q angle documented by a trochlear groove to
    tibial tubercle distance of more than 20 mm on axial
    CT scan. In most cases, this consists of an anteromedialization tibial tubercle osteotomy. The amount of anterior and medial displacement of the osteotomy can be
    tailored to the specific patients pathology. Combined
    procedures are reserved for when a patient has deficient
    soft-tissue restraints as well as increased extensor
    mechanism valgus alignment. When a patient has a
    dysplastic trochlear groove, this may have to be specifically addressed with a trochlear groove deepening procedure.70 Also, patella alta can be treated with a patellar tendon imbrication or tibial tubercle distalization.

    461

    Section 4: Lower Extremity

    Clinical outcomes of arthroscopically assisted ACL reconstruction with four-stranded hamstring autograft
    were retrospectively evaluated in 21 patients older than
    40 years at mean 2-year follow-up. Satisfactory results
    were observed in Lysholm, International Knee Documentation Committee, Tegner, and KT-1000 arthrometer measurements.
    8.

    4: Lower Extremity

    Tayton E, Verma R, Higgins B, Gosal H: A correlation


    of time with meniscal tears in anterior cruciate ligament
    deficiency: Stratifying the risk of surgical delay. Knee
    Surg Sports Traumatol Arthrosc 2009;17(1):30-34.
    This retrospective review of patients who underwent
    ACL reconstruction found that those patients with no
    meniscal damage at the time of diagnosis and who had
    no further damage at surgery had a median time to surgery of 6 months. This time was significantly different
    from those with no meniscal damage at diagnosis, but
    who were found subsequently to have sustained damage
    to one meniscus, when the median time was 11 months
    (P = 0.0017), or both menisci, when the median time
    was 32 months (P = 0.0184).

    10.

    462

    13.

    Stanford FC, Kendoff D, Warren RF, Pearle AD: Native


    anterior cruciate ligament obliquity versus anterior cruciate ligament graft obliquity: An observational study
    using navigated measurements. Am J Sports Med 2009;
    37(1):114-119.
    This laboratory study compared transtibial ACL reconstruction to the native anatomy. The sagittal and coronal plane obliquity of well-functioning grafts placed using the transtibial technique were more vertical than
    anatomic fibers.

    14.

    Harner CD, Honkamp NJ, Ranawat AS: Anteromedial


    portal technique for creating the anterior cruciate ligament femoral tunnel. Arthroscopy 2008;24(1):113-115.
    The authors describe the technique of using an anteromedial portal for femoral tunnel drilling in ACL reconstruction.

    15.

    Kanaya A, Ochi M, Deie M, Adachi N, Nishimori M,


    Nakamae A: Intraoperative evaluation of anteroposterior and rotational stabilities in anterior cruciate ligament reconstruction: Lower femoral tunnel placed
    single-bundle versus double-bundle reconstruction.
    Knee Surg Sports Traumatol Arthrosc 2009;17(8):907913.
    This prospective, randomized trial evaluated stability after single- versus double-bundle ACL reconstruction
    with hamstring tendons in 26 patients with anteroposterior knee laxity. No differences were found in AP displacement or tibial rotation at 30 and 60 of flexion
    between groups.

    16.

    Markolf KL, Park S, Jackson SR, McAllister DR: Simulated pivot-shift testing with single and double-bundle
    anterior cruciate ligament reconstructions. J Bone Joint
    Surg Am 2008;90(8):1681-1689.
    The authors cadaver model of ACL reconstruction
    found that a single-bundle reconstruction was sufficient
    to restore intact knee kinematics during a simulated
    pivot-shift event. The higher graft forces with some
    double-bundle graft-tensioning protocols reduced the
    coupled rotations and displacements from an applied
    valgus moment to less than the intact levels. This overcorrection should theoretically make the knee less likely
    to pivot but could have unknown clinical consequences.

    17.

    Markolf KL, Park S, Jackson SR, McAllister DR:


    Anterior-posterior and rotatory stability of single and
    double-bundle anterior cruciate ligament reconstructions. J Bone Joint Surg Am 2009;91(1):107-118.

    Lebel B, Hulet C, Galaud B, Burdin G, Locker B, Vielpeau C: Arthroscopic reconstruction of the anterior cruciate ligament using bone-patellar tendon-bone autograft: A minimum 10-year follow-up. Am J Sports
    Med 2008;36(7):1275-1282.
    This was a retrospective study of patients undergoing
    ACL reconstruction using bonepatellar tendonbone
    autograft. The authors found high patient satisfaction
    levels and good clinical results after 10 years. Moreover,
    a high percentage of patients remained involved in
    sports activities, and ACL reconstruction protected the
    meniscus from a secondary tear. However, knee osteoarthritis developed in 17.8% of patients so treated.

    11.

    Taylor DC, Posner M, Curl WW, Feagin JA: Isolated


    tears of the anterior cruciate ligament: Over 30-year
    follow-up of patients treated with arthrotomy and primary repair. Am J Sports Med 2009;37(1):65-71.
    At more than 30-year follow-up, patients have decreased activity levels and an equal mix of acceptable
    and unacceptable outcomes. The authors were unable to
    identify any predictive factors that correlated with the
    results; however, subsequent meniscal surgery did correlate with poor results. The results at greater than 30
    years reinforce the 5-year results that showed unsatisfactory results after the open evaluation and treatment
    of ACL injuries with or without repair.

    Granan LP, Bahr R, Lie SA, Engebretsen L: Timing of


    anterior cruciate ligament reconstructive surgery and
    risk of cartilage lesions and meniscal tears: A cohort
    study based on the Norwegian National Knee Ligament
    Registry. Am J Sports Med 2009;37(5):955-961.
    This study evaluated a cohort of patients undergoing
    ACL reconstructions in the Norwegian National Knee
    Ligament Registry. The odds of a cartilage lesion in the
    adult knee increased by nearly 1% for each month that
    elapsed from the injury date until the surgery date, and
    that of cartilage lesions were nearly twice as frequent if
    there was a meniscal tear, and vice versa.

    9.

    12.

    Lidn M, Sernert N, Rostgrd-Christensen L, Kartus C,


    Ejerhed L: Osteoarthritic changes after anterior cruciate
    ligament reconstruction using bone-patellar tendonbone or hamstring tendon autografts: A retrospective,
    7-year radiographic and clinical follow-up study. Arthroscopy 2008;24(8):899-908.
    This retrospective review found at a median of 7 years
    after ACL reconstruction with either bonepatellar-tendonbone or hamstring tendon autografts, the prevalence of osteoarthritis as seen on standard weightbearing radiographs and the clinical outcome were
    comparable. The presence of meniscal injuries increased
    the prevalence of osteoarthritis.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 35: Soft-Tissue Injuries About the Knee

    The authors cadaver model of ACL reconstruction


    found that the single-bundle reconstruction produced
    graft forces, knee laxities, and coupled tibial rotations
    that were closest to normal. Adding a posterolateral
    graft to an anteromedial graft tended to reduce laxities
    and tibial rotations, but the reductions were accompanied by markedly higher forces in the posterolateral
    graft near 0 that occasionally caused it to fail during
    tests with internal torque or anterior tibial force.
    Lewis PB, Parameswaran AD, Rue JP, Bach BR Jr: Systematic review of single-bundle anterior cruciate ligament reconstruction outcomes: A baseline assessment
    for consideration of double-bundle techniques. Am J
    Sports Med 2008;36(10):2028-2036.
    This systematic review of one single-bundle anterior cruciate ligament reconstruction demonstrates it to be a safe,
    consistent surgical procedure affording reliable results.

    19.

    Meredick RB, Vance KJ, Appleby D, Lubowitz JH: Outcome of single-bundle versus double-bundle reconstruction of the anterior cruciate ligament: A meta-analysis.
    Am J Sports Med 2008;36(7):1414-1421.
    This meta-analysis of single-bundle and double-bundle
    reconstruction found that double-bundle reconstruction
    does not result in clinically significant differences in KT1000 arthrometer or pivot shift testing. The pivot shift
    results have particular clinical relevance because the test
    is designed to evaluate knee rotational instability; the results do not support the theory that double-bundle reconstruction better controls knee rotation.

    20.

    21.

    22.

    Cohen SB, Sekiya JK: Allograft safety in anterior cruciate ligament reconstruction. Clin Sports Med 2007;
    26(4):597-605.
    This review article discusses the risks and benefits of using allograft tissue for ACL reconstruction and advocates providing this information to patients before their
    procedure.
    Borchers JR, Pedroza A, Kaeding C: Activity level and
    graft type as risk factors for anterior cruciate ligament
    graft failure: A case-control study. Am J Sports Med
    2009;37(12):2362-2367.
    This case-control study compared activity level and
    graft selection in 21 patients with ACL graft failure to a
    2:1 age- and sex-matched control group, determining a
    roughly 5.5 odds ratio for higher activity levels and allograft versus autograft for failure.
    Prodromos C, Joyce B, Shi K: A meta-analysis of stability of autografts compared to allografts after anterior
    cruciate ligament reconstruction. Knee Surg Sports
    Traumatol Arthrosc 2007;15(7):851-856.
    This meta-analysis found that allografts had significantly lower normal stability rates than autografts. The
    allograft abnormal stability rate, which usually represents graft failure, was significantly higher than that of
    autografts: nearly three times greater. It would therefore
    appear that autografts are the graft of choice for routine
    ACL reconstruction with allografts better reserved for
    multiple ligamentinjured knees where extra tissue may
    be required.

    2011 American Academy of Orthopaedic Surgeons

    Maletis GB, Cameron SL, Tengan JJ, Burchette RJ: A


    prospective randomized study of anterior cruciate ligament reconstruction: A comparison of patellar tendon
    and quadruple-strand semitendinosus/gracilis tendons
    fixed with bioabsorbable interference screws. Am J
    Sports Med 2007;35(3):384-394.
    The authors found that the bonepatellar tendonbone
    group had better flexion strength in the operated leg
    than in the nonoperated leg (102% versus 90%, P =
    0.0001), fewer patients reporting difficulty jumping
    (3% vs 17%, P = 0.03), and a greater number of patients returning to preinjury Tegner level (51% vs 26%,
    P = 0.01). The quadruple-strand semitendinosus/gracilis
    group had better extension strength in the operated leg
    than in the nonoperated leg (92% versus 85%, P =
    0.04), fewer patients with sensory deficits (14% versus
    83%, P = 0.0001), and fewer patients with difficulty
    kneeling (6% versus 20%, P = 0.04). Both groups
    showed significant improvement in KT-1000 arthrometer manual maximum difference, Lysholm score, Tegner
    activity level, International Knee Documentation Committee grade, and patient knee rating score.

    24.

    Poolman RW, Abouali JA, Conter HJ, Bhandari M:


    Overlapping systematic reviews of anterior cruciate ligament reconstruction comparing hamstring autograft
    with bone-patellar tendon-bone autograft: Why are they
    different? J Bone Joint Surg Am 2007;89(7):1542-1552.
    The currently available best evidence, derived from a
    methodologically sound meta-analysis, suggests that
    hamstring tendon autografts are superior for preventing
    anterior knee pain, and there is limited evidence that
    bone-atellar tendonbone autografts provide better stability.

    25.

    Pinczewski LA, Lyman J, Salmon LJ, Russell VJ, Roe J,


    Linklater J: A 10-year comparison of anterior cruciate
    ligament reconstructions with hamstring tendon and patellar tendon autograft: A controlled, prospective trial.
    Am J Sports Med 2007;35(4):564-574.
    The authors found it possible to obtain excellent results
    with both hamstring tendon and patellar tendon autografts. They recommend hamstring tendon reconstructions because of decreased harvest-site symptoms and
    radiographic osteoarthritis.

    26.

    Birmingham TB, Bryant DM, Giffin JR, et al: A randomized controlled trial comparing the effectiveness of
    functional knee brace and neoprene sleeve use after anterior cruciate ligament reconstruction. Am J Sports
    Med 2008;36(4):648-655.
    This randomized controlled trial of functional knee
    bracing versus neoprene sleeve in 150 patients after
    ACL reconstruction with hamstring autograft demonstrated no significant differences in functional or clinical
    outcomes at 1- and 2-year follow-up visits.

    27.

    Matava MJ, Prickett WD, Khodamoradi S, Abe S, Garbutt J: Femoral nerve blockade as a preemptive anesthetic in patients undergoing anterior cruciate ligament
    reconstruction: A prospective, randomized, doubleblinded, placebo-controlled study. Am J Sports Med
    2009;37(1):78-86.
    This randomized controlled trial evaluated the effectiveness of preemptive femoral nerve blockade versus pla-

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    18.

    23.

    463

    Section 4: Lower Extremity

    instabilities: Surgical concepts and clinical outcome.


    Knee Surg Sports Traumatol Arthrosc 2008;16(8):763769.

    cebo for pain control after patellar tendon ACL reconstruction in 56 patients. No significant differences in
    postoperative pain, narcotic use, or hospital stay data
    were noted.
    28.

    4: Lower Extremity

    29.

    30.

    31.

    32.

    33.

    464

    Andersson D, Samuelsson K, Karlsson J: Treatment of


    anterior cruciate ligament injuries with special reference
    to surgical technique and rehabilitation: An assessment
    of randomized controlled trials. Arthroscopy 2009;
    25(6):653-685.
    This systematic review of the literature found 70 articles
    dealing with surgical technique and rehabilitation after
    ACL reconstruction, determining from these that closed
    kinetic chain exercises promote better subjective outcomes, decreased laxity, and less pain compared to open
    chain exercises.
    Shelbourne KD, Gray T, Haro M: Incidence of subsequent injury to either knee within 5 years after anterior
    cruciate ligament reconstruction with patellar tendon
    autograft. Am J Sports Med 2009;37(2):246-251.
    The authors found that women have a higher incidence
    of ACL injury to the contralateral knee than men after
    reconstruction. The incidence of injury to either knee after reconstruction is associated with younger age and
    higher activity level, but returning to full activities before 6 months postoperatively does not increase the risk
    of subsequent injury.
    LaPrade RF, Engebretsen AH, Ly TV, Johansen S, Wentorf FA, Engebretsen L: The anatomy of the medial part
    of the knee. J Bone Joint Surg Am 2007;89(9):20002010.
    Anatomic dimensions and attachment sites for the main
    medial knee structures were recorded in eight cadaver
    knees, confirming a consistent attachment pattern for
    these structures.
    Kim SJ, Lee DH, Kim TE, Choi NH: Concomitant reconstruction of the medial collateral and posterior
    oblique ligaments for medial instability of the knee.
    J Bone Joint Surg Br 2008;90(10):1323-1327.
    This article describes a surgical technique for and clinical outcomes of concomitant reconstruction of the MCL
    and POL with semitendinosus autograft in 24 patients
    at mean 52.6-month follow-up, demonstrating satisfactory improvement in medial-side stability.
    Kovachevich R, Shah JP, Arens AM, Stuart MJ, Dahm
    DL, Levy BA: Operative management of the medial collateral ligament in the multi-ligament injured knee: An
    evidence-based systematic review. Knee Surg Sports
    Traumatol Arthrosc 2009;17(7):823-829.
    This systematic review examined evidence in the literature comparing outcomes of repair versus reconstruction of the MCL in multiligament knee injuries. Satisfactory results were observed with both techniques.
    Treatment decisions should be made on a case-by-case
    basis.
    Hayashi R, Kitamura N, Kondo E, Anaguchi Y,
    Tohyama H, Yasuda K: Simultaneous anterior and posterior cruciate ligament reconstruction in chronic knee

    Orthopaedic Knowledge Update 10

    This case series of 19 patients with chronic multiligament knee injuries demonstrated single-stage reconstruction of two or more knee ligaments with autograft to be
    safe and effective, with satisfactory postoperative outcomes at a mean 42-month follow-up.
    34.

    Lind M, Jakobsen BW, Lund B, Hansen MS, Abdallah


    O, Christiansen SE: Anatomical reconstruction of the
    medial collateral ligament and posteromedial corner of
    the knee in patients with chronic medial collateral ligament instability. Am J Sports Med 2009;37(6):11161122.
    This case series of 61 patients with medial-sided knee
    instability described satisfactory clinical, functional, and
    subjective outcomes at a minimum of 2 years after
    MCL/PMC reconstruction using an anatomic technique.

    35.

    LaPrade RF, Heikes C, Bakker AJ, Jakobsen RB: The


    reproducibility and repeatability of varus stress radiographs in the assessment of isolated fibular collateral
    ligament and grade-III posterolateral knee injuries: An
    in vitro biomechanical study. J Bone Joint Surg Am
    2008;90(10):2069-2076.
    This study of 10 cadaver knees measured lateral compartment opening on varus stress radiography after PLC
    sectioning, determining that an isolated FCL injury or
    grade III PLC injury was likely if 2.7 mm or 4.0 mm of
    opening was found, respectively.

    36.

    Sekiya JK, Whiddon DR, Zehms CT, Miller MD: A


    clinically relevant assessment of posterior cruciate ligament and posterolateral corner injuries: Evaluation of
    isolated and combined deficiency. J Bone Joint Surg Am
    2008;90(8):1621-1627.
    Twenty cadaver knees underwent sectioning of the PCL
    and PLC structures. A grade 3 posterior drawer test and
    >10 mm of posterior tibial translation on stress radiography were associated with PLC injury in addition to
    complete disruption of the PCL.

    37.

    Levy BA, Dajani KA, Morgan JA, Shah JP, Dahm DL,
    Stuart MJ: Repair versus reconstruction of the fibular
    collateral ligament and posterolateral corner in the
    multiligament-injured knee. Am J Sports Med 2010;
    38(4):804-809.
    The authors found a statistically significant higher rate
    of failure for repair compared with reconstruction of the
    FCL and PLC. Level of evidence: III.

    38.

    Schechinger SJ, Levy BA, Dajani KA, Shah JP, Herrera


    DA, Marx RG: Achilles tendon allograft reconstruction
    of the fibular collateral ligament and posterolateral corner. Arthroscopy 2009;25(3):232-242.
    FCL and PLC reconstruction via a single Achilles tendon allograft construct was evaluated in 16 knees (minimum 2-year follow-up). No significant difference in
    clinical or functional outcomes was observed between
    two-ligament and multiligament PLC-based reconstructions. Level of evidence: IV.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 35: Soft-Tissue Injuries About the Knee

    39.

    40.

    42.

    Moorman CT III, Murphy Zane MS, Bansai S, et al:


    Tibial insertion of the posterior cruciate ligament: A
    sagittal plane analysis using gross, histologic, and radiographic methods. Arthroscopy 2008;24(3):269-275.
    This study of 14 cadaver knees describes the anatomy of
    the tibial attachment site of the posterior cruciate ligament and recommends measurement for tunnel placement along the posterior cruciate ligament facet seen on
    a lateral radiographic view.
    Forsythe B, Harner C, Martins CA, Shen W, Lopes OV
    Jr, Fu FH: Topography of the femoral attachment of the
    posterior cruciate ligament: Surgical technique. J Bone
    Joint Surg Am 2009;91(suppl 2 pt 1):89-100.
    This study of 20 cadaver knees describes the anatomic
    dimensions and femoral attachment sites of both bundles of the PCL as well as a related surgical technique
    for double-bundle PCL reconstruction.
    Lee YS, Ahn JH, Jung YB, et al: Transtibial double bundle posterior cruciate ligament reconstruction using
    TransFix tibial fixation. Knee Surg Sports Traumatol
    Arthrosc 2007;15(8):973-977.
    A transtibial double-bundle PCL reconstruction technique is described using TransFix tibial fixation.

    43.

    Fanelli GC, Edson CJ: Arthroscopically assisted combined anterior and posterior cruciate ligament reconstruction in the multiple ligament injured knee: 2- to 10year follow-up. Arthroscopy 2002;18(7):703-714.

    44.

    Markolf KL, Feeley BT, Jackson SR, McAllister DR:


    Biomechanical studies of double-bundle posterior cruciate ligament reconstructions. J Bone Joint Surg Am
    2006;88(8):1788-1794.

    45.

    46.

    47.

    Whiddon DR, Zehms CT, Miller MD, Quinby JS,


    Montgomery SL, Sekiya JK: Double compared with
    single-bundle open inlay posterior cruciate ligament reconstruction in a cadaver model. J Bone Joint Surg Am
    2008;90(9):1820-1829.
    Posterior tibial translation and external rotation after
    single- and double-bundle PCL tibial-inlay reconstruction were compared in nine cadaver knees with a deficient and repaired posterolateral corner. The doublebundle technique resulted in significantly greater
    rotational and anterior-posterior stability.
    Levy BA, Zlowodzki MP, Graves M, Cole PA: Screening
    for extremity arterial injury with the arterial pressure
    index. Am J Emerg Med 2005;23(5):689-695.
    Redmond JM, Levy BA, Dajani KA, Cass JR, Cole PA:
    Detecting vascular injury in lower-extremity orthopedic

    2011 American Academy of Orthopaedic Surgeons

    trauma: The role of CT angiography. Orthopedics


    2008;31(8):761-767.
    CT angiography demonstrates excellent sensitivity and
    specificity as a screening tool for vascular injury in the
    setting of trauma to the lower extremity and has several
    advantages compared to conventional arteriography.
    48.

    Bodily KD, Spinner RJ, Bishop AT: Restoration of motor function of the deep fibular (peroneal) nerve by direct nerve transfer of branches from the tibial nerve: An
    anatomical study. Clin Anat 2004;17(3):201-205.

    49.

    Levy BA, Dajani KA, Whelan DB, et al: Decision making in the multiligament-injured knee: An evidencebased systematic review. Arthroscopy 2009;25(4):430438.
    This systematic review suggested that early surgical
    treatment of the multiligament-injured knee produces
    improved functional and clinical outcomes compared
    with nonsurgical management or delayed surgery, and
    that repair of the PLC yields higher revision rates compared with reconstruction.

    50.

    Allaire R, Muriuki M, Gilbertson L, Harner CD: Biomechanical consequences of a tear of the posterior root
    of the medial meniscus: Similar to total meniscectomy.
    J Bone Joint Surg Am 2008;90(9):1922-1931.
    This laboratory study found significant changes in contact pressure and knee joint kinematics due to a posterior root tear of the medial meniscus. Root repair was
    successful in restoring joint biomechanics to within normal conditions.

    51.

    Marzo JM, Gurske-DePerio J: Effects of medial meniscus posterior horn avulsion and repair on tibiofemoral
    contact area and peak contact pressure with clinical implications. Am J Sports Med 2009;37(1):124-129.
    This laboratory study found that posterior horn medial
    meniscal root avulsion leads to deleterious alteration of
    the loading profiles of the medial joint compartment
    and results in loss of hoop stress resistance, meniscus
    extrusion, abnormal loading of the joint, and early knee
    medial compartment degenerative changes.

    52.

    Chen NC, Martin SD, Gill TJ: Risk to the lateral geniculate artery during arthroscopic lateral meniscal suture
    passage. Arthroscopy 2007;23(6):642-646.
    This laboratory study found that the lateral geniculate
    artery is in close proximity to the lateral meniscus and is
    punctured often during in vitro inside-out meniscal repair in the embalmed cadaver model.

    53.

    Logan M, Watts M, Owen J, Myers P: Meniscal repair


    in the elite athlete: Results of 45 repairs with a minimum 5-year follow-up. Am J Sports Med 2009;37(6):
    1131-1134.
    This retrospective review found that meniscal repair and
    healing are possible, and most elite athletes can return
    to their preinjury level of activity.

    54.

    Pujol N, Panarella L, Selmi TA, Neyret P, Fithian D,


    Beaufils P: Meniscal healing after meniscal repair: A CT
    arthrography assessment. Am J Sports Med 2008;36(8):
    1489-1495.

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    41.

    Lopes OV Jr, Ferretti M, Shen W, Ekdahl M, Smolinski


    P, Fu FH: Topography of the femoral attachment of the
    posterior cruciate ligament. J Bone Joint Surg Am 2008;
    90(2):249-255.
    This study of 20 cadaver knees described the dimensions
    and anatomy of the femoral footprints of each bundle of
    the PCL using gross observation and three-dimensional
    laser photography. A medial intercondylar ridge and
    medial bifurcate ridge are described.

    465

    Section 4: Lower Extremity

    This retrospective review found that using all-inside fixation or outside-in sutures provided good clinical and
    anatomic outcomes. No statistically significant effect of
    ACL reconstruction or laterality (medial versus lateral)
    on overall healing after meniscal repair was identified.
    Partial healing occurred often, with a stable tear on a
    narrowed and painless meniscus. The posterior segment
    healing rate remained low, suggesting a need for further
    technical improvements.

    4: Lower Extremity

    55.

    56.

    Lee DH, Kim TH, Lee SH, Kim CW, Kim JM, Bin SI:
    Evaluation of meniscus allograft transplantation with
    serial magnetic resonance imaging during the first postoperative year: Focus on graft extrusion. Arthroscopy
    2008;24(10):1115-1121.
    This retrospective review found that a meniscus that extrudes early remains extruded and does not progressively worsen, whereas one that does not extrude early
    is unlikely to extrude within the first postoperative year.

    57.

    Hommen JP, Applegate GR, Del Pizzo W: Meniscus allograft transplantation: Ten-year results of cryopreserved allografts. Arthroscopy 2007;23(4):388-393.
    This retrospective review found that transplantation of
    cryopreserved allografts improved knee pain and function, and the average knee function was fair at longterm follow-up. Fifty-five percent of allografts failed
    when failure criteria for second-look surgery, knee improvement surveys, and MRI were added to Lysholm
    and pain score failure rates. The protective benefits of
    meniscus allografts remain debatable, and inferences
    cannot be made from this study.

    58.

    59.

    466

    Feng H, Hong L, Geng XS, Zhang H, Wang XS, Jiang


    XY: Second-look arthroscopic evaluation of buckethandle meniscus tear repairs with anterior cruciate ligament reconstruction: 67 consecutive cases. Arthroscopy
    2008;24(12):1358-1366.
    This retrospective review found that for large buckethandle meniscus tears involving red-red and red-white
    zones, an arthroscopic hybrid suture technique with
    ACL reconstruction achieves high anatomic healing results, with an overall meniscal healing rate of 89.6%,
    including 82.1% completely healed and 7.5% incompletely healed. The failure rate was 10.4% in the average 26-month follow-up period.

    Widuchowski W, Widuchowski J, Koczy B, Szyluk K:


    Untreated asymptomatic deep cartilage lesions associated with anterior cruciate ligament injury: Results at
    10- and 15-year follow-up. Am J Sports Med 2009;
    37(4):688-692.
    The authors found that untreated deep cartilage lesions
    found during ACL reconstruction do not appear to affect clinical outcome at 10- to 15-year follow-up. Level
    of evidence: III.
    Mithoefer K, McAdams T, Williams RJ, Kreuz PC,
    Mandelbaum BR: Clinical efficacy of the microfracture
    technique for articular cartilage repair in the knee: An
    evidence-based systematic analysis. Am J Sports Med
    2009;37(10):2053-2063.
    This systematic analysis shows that microfracture provides effective short-term functional improvement of

    Orthopaedic Knowledge Update 10

    knee function but insufficient data are available on its


    long-term results. Shortcomings of the technique include
    limited hyaline repair tissue, variable repair cartilage
    volume, and possible functional deterioration. The quality of the currently available data on microfracture is
    still limited by the variability of results and study designs.
    60.

    Knutsen G, Drogset JO, Engebretsen L, et al: A randomized trial comparing autologous chondrocyte implantation with microfracture. Findings at five years.
    J Bone Joint Surg Am 2007;89(10):2105-2112.
    This randomized controlled trial found that both methods provided satisfactory results in 77% of the patients
    at 5 years. There was no significant difference in the
    clinical and radiographic results between the two treatment groups and no correlation between the histologic
    findings and the clinical outcome. One third of the patients had early radiographic signs of osteoarthritis 5
    years after the surgery.

    61.

    Kon E, Gobbi A, Filardo G, Delcogliano M, Zaffagnini


    S, Marcacci M: Arthroscopic second-generation autologous chondrocyte implantation compared with microfracture for chondral lesions of the knee: Prospective
    nonrandomized study at 5 years. Am J Sports Med
    2009;37(1):33-41.
    This nonrandomized trial found that both methods have
    shown satisfactory clinical outcome at medium-term
    follow-up. Better clinical results and sports activity resumption were noted in the group treated with secondgeneration autologous chondrocyte transplantation.

    62.

    Marcacci M, Kon E, Delcogliano M, Filardo G, Busacca


    M, Zaffagnini S: Arthroscopic autologous osteochondral grafting for cartilage defects of the knee: Prospective study results at a minimum 7-year follow-up. Am J
    Sports Med 2007;35(12):2014-2021.
    This retrospective review found that the results of this
    technique at medium- to long-term follow-up are encouraging. This arthroscopic one-step surgery appears
    to be a valid solution for treatment of small grade III to
    IV cartilage defects.

    63.

    Williams RJ III, Ranawat AS, Potter HG, Carter T,


    Warren RF: Fresh stored allografts for the treatment of
    osteochondral defects of the knee. J Bone Joint Surg Am
    2007;89(4):718-726.
    This prospective study found that fresh osteochondral
    allografts that were hypothermically stored between 17
    and 42 days were effective in the short term both structurally and functionally in reconstructing symptomatic
    chondral and osteochondral lesions of the knee.

    64.

    Zaslav K, Cole B, Brewster R, et al; STAR Study Principal Investigators: A prospective study of autologous
    chondrocyte implantation in patients with failed prior
    treatment for articular cartilage defect of the knee: Results of the Study of the Treatment of Articular Repair
    (STAR) clinical trial. Am J Sports Med 2009;37(1):4255.
    This prospective study found that patients with moderate to large chondral lesions with failed prior cartilage
    treatments can expect sustained and clinically meaning-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 35: Soft-Tissue Injuries About the Knee

    tralateral patellofemoral instability. Routine repair of


    the torn medial stabilizing soft tissues is not advocated
    for the treatment of acute patellar dislocation in children and adolescents.

    ful improvement in pain and function after ACI. The


    subsequent surgical procedure rate observed in this
    study (49% overall; 40% related to autologous chondrocyte implantation) appears higher than generally reported after autologous chondrocyte implantation.
    65.

    67.

    Christiansen SE, Jakobsen BW, Lund B, Lind M: Isolated repair of the medial patellofemoral ligament in
    primary dislocation of the patella: A prospective randomized study. Arthroscopy 2008;24(8):881-887.
    This randomized controlled trial found that delayed primary repair of the MPFL by use of an anchor-based reattachment to the adductor tubercle without vastus medialis obliquus repair after primary patella dislocation
    does not reduce the risk of redislocation nor does it produce any significantly better subjective functional outcome based on the Kujala knee score. Only the specific
    subjective patella stability score was improved by MPFL
    repair compared with conservative treatment.
    Palmu S, Kallio PE, Donell ST, Helenius I, Nietosvaara
    Y: Acute patellar dislocation in children and adolescents: A randomized clinical trial. J Bone Joint Surg Am
    2008;90(3):463-470.
    This randomized controlled trial found that long-term
    subjective and functional results after acute patellar dislocation are satisfactory in most patients. Initial surgical
    repair of the medial structures combined with lateral release did not improve the long-term outcome, despite
    the very high rate of recurrent instability. A positive
    family history is a risk factor for recurrence and for con-

    2011 American Academy of Orthopaedic Surgeons

    68.

    Sillanp PJ, Mattila VM, Menp H, Kiuru M, Visuri


    T, Pihlajamki H: Treatment with and without initial
    stabilizing surgery for primary traumatic patellar dislocation: A prospective randomized study. J Bone Joint
    Surg Am 2009;91(2):263-273.
    This randomized controlled trial found that in a study
    of young, mostly male adults with primary traumatic
    patellar dislocation, the rate of redislocation for those
    treated with surgical stabilization was significantly
    lower than the rate for those treated without surgical
    stabilization. However, no clear subjective benefits of
    initial stabilizing surgery were seen at the time of longterm follow-up.

    69.

    4: Lower Extremity

    66.

    Agneskirchner JD, Hurschler C, Wrann CD, Lobenhoffer P: The effects of valgus medial opening wedge
    high tibial osteotomy on articular cartilage pressure of
    the knee: A biomechanical study. Arthroscopy 2007;
    23(8):852-861.
    This cadaver study found that a medial opening wedge
    high tibial osteotomy (HTO) maintains high medial
    compartment pressure despite the fact that the loading
    axis has been shifted into valgus. Only after complete
    release of the distal fibers of the MCL does the opening
    wedge HTO produce a decompression of the medial
    joint compartment.

    Schttle PB, Schmeling A, Rosenstiel N, Weiler A: Radiographic landmarks for femoral tunnel placement in
    medial patellofemoral ligament reconstruction. Am J
    Sports Med 2007;35(5):801-804.
    This cadaver study found that a reproducible anatomic
    and radiographic point, 1 mm anterior to the posterior
    cortex extension line, 2.5 mm distal to the posterior origin of the medial femoral condyle, and proximal to the
    level of the posterior point of the Blumensaat line on a
    lateral radiograph with both posterior condyles projected in the same plane, shows the mean femoral MPFL
    center.

    70.

    Koter S, Pakvis D, van Loon CJ, van Kampen A:


    Trochlear osteotomy for patellar instability: Satisfactory
    minimum 2-year results in patients with dysplasia of the
    trochlea. Knee Surg Sports Traumatol Arthrosc 2007;
    15(3):228-232.
    This retrospective review found that anterior femoral
    osteotomy of the lateral condyle appears to be a satisfactory and safe method for treating patients with patellofemoral joint instability caused by trochlear dysplasia.

    Orthopaedic Knowledge Update 10

    467

    Chapter 36

    Knee Reconstruction and


    Replacement
    Raymond H. Kim, MD

    Bryan D. Springer, MD

    Douglas A. Dennis, MD

    Introduction

    Clinical Evaluation

    History and Physical Examination


    The clinical evaluation of the patient with a painful
    knee begins with a thorough history and physical examination. The history includes the duration of symptoms, previous trauma, and any prior surgeries on the
    affected extremity. In addition, any medical conditions
    that may affect the limb such as rheumatoid arthritis,
    childhood musculoskeletal conditions (such as Blount
    disease), or blood dyscrasias (sickle cell anemia) should
    be ascertained. The location of the pain along with the
    exacerbating activities may be an important indicator
    of the underlying pathology. It is important to remem-

    Dr. Kim or an immediate family member is a member of


    a speakers bureau or has made paid presentations on
    behalf of DePuy, A Johnson & Johnson Company. Dr.
    Springer or an immediate family member is a member
    of a speakers bureau or has made paid presentations
    on behalf of DePuy, A Johnson & Johnson Company and
    serves as a paid consultant to Stryker Convatec. Dr. Dennis or an immediate family member has received royalties from DePuy, A Johnson & Johnson Company and Innomed; is a member of a speakers bureau or has made
    paid presentations on behalf of DePuy, A Johnson &
    Johnson Company; serves as a paid consultant to DePuy,
    A Johnson & Johnson Company; has received research or
    institutional support from DePuy, A Johnson & Johnson
    Company; and serves as a board member, owner, officer,
    or committee member of the American Academy of Orthopaedic Surgeons, the Hip Society, and the Knee Society.

    2011 American Academy of Orthopaedic Surgeons

    4: Lower Extremity

    Arthritic conditions of the knee remain one of the most


    common reasons for disability. With the aging population, the number of patients with arthritis is expected
    to reach 67 million Americans by the year 2030.1 Demographic projections estimate a 673% increase in the
    number of total knee arthroplasties (TKAs) and a
    601% increase in revision TKAs by the year 2030.2

    ber that referred pain from both the lumbar spine as


    well as the ipsilateral hip may also present as knee pain.
    Anterior knee pain that is exacerbated with squatting
    or stair climbing may indicate patellofemoral involvement. Pain located at the joint line associated with mechanical symptoms may indicate meniscal pathology.
    Additionally, it is important to assess the impact of the
    patients pain and disability on quality of life.
    The physical examination should begin with an evaluation of gait, including assessment of antalgia, stride
    length, and muscle weakness (Trendelenburg gait).
    Overall standing limb alignment (varus or valgus)
    should be noted along with the contribution of this
    alignment from the hip, knee, and foot. To rule out referred pain, the contribution of the spine and hip as
    part of the examination should be assessed. The knee
    examination should always include a comparison with
    the opposite side and any discrepancy noted. Range of
    motion, patellar alignment (Q angle), and joint line tenderness should be noted. Tenderness over soft-tissue
    structures such as pes anserine bursae, patellar tendon,
    or iliotibial band should also be evaluated. Ligamentous stability should be tested with varus stress (fibular
    collateral ligament), valgus stress (medial collateral ligament), anteriorly with the Lachman or anterior
    drawer test (anterior cruciate ligament), or posteriorly
    with the posterior drawer test (posterior cruciate ligament).

    Radiographic Evaluation
    A proper evaluation of the knee begins with plain radiographs. Standard radiographs should include standing AP, lateral, and Merchant views. It is important
    that these views be obtained with the patient in a standing position; otherwise; the amount of joint space narrowing and deformity may be minimized (Figure 1, A).
    These radiographs should be evaluated for bone quality, alignment, and joint space narrowing. Additional
    plain radiographs may be indicated when standard
    films are equivocal or to further assess pathology. A
    45 PA flexion view is useful to evaluate the posterior
    aspect of the medial compartment. Stress radiographs
    may be obtained to assess ligamentous instability or as
    an indirect measure of cartilage thickness or deformity
    correction in the medial or lateral compartment in patients with arthritic knees (Figure 1, B). MRI provides a

    Orthopaedic Knowledge Update 10

    469

    Section 4: Lower Extremity

    detailed evaluation of soft-tissue structures, including


    tendons, ligaments, meniscus, articular cartilage, and
    bone marrow. Newer delayed gadolinium-enhanced
    MRI of cartilage (dGEMRIC) allows for detailed evaluation of articular cartilage and associated lesions.3

    Nonsurgical Treatment
    Nonsurgical treatment is generally indicated for patients with knee pain. Initial management may include
    the use of analgesics such as acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs), ice, activity modification, and physical therapy.4 In December
    2008, the American Academy of Orthopaedic Surgeons
    (AAOS) released the clinical practice guidelines for the
    treatment of osteoarthritis of the knee5 based on the
    best available scientific evidence. Table 1 summarizes
    these guidelines for the nonsurgical management of osteoarthritis.

    4: Lower Extremity

    Joint-Preserving Procedures

    Arthroscopic Dbridement

    Figure 1

    A, Standing weight-bearing AP radiograph


    demonstrating medial compartment narrowing.
    B, Stress radiograph demonstrating passive
    correction of varus deformity.

    Controversy exists over whether arthroscopy for degenerative knee arthritis provides palliative relief.6-8 The
    authors of one study conducted a prospective, randomized study comparing arthroscopic lavage, dbridement, and a sham procedure; no significant therapeutic
    benefit was shown.6 Careful assessment of the study design, however, revealed poor preoperative disease classification with inadequate radiographic assessment, and
    concerns with patient selection criteria and selection
    bias.9 In another study, long-term results of patients undergoing arthroscopic knee dbridement in the context
    of degenerative arthritis were reviewed. Sixty-seven percent of patients at a mean 13.2 years postoperatively
    had not undergone arthroplasty, and satisfaction scores
    rating the success of the arthroscopic procedure was
    8.6 on a scale of 0 to 10.10 In a prospective study done

    Table 1

    AAOS Clinical Practice Guideline on the Treatment of Osteoarthritis of the Knee


    Treatment

    Recommendation

    Level of Evidence

    Self-management and education programs

    Yes

    II B

    Promotion of self-care

    Yes

    IV C

    Weight loss with diet and exercise

    Yes

    IA

    Low-impact exercise

    Yes

    IA

    Patellar taping

    Yes

    II B

    NSAIDs or acetaminophen

    Yes

    II B

    Intra-articular cortisone injection

    Yes

    II B

    Heel wedges

    No

    II B

    Glucosamine and/or chondroitin sulfate

    No

    IA
    I and II B

    Needle lavage of joint

    No

    Medial or lateral unloader braces

    Inconclusive

    Accupuncture therapy

    Inconclusive

    Intra-articular hyaluronic acid injection

    Inconclusive

    (Adapted from American Academy of Orthopaedic Surgeons: Clinical Practice Guideline on the Treatment of Osteoarthritis (OA) of the Knee. Rosemont, IL, American
    Academy of Orthopaedic Surgeons, December 2008.)

    470

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 36: Knee Reconstruction and Replacement

    on patients older than 50 years, surgical (partial meniscectomy, dbridement of loose articular cartilage, and
    loose body removal) and nonsurgical treatment of limited degenerative knee arthritis were compared.11 At
    follow-up of 1 to 3 years, 75% of the group that had
    surgery obtained symptomatic improvement, compared
    to 16% of the nonsurgical group.

    Proximal Tibial Osteotomy

    Total Knee Arthroplasty


    TKA is an effective procedure that has been shown to
    relieve pain and restore function to most patients with
    advanced arthritis of the knee, and is indicated for
    these patients when nonsurgical measures have failed.
    Multiple studies have demonstrated excellent outcomes
    for TKA. In one study, a 98.1% survival rate at 14
    years was observed for a cemented posterior cruciate
    substituting (PS) TKA design.15 Similar excellent survivorship of 96.8% at 15 years for a modular cemented

    2011 American Academy of Orthopaedic Surgeons

    Disease Variables Affecting Outcome


    Diabetes
    Following surgery, patients with diabetes have been
    shown to have a statistically significant increased risk
    of pneumonia, stroke, and blood transfusion compared
    to nondiabetic patients.17 In addition to systemic complications, patients with poorly controlled diabetes
    have an increased likelihood of superficial and deep
    periprosthetic infections.18 Measures should be taken to
    ensure adequate control of blood glucose before surgery (Hgb A1C) and appropriate management in the
    postoperative period.
    Obesity
    Obese patients have a higher incidence of osteoarthritis
    and tend to be a younger cohort of patients requiring
    TKA. The clinical and mechanical survival of TKA in
    obese patients, however, has been shown to be comparable to that of a nonobese population.19 Superficial
    and deep periprosthetic infection following TKA in the
    obese population remains a concern. Studies in the literature indicate a sixfold to eightfold increase in the incidence of superficial and deep infection in patients
    with a body mass index above 35.20,21 There are no
    data to suggest that obese patients tend to lose weight
    or increase activity level after successful TKA.22

    4: Lower Extremity

    Proximal tibial osteotomy remains a reasonable option


    for a particular subset of patients. Patients younger
    than 55 to 60 years with medial compartment degenerative arthritis associated with malalignment, or malalignment in conjunction with ligamentous reconstruction,
    meniscal
    transplantation,
    or
    cartilage
    transplantation may obtain pain relief and functional
    improvement with a proximal tibial osteotomy. Contraindications for proximal tibial osteotomy include
    diffuse knee pain, patellofemoral pain, instability, previous meniscectomy or arthrosis in the lateral compartment, inflammatory disease, obesity (1.3 times ideal
    body weight), and unrealistic patient expectations.
    Proximal tibial osteotomy can be performed with either a medial opening wedge or a lateral closing wedge
    technique. Advantages of the opening wedge technique
    include avoidance of the proximal tibiofibular joint, anterior compartment, and peroneal nerve; and better control of multiplanar deformity correction. Disadvantages
    include the need for bone grafting, slower progression
    to union compared to the closing wedge technique, and
    limitations to mild to moderate corrections. A closing
    wedge provides the advantages of allowing accelerated
    weight bearing postoperatively and no required bone
    grafting. Disadvantages include violation of the tibiofibular joint and alteration of patellar height.
    Most clinical studies reviewing proximal tibial osteotomy results reveal modest clinical outcomes. One
    study revealed a 57% satisfactory outcome with 15year follow-up.12 According to another study, there was
    a 75% rate of survival free of failure with 10-year
    follow-up, with failure defined as arthroplasty.13 In a
    review of 106 high tibial valgus osteotomies, improved
    survivorship was noted with careful selection of patients younger than 50 years who also had preoperative
    flexion greater than 120.14 Properly performed proximal tibial osteotomy yields satisfactory clinical results
    with appropriate patient selection.

    PS TKA with mechanical failure as an end point has


    been noted.16

    Systemic Risk Factors for Infection


    In addition to obesity and diabetes, several other systemic factors increase a patients risk for deep periprosthetic infection following TKA,23 such as rheumatoid
    arthritis and chronic steroid use. The contribution of
    disease-modifying drugs used to treat inflammatory arthritis remains uncertain. These drugs that alter the immune system may affect wound healing and increase
    the risk for development of infection. No set guidelines
    are available regarding the discontinuation of these
    drugs before surgery or resumption after surgery.

    Surgical Technique
    Because malalignment and instability are two common
    causes of TKA failure, careful attention to surgical
    technique is critical to optimize clinical outcome. Key
    principles include achieving adequate exposure while
    respecting the soft tissues, restoration of the mechanical
    alignment, and proper balancing of the soft tissues.
    Despite significant enthusiasm for minimally invasive TKA, there are no data that show improved longterm clinical results with minimally invasive surgical
    exposures. The short-term benefits of improved function, less pain, and better cosmetic appearance of incisions should be tempered by data that demonstrate
    increased complication risks due to inadequate exposure.24 The ability to adequately visualize component
    positioning, alignment, and soft-tissue balancing should
    never be compromised by a limited exposure.
    Restoration of the mechanical axis can be achieved

    Orthopaedic Knowledge Update 10

    471

    Section 4: Lower Extremity

    4: Lower Extremity

    Figure 2

    Use of a spacer block to determine symmetry of


    ligament tensioning.

    using contemporary instrumentation to make the appropriate distal femoral and proximal tibial cuts. Intramedullary referencing is commonly used for the distal femoral cut, whereas extramedullary jigs are more
    commonly used for the proximal tibial cut. Once the
    distal femur and proximal tibia are resected, attention
    can then be turned to ligament balancing in extension.
    A titrated release of soft tissues may be performed on
    the medial or lateral side of the knee to accommodate
    for a fixed varus or valgus deformity, respectively. Use
    of spacer blocks or tensioning devices is helpful to determine symmetry of ligament tension (Figure 2).
    The method of determining femoral component rotation remains controversial. The measured resection
    technique references one of several axes defined by
    bony landmarks on the femur: the posterior condylar
    axis, the transepicondylar axis, or the AP axis. Because
    of anatomic variations in the osseous anatomy, advocates of the gap-balancing method reference the tibial
    cut surface to establish the femoral component rotation
    with the use of a flexion gaptensioning device.

    Design Issues
    PS Compared With Cruciate-Retaining TKA
    Advantages of using a PS design include ease of technique, minimization of tibial resection, restoration of
    knee kinematics, improved motion, potential reduction
    in polyethylene wear due to ability to use a more conforming bearing surface, and ease of deformity correction. Disadvantages include potential post wear caused
    by post impingement, fixation stresses due to post constraint, removal of intercondylar bone stock, and patellar clunk or crepitus complications. Specific indications
    for the use of a PS design over a cruciate-retaining (CR)
    design include severe deformity, severe flexion contracture, preoperative ankylosis of the knees, previous patellectomy, and revision of a TKA. When comparing
    CR to PS designs, a meta-analysis that reviewed eight
    randomized controlled trials noted no differences in
    function, patient satisfaction, and survivorship.25 However, 8.1 higher range of motion was noted for the PS
    group compared to the CR group (P = 0.01).
    472

    Orthopaedic Knowledge Update 10

    Mobile-Bearing Design
    Mobile-bearing TKA designs offer the advantage of allowing increased implant conformity and contact area
    without dramatically increasing stresses transmitted to
    the fixation interface. The incorporation of polyethylene bearing mobility, such as in a rotating platform
    TKA design, allows rotation through the tibial traypolyethylene articulation and effectively minimizes the
    transfer of torsional stresses to the fixation interface
    that have been associated with fixed-bearing TKA implants. This is supported by the excellent long-term
    clinical results with minimal loosening reported in numerous studies of mobile-bearing TKA. The 9- to 12year results of the Low Contact Stress (LCS) rotating
    platform design (DePuy, Warsaw, IN) were evaluated;
    100% survivorship was reported.26 Survivorship of the
    cementless LCS rotating platform system with loosening as the end point was determined to be 99.4% at 20
    years.27 Various studies evaluating primary TKA using
    the rotating platform system reported no evidence of
    radiographic loosening, even at 20-year radiographic
    follow-up; revision TKA reportedly was required in up
    to 0.2% of patients because of aseptic loosening.26,27

    Patellar Resurfacing
    Patellar resurfacing has remained a source of controversy with varying trends across countries. Advantages
    of patellar resurfacing in TKA include reduced anterior
    knee pain, removal of articular cartilage antigens in
    rheumatoid arthritis patients, decreased reoperation
    rates, and functional improvement with stair climbing.
    Disadvantages include extensor mechanism complications (rupture, patellar osteonecrosis, patellar fracture),
    component failure (polyethylene wear, aseptic loosening, osteolysis), and mechanical complications (overstuffing the patellofemoral compartment limiting flexion, patellar clunk). The authors of one study
    performed a meta-analysis of 14 studies and observed a
    higher incidence of anterior knee pain and an 8.7% incidence of secondary resurfacing in nonresurfaced
    knees.28 In a meta-analysis of 10 randomized controlled
    trials, a 40% reduction in anterior knee pain and a
    48% lower reoperation rate in the resurfacing group
    were noted.29 In contrast, a 2007 study reviewed 32 patients who underwent bilateral TKA and were randomized to have the first knee resurfaced or nonresurfaced
    and the second knee received the opposite treatment.
    With minimum follow-up of 10 years, no difference in
    range of motion, Knee Society clinical scores, satisfaction, revision rates, or anterior knee pain was observed.30 The differing reported results mirror the lack
    of consensus within the arthroplasty community regarding patellar resurfacing.

    Computer-Assisted Surgery and


    Patient-Specific Instruments
    Recent technology has sought to improve the accuracy
    and precision of component alignment and position.
    Based on intraoperative registered data, computerassisted surgery allows the surgeon to understand the

    2011 American Academy of Orthopaedic Surgeons

    Chapter 36: Knee Reconstruction and Replacement

    High-Flexion Designs
    A popular trend in TKA design has been the advent of
    high-flexion knees. The designs by multiple companies permit greater flexion without increasing polyethylene contact stresses at high flexion. Despite the hope
    that the high-flexion designs would improve motion,
    studies demonstrate no significant difference in motion
    between standard and high-flexion prostheses. A metaanalysis of high-flexion TKAs reviewed 9 studies that
    included 399 TKAs.36 Although five studies reported
    greater motion, the methodology of these studies was
    criticized for inadequate blinding, flawed patient selection, and short follow-up. It was concluded that there
    was inadequate evidence for improved motion or function with high-flexion designs. Several recent studies
    also revealed no significant differences between motion
    comparing high-flexion with standard knee designs.37,38

    2011 American Academy of Orthopaedic Surgeons

    Unicompartmental Knee Arthroplasty


    Classic indications for unicompartmental knee arthroplasty (UKA) include isolated unicompartmental arthrosis in low-demand patients older than 60 years,
    weighing less than 82 kg (180 lb), with a range-ofmotion arc of greater than 90 and flexion contracture
    less than 5, and having a minimal deformity of less
    than 15 that is passively correctable.39 Controversy
    currently exists regarding specific contraindications related to age, presence of patellofemoral degenerative
    changes, anterior cruciate ligament deficiency, and obesity. Clinical results of both fixed-bearing and mobilebearing knees have demonstrated excellent long-term
    results. One study reviewed 49 knees with a minimum
    10-year follow-up using a fixed-bearing metal-backed
    modular tibial component, and a 98% 10-year survivorship was reported.40 Mobile-bearing UKAs have
    also demonstrated excellent clinical results. One study
    reviewed 439 knees, and a 93% 15-year survivorship
    using the Oxford knee (Biomet, Warsaw, IN), a mobilebearing UKA, was observed.41 Failure of UKA commonly occurs due to polyethylene wear, component
    loosening, and progression of arthritis. Revision procedures may be relatively straightforward with minimal
    complexity.42,43 However, if failure occurs because of
    collapse of the medial tibial plateau, revision is technically more demanding to address significant bony defects.44

    4: Lower Extremity

    three-dimensional morphology of the knee and its relative position to the overall alignment of the entire extremity. Bone cuts can be planned and checked with improved accuracy and precision compared to traditional
    instrumentation. Although multiple studies have demonstrated improved radiographic alignment and component positioning, no articles have suggested any improvement in the clinical outcome of patients
    undergoing TKA using computer navigation.
    Patient-specific instruments are similar in concept
    while allowing the surgeon to establish the desired
    component position and alignment based on preoperative imaging (MRI or CT). Two drastically different
    philosophies have been developed to custom fit TKA
    components. Anatomic shape fitting identifies kinematic axes, which can be defined by the articular surface of the femoral condyles based on an individual patients MRI, and templates the position of the femoral
    component using a single-radius TKA design. Custom
    jigs are then manufactured to allow the surgeon to
    carry out the planned bone resection. Critics of this
    technology have observed malalignment of the components, particularly the tibial component,31 whereas advocates describe its ease of application, the avoidance
    of ligament balancing, and a better functioning knee.32
    No data are available to discern the clinical differences
    in functional outcome.
    The alternative form of patient-specific instrumentation holds to the traditional principle that mechanical
    alignment is paramount. Intraoperative registration of
    the anatomic morphology of the knee allows the surgeon to position and align the components to restore
    the limb to a neutral mechanical axis. Multiple studies
    have confirmed the improved component position and
    alignment with fewer outliers while using computer
    navigation.33 Additional benefits include reduced blood
    loss,33reduced embolic phenomenon,34 and advantages
    in complex situations/conditions such as severe deformity, retained hardware, previous osteomyelitis, and
    obesity.35

    Patellofemoral Arthroplasty
    Patellofemoral arthroplasty is a surgical option for the
    treatment of isolated patellofemoral arthritis with variable success rates. Outcomes of early designs were
    complicated by patellar instability and mechanical
    catching.45,46 More recent designs have demonstrated
    improved clinical outcomes. A 95.8% 5-year survivorship was reported after a review of 109 patellofemoral
    arthroplasties.47 In a longer term series 66 patients were
    reviewed at an average follow-up of 16.2 years (range,
    12 to 20 years) and a 58% survivorship at 16 years was
    noted.48

    Infection in TKA
    Treatment of infection following TKA depends on timing of the infection, the condition of the patient, the
    fixation of the components, and the infecting organism.
    Acute infections (less than 3 weeks of symptom duration) can occur in the early postoperative period or secondary to hematogenous seeding. In these situations,
    open irrigation and dbridement with complete synovectomy and polyethylene exchange may be considered. A successful outcome is dependent on well-fixed
    and functioning components, the absence of immunocompromise, and a susceptible organism. Regardless of
    timing of the infection, the presence of drug-resistant
    organisms has a negative impact on the outcome of
    component retention.

    Orthopaedic Knowledge Update 10

    473

    Section 4: Lower Extremity

    For patients with chronic infections (present longer


    than 3 to 4 weeks), two-stage exchange arthroplasty
    has the highest rate of success with regard to eradication of infection (88% to 93% in most studies).49,50 The
    procedure consists of removal of all components, a
    thorough dbridement, and placement of a high-dose
    antibiotic cement spacer. Both articulating and static
    spacers have been used with success. Articulating spacers that allow for motion between surgeries may have a
    better functional outcome with technically easier exposure at the time of reimplantation.51 Following the initial resection arthroplasty, patients are generally treated
    with a course of intravenous antibiotics. The resolution
    of infection is based on clinical examination, trend in
    serologic markers, and joint aspiration.
    4: Lower Extremity

    Deep Venous Thrombosis and


    Pulmonary Embolism
    This topic is discussed in chapter 12. Please refer to the
    AAOS clinical practice guideline on pulmonary embolism. The guideline can be accessed at www.aaos.org/
    research/guidelines/guide.asp.

    Revision TKA

    Evaluation of the Patient With a Painful TKA


    Evaluation should proceed in a stepwise and systemic
    manner. A thorough history, physical examnation, radiographic evaluation, and appropriate ancillary testing
    should be used to evaluate the patient with a painful
    TKA. Whenever possible, old radiographs should be
    obtained and evaluated. Serial radiographic evaluation
    can provide clues to progression of radiolucencies that
    may indicate loosening and polyethylene wear and osteolysis. In most instances plain radiographs are sufficient to make or confirm the diagnosis. Other tests may
    include fluoroscopic views to assess the bone-implant
    interface to look for subtle lucencies, stress views to
    evaluate for instability, or CT to evaluate for femoral
    or tibial component malrotation.52 Metal suppression
    MRI techniques may be useful to evaluate the size and
    extent of osteolytic lesions that are not readily apparent
    on plain radiographs.53 Serologic tests and joint aspiration are important, cost-effective assessments to rule
    out infection in the patient with a painful TKA. No single serologic test is 100% sensitive or specific for the
    diagnosis of infection. When used in combination, the
    erythrocyte sedimentation rate and C-reactive protein
    level are useful screening tests in the initial evaluation
    of the patient with a painful TKA. Other serologic
    markers such as interleukin-6, tumor necrosis factor,
    and procalcitonin are being evaluated as other potential
    markers for infection.54 Joint aspiration should be performed in any patient with elevated serologic markers
    or when there is high clinical suspicion for infection. A
    synovial leukocyte count greater than 1,700 with a differential neutrophil count greater than 65% is considered diagnostic of deep periprosthetic infection.55
    474

    Orthopaedic Knowledge Update 10

    Surgical Management
    Adequate surgical exposure is essential for successful
    surgery in revision TKA. Exposure begins with the incision. The vascular anatomy of the knee must be understood by the surgeon. The blood supply to the anterior aspect of the knee is medially based, with the
    vessels traveling in the subcutaneous layer. A patient often may have multiple incisions about the knee from
    previous surgeries. It is generally advised to use the lateralmost incision to maintain the blood supply to the
    medial flap.
    The goal of the exposure in revision TKA is to allow
    easy access to the components and bony anatomy without jeopardizing the ligaments or extensor mechanism.
    Exposure should occur in a stepwise manner. Rarely is
    there a need to evert the patella during revision. Reestablishment of the medial and lateral gutters of the femur and the suprapatellar pouch along with an early
    lateral release will provide adequate exposure in most
    instances. A multitude of other exposure options exist
    that may be used in the difficult knee, including a quadriceps snip, V-Y turndown, and tibial tubercle osteotomy.

    Component Removal
    Component removal should be methodical and proceed
    in a stepwise fashion. The goal of component removal
    is to extract the components with minimal bone loss. In
    general, the polyethylene is removed first, followed by
    the femoral and tibial components. Meticulous technique is required to disrupt the bone-cement interface.
    Proper tools such as osteotomes and microsagittal saws
    can help to facilitate this process.

    Dealing With Bone Loss and


    Component Fixation
    Dealing with bone loss at the time of revision can be
    challenging. Options include cement augmentation for
    small defects, modular metal augments, and allografts.56 Tibial and femoral porous cones and sleeves
    are available to deal with segmental bone defects (Figure 3). These augments have highly porous surfaces
    that allow for rapid ingrowth in addition to providing
    mechanical support of the implants. Recent data at
    short-term follow-up show promising results with these
    materials.57,58 The patella may be retained in many
    cases if it is well fixed, has minimal wear, and a congruent tracking with the new implants. When the patella is
    removed, adequate bone should be available for reconstruction. In general, thickness below 12 mm increases
    the risk of patella fracture. If severe patellar bone loss is
    present, the patella may be left unresurfaced or augmented with bone graft or porous tantalum augmentation.59 A patellectomy is rarely indicated.
    In the revision setting, condylar bone loss on both
    the femur and tibia make these surfaces inadequate
    alone for support of the revision components. Stem fixation should be used to bypass defects and unload the
    deficient condylar bone. Both cemented and cementless
    press-fit stems can be used with success.60,61 Cementless

    2011 American Academy of Orthopaedic Surgeons

    Chapter 36: Knee Reconstruction and Replacement

    The demand for primary TKA is projected to grow by


    673% to 3.48 million procedures. The demand for knee
    revisions is expected to grow by 601% by the year
    2030.

    Metaphyseal sleeves are used in revision TKA to


    address metaphyseal bone deficiency.

    stems, when used, should engage the diaphysis of both


    the femur and tibia to allow for adequate fixation.

    Miller TT: MR imaging of the knee. Sports Med Arthrosc 2009;17(1):56-67.


    This article provides an excellent review of MRI of the
    knee, including the role of dGEMRIC imaging.

    4.

    Richmond J, Hunter D, Irrgang J, et al; American Academy of Orthopaedic Surgeons: Treatment of osteoarthritis of the knee (nonarthroplasty). J Am Acad Orthop
    Surg 2009;17(9):591-600.
    This article provides clinical guidlelines for less invasive
    treatments than knee arthroplasty for symptomatic knee
    osteoarthritis.

    5.

    American Academy of Orthopaedic Surgeons Clinical


    Practice Guideline on the Treatment of Osteoarthritis of
    the Knee. American Academy of Orthopaedic Surgeons
    (AAOS), Rosemont, Illinois. 2008. http://www.aaos.org/
    research/guidelines/GuidelineOAKnee.asp
    This clinical practice guideline is published on the Website of the AAOS (www.aaos.org). It provides a comprehensive review of the literature and guidelines for the nonsurgical and nonarthroplastic treatment of knee arthritis.

    6.

    Moseley JB, OMalley K, Petersen NJ, et al: A controlled trial of arthroscopic surgery for osteoarthritis of
    the knee. N Engl J Med 2002;347(2):81-88.

    7.

    Kirkley A, Birmingham TB, Litchfield RB, et al: A randomized trial of arthroscopic surgery for osteoarthritis
    of the knee. N Engl J Med 2008;359(11):1097-1107.
    A randomized controlled study comparing arthroscopic
    lavage and debridement with optimized physical and
    medical therapy to physical and medical therapy alone
    for patients with moderate to severe knee osteoarthritis
    demonstrated no additional benefit with arthroscopic
    surgery. Level of evidence: I.

    8.

    Marx RG: Arthroscopic surgery for osteoarthritis of the


    knee? N Engl J Med 2008;359(11):1169-1170.
    This is an editorial in response to the study by Kirkley et
    al stating that although knee osteoarthritis is not an indication for arthroscopic surgery, it is not a contraindication for arthroscopic surgery in specific situations
    such as a symptomatic meniscal tear.

    9.

    Johnson LL: A controlled trial of arthroscopic surgery


    for osteoarthritis of the knee. Arthroscopy 2002;18(7):
    683-687.

    10.

    McGinley BJ, Cushner FD, Scott WN: Debridement arthroscopy: 10-year followup. Clin Orthop Relat Res
    1999;367(367):190-194.

    11.

    Merchan EC, Galindo E: Arthroscope-guided surgery


    versus nonoperative treatment for limited degenerative
    osteoarthritis of the femorotibial joint in patients over
    50 years of age: A prospective comparative study. Arthroscopy 1993;9(6):663-667.

    Constraint in Revision TKA


    Constraint in revision TKA should be viewed as a spectrum from standard posterior stabilized to hinged arthroplasty. In most revision settings with proper component position and ligament balancing, a standard
    posterior stabilized insert can be used. Constraint is indicated when there is collateral ligament compromise
    or the inability to obtain proper flexion and extension
    balance. Results of constrained TKA in the revision setting have demonstrated excellent survivorship.62 A
    hinged prosthesis is indicated in patients with global instability, a deficient extensor mechanism, or severe
    bone loss from fracture, tumor, or multiple surgeries.

    Annotated References
    1.

    Hootman JM, Helmick CG: Projections of US prevalence of arthritis and associated activity limitations. Arthritis Rheum 2006;54(1):226-229.

    2.

    Kurtz S, Ong K, Lau E, Mowat F, Halpern M: Projections of primary and revision hip and knee arthroplasty
    in the United States from 2005 to 2030. J Bone Joint
    Surg Am 2007;89(4):780-785.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    Figure 3

    3.

    475

    4: Lower Extremity

    Section 4: Lower Extremity

    12.

    Aglietti P, Buzzi R, Vena LM, Baldini A, Mondaini A:


    High tibial valgus osteotomy for medial gonarthrosis: A
    10- to 21-year study. J Knee Surg 2003;16(1):21-26.

    13.

    Coventry MB, Ilstrup DM, Wallrichs SL: Proximal tibial


    osteotomy: A critical long-term study of eighty-seven
    cases. J Bone Joint Surg Am 1993;75(2):196-201.

    14.

    Naudie D, Bourne RB, Rorabeck CH, Bourne TJ: Survivorship of the high tibial valgus osteotomy: A 10- to
    -22-year followup study. Clin Orthop Relat Res 1999;
    367:18-27.

    15.

    Colizza WA, Insall JN, Scuderi GR: The posterior stabilized total knee prosthesis: Assessment of polyethylene
    damage and osteolysis after a ten-year-minimum followup. J Bone Joint Surg Am 1995;77(11):1713-1720.

    16.

    Lachiewicz PF, Soileau ES: Fifteen-year survival and osteolysis associated with a modular posterior stabilized
    knee replacement: A concise follow-up of a previous report. J Bone Joint Surg Am 2009;91(6):1419-1423.
    This is a follow-up study of a previous report on a consecutive series of patients with a modular posterior stabilized TKA. With reoperation for mechanical failure as
    the end point, 15-year survival rate was 96.8%. Level of
    evidence: IV.

    17.

    Marchant MH Jr, Viens NA, Cook C, Vail TP, Bolognesi MP: The impact of glycemic control and diabetes
    mellitus on perioperative outcomes after total joint arthroplasty. J Bone Joint Surg Am 2009;91(7):16211629.
    The goal of the present study was to determine whether
    the quality of preoperative glycemic control affected the
    prevalence of in-hospital perioperative complications
    following lower extremity total joint arthroplasty.

    18.

    Yang K, Yeo SJ, Lee BP, Lo NN: Total knee arthroplasty


    in diabetic patients: A study of 109 consecutive cases.
    J Arthroplasty 2001;16(1):102-106.

    19.

    Krushell RJ, Fingeroth RJ: Primary total knee arthroplasty in morbidly obese patients: A 5- to 14-year
    follow-up study. J Arthroplasty 2007;22(6, suppl 2):7780.
    This retrospective study examined the results of 39
    TKAs in morbidly obese patients with 5- to 14-year
    follow-up compared with a case-controlled group of
    nonobese patients. Although there was a somewhat
    higher rate of minor wound complications, suboptimal
    alignment, and late revision (5%) in the morbidly obese
    group compared with the case-controlled group overall,
    the problems in morbidly obese patients have been relatively few thus far. The substantial improvement in
    scores and high rate of patient satisfaction (85%) suggests that TKA should continue to be offered to morbidly obese patients. Level of evidence: III.

    20.

    476

    Namba RS, Paxton L, Fithian DC, Stone ML: Obesity


    and perioperative morbidity in total hip and total knee
    arthroplasty patients. J Arthroplasty 2005;20(7, suppl
    3):46-50.

    Orthopaedic Knowledge Update 10

    21.

    Rajgopal V, Bourne RB, Chesworth BM, MacDonald


    SJ, McCalden RW, Rorabeck CH: The impact of morbid obesity on patient outcomes after total knee arthroplasty. J Arthroplasty 2008;23(6):795-800.
    Five hundred fifty patients who underwent primary
    TKA between 1987 and 2004 with a primary diagnosis
    of osteoarthritis and 1-year outcome data (Western Ontario and McMaster Osteoarthritis Index [WOMAC])
    were evaluated. Patients were stratified into body mass
    index categories based on the World Health Organization classification of obesity. Although 1-year outcomes
    were worse for morbidly obese patients (P < 0.05), they
    showed greater improvement in function compared with
    nonmorbidly obese patients. Morbid obesity does not
    affect 1-year outcomes in patients who have had a TKA.
    Level of evidence: IV.

    22.

    Lachiewicz AM, Lachiewicz PF: Weight and activity


    change in overweight and obese patients after primary
    total knee arthroplasty. J Arthroplasty 2008;23(1):3340.
    A prospective study of changes in mean weight, body
    mass index (BMI), and physical activity over 2 years in
    188 consecutive overweight or obese patients. Weight,
    BMI, and physical activity, evaluated using the Lower
    Extremity Activity Scale (LEAS), were assessed preoperatively and at 1 and 2 years. At 2 years, no significant
    weight change was found (P = 0.80), but BMI increased
    by 0.46 kg/m2 (P = 0.049). The LEAS score increased
    from preoperatively to 2 years (P < 0.001). Preoperative
    LEAS score was not associated with weight or BMI at 2
    years. This finding has implications for patient expectations and preoperative counseling. Level of evidence: IV.

    23.

    Jmsen E, Huhtala H, Puolakka T, Moilanen T: Risk


    factors for infection after knee arthroplasty: A registerbased analysis of 43,149 cases. J Bone Joint Surg Am
    2009;91(1):38-47.
    The purpose of the present study was to determine the
    risk factors for infection following primary and revision
    TKA in a large register-based series. There was an increased risk of deep postoperative infection in male patients and in patients with rheumatoid arthritis or a
    fracture around the knee as the underlying diagnosis for
    TKA. The results of the present study suggest that the
    infection rate is similar after partial revision and complete revision TKA. Combining intravenous antibiotic
    prophylaxis with antibiotic-impregnated cement seems
    advisable in revision arthroplasty. Level of evidence: III.

    24.

    Dalury DF, Dennis DA: Mini-incision total knee arthroplasty can increase risk of component malalignment.
    Clin Orthop Relat Res 2005;440:77-81.

    25.

    Jacobs WC, Clement DJ, Wymenga AB: Retention versus removal of the posterior cruciate ligament in total
    knee replacement: A systematic literature review within
    the Cochrane framework. Acta Orthop 2005;76(6):757768.

    26.

    Callaghan JJ, ORourke MR, Iossi MF, et al: Cemented


    rotating-platform total knee replacement: A concise
    follow-up, at a minimum of fifteen years, of a previous
    report. J Bone Joint Surg Am 2005;87(9):1995-1998.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 36: Knee Reconstruction and Replacement

    Buechel FF Sr: Long-term followup after mobile-bearing


    total knee replacement. Clin Orthop Relat Res 2002;
    404(404):40-50.

    28.

    Parvizi J, Rapuri VR, Saleh KJ, Kuskowski MA, Sharkey PF, Mont MA: Failure to resurface the patella during total knee arthroplasty may result in more knee pain
    and secondary surgery. Clin Orthop Relat Res 2005;
    438:191-196.

    29.

    Pakos EE, Ntzani EE, Trikalinos TA: Patellar resurfacing in total knee arthroplasty: A meta-analysis. J Bone
    Joint Surg Am 2005;87(7):1438-1445.

    30.

    Burnett RS, Boone JL, McCarthy KP, Rosenzweig S,


    Barrack RL: A prospective randomized clinical trial of
    patellar resurfacing and nonresurfacing in bilateral
    TKA. Clin Orthop Relat Res 2007;464:65-72.
    A randomized trial was performed to study the outcomes of patella resurfacing versus nonresurfacing in
    patients undergoing bilateral TKA. No differences were
    noted with regard to range of motion, Knee Society
    Clinical Rating Score, satisfaction, revision rates, or anterior knee pain. Level of evidence: I.

    31.

    Klatt BA, Goyal N, Austin MS, Hozack WJ: Custom-fit


    total knee arthroplasty (OtisKnee) results in malalignment. J Arthroplasty 2008;23(1):26-29.
    A case series of four patients who underwent TKA with
    the OtisKnee system resulted in malalignment of the
    components more than 3 off of a neutral mechanical
    axis. Level of evidence: IV.

    32.

    33.

    Howell SM, Kuznik K, Hull ML, Siston RA: Results of


    an initial experience with custom-fit positioning total
    knee arthroplasty in a series of 48 patients. Orthopedics
    2008;31(9):857-863.
    A series of TKAs utilizing a custom-fit positioning system in 48 patients demonstrated rapid return to function, restoration of motion, restoration of alignment,
    and high patient satisfaction. Level of evidence: IV.
    Chauhan SK, Scott RG, Breidahl W, Beaver RJ:
    Computer-assisted knee arthroplasty versus a conventional jig-based technique: A randomised, prospective
    trial. J Bone Joint Surg Br 2004;86(3):372-377.

    34.

    Kalairajah Y, Cossey AJ, Verrall GM, Ludbrook G,


    Spriggins AJ: Are systemic emboli reduced in computerassisted knee surgery? A prospective, randomised, clinical trial. J Bone Joint Surg Br 2006;88(2):198-202.

    35.

    Fehring TK, Mason JB, Moskal J, Pollock DC, Mann J,


    Williams VJ: When computer-assisted knee replacement
    is the best alternative. Clin Orthop Relat Res 2006;452:
    132-136.

    36.

    Murphy M, Journeaux S, Russell T: High-flexion total


    knee arthroplasty: A systematic review. Int Orthop
    2009;33(4):887-893.
    This systematic literature review identified nine studies
    representing 399 high-flexion TKAs in 370 patients. It
    was concluded that there was not sufficient evidence

    2011 American Academy of Orthopaedic Surgeons

    demonstrating improved range of motion or functional


    outcome with high-flexion designs.
    37.

    Kim YH, Choi Y, Kim JS: Range of motion of standard


    and high-flexion posterior cruciate-retaining total knee
    prostheses: A prospective randomized study. J Bone
    Joint Surg Am 2009;91(8):1874-1881.
    This randomized study compared standard cruciateretaining total knees to high-flexion posterior cruciateretaining total knees in bilateral TKA patients and found
    no significant differences in range of motion or any clinical or radiographic parameters. Level of evidence: I.

    38.

    Seon JK, Park SJ, Lee KB, Yoon TR, Kozanek M, Song
    EK: Range of motion in total knee arthroplasty: A prospective comparison of high-flexion and standard
    cruciate-retaining designs. J Bone Joint Surg Am 2009;
    91(3):672-679.
    The range of motion was found to be similar in 50 knees
    treated with a standard cruciate-retaining TKA compared
    to 50 knees treated with a high-flexion cruciate-retaining
    design under both nonweight-bearing and weightbearing conditions. Level of evidence: II.

    39.

    Kozinn SC, Scott R: Unicondylar knee arthroplasty.


    J Bone Joint Surg Am 1989;71(1):145-150.

    40.

    Berger RA, Meneghini RM, Jacobs JJ, et al: Results of


    unicompartmental knee arthroplasty at a minimum of
    ten years of follow-up. J Bone Joint Surg Am 2005;
    87(5):999-1006.

    41.

    Price AJ, Waite JC, Svard U: Long-term clinical results


    of the medial Oxford unicompartmental knee arthroplasty. Clin Orthop Relat Res 2005;435:171-180.

    42.

    McAuley JP, Engh GA, Ammeen DJ: Revision of failed


    unicompartmental knee arthroplasty. Clin Orthop Relat
    Res 2001;392(392):279-282.

    43.

    Levine WN, Ozuna RM, Scott RD, Thornhill TS: Conversion of failed modern unicompartmental arthroplasty
    to total knee arthroplasty. J Arthroplasty 1996;11(7):
    797-801.

    44.

    Aleto TJ, Berend ME, Ritter MA, Faris PM, Meneghini


    RM: Early failure of unicompartmental knee arthroplasty leading to revision. J Arthroplasty 2008;23(2):
    159-163.
    This retrospective review of 32 consecutive revisions
    from UKA to TKA revealed the predominant mode of
    failure was medial tibial collapse (47%). Those knees
    that failed by medial tibial collapse required more complex reconstructions due to more significant bone defects. Level of evidence: IV.

    45.

    Krajca-Radcliffe JB, Coker TP: Patellofemoral arthroplasty: A 2- to 18-year followup study. Clin Orthop
    Relat Res 1996;330(330):143-151.

    46.

    Lonner JH: Patellofemoral arthroplasty: Pros, cons, and


    design considerations. Clin Orthop Relat Res 2004;
    428(428):158-165.

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    27.

    477

    Section 4: Lower Extremity

    4: Lower Extremity

    47.

    Ackroyd CE, Newman JH, Evans R, Eldridge JD, Joslin


    CC: The Avon patellofemoral arthroplasty: Five-year
    survivorship and functional results. J Bone Joint Surg Br
    2007;89(3):310-315.

    56.

    Bush JL, Wilson JB, Vail TP: Management of bone loss


    in revision total knee arthroplasty. Clin Orthop Relat
    Res 2006;452:186-192.

    A retrospective review of 109 consecutive patellofemoral arthroplasties in 85 patients with a minimum


    follow-up of 5 years revealed a 95.8% 5-year survivorship with revision as the end point. The main complication was radiographic progression of arthritis in other
    compartments in 28% of patients. Level of evidence: IV.

    57.

    Radnay CS, Scuderi GR: Management of bone loss:


    Augments, cones, offset stems. Clin Orthop Relat Res
    2006;446:83-92.

    58.

    Meneghini RM, Lewallen DG, Hanssen AD: Use of porous tantalum metaphyseal cones for severe tibial bone
    loss during revision total knee replacement: Surgical
    technique. J Bone Joint Surg Am 2009;91(suppl 2 pt 1):
    131-138.
    The purpose of this study was to determine the initial
    results obtained with a unique reconstructive implant,
    the porous tantalum metaphyseal cone, designed as an
    alternative treatment of severe tibial bone loss following
    TKA. The porous tantalum metaphyseal tibial cones effectively provided structural support for the tibial implants in this series. The potential for long-term biologic
    fixation may provide durability for these tibial reconstructions. Level of evidence: IV.

    59.

    Nelson CL, Lonner JH, Lahiji A, Kim J, Lotke PA: Use


    of a trabecular metal patella for marked patella bone
    loss during revision total knee arthroplasty. J Arthroplasty 2003;18(7, suppl 1):37-41.

    60.

    Wood GC, Naudie DD, MacDonald SJ, McCalden RW,


    Bourne RB: Results of press-fit stems in revision knee
    arthroplasties. Clin Orthop Relat Res 2009;467(3):810817.
    The aim of this study was to report the authors experience with press-fit uncemented stems and metaphyseal
    cement fixation in a selected series of patients undergoing revision TKA. One hundred twenty-seven patients
    (135 knees) who underwent revision TKA using a pressfit technique (press-fit diaphyseal fixation and cemented
    metaphyseal fixation) were reviewed. Minimum
    follow-up was 2 years. Survivorship analysis revealed a
    probability of survival free of revision for aseptic loosening of 98% at 12 years. Survivorship of press-fit
    stems for revision TKA is comparable to reported survivorship of cemented stem revision TKA.

    61.

    Whaley AL, Trousdale RT, Rand JA, Hanssen AD: Cemented long-stem revision total knee arthroplasty. J Arthroplasty 2003;18(5):592-599.

    62.

    Kim YH, Kim JS: Revision total knee arthroplasty with


    use of a constrained condylar knee prosthesis. J Bone
    Joint Surg Am 2009;91(6):1440-1447.
    A retrospective review of a case series of revision TKA
    with a constrained condylar prosthesis by a single surgeon was performed to ascertain the role of this prosthesis and to determine whether it provided satisfactory
    results. Kaplan-Meier survivorship analysis, with revision or radiographic failure as the end point, revealed
    that the 10-year rate of survival of the components was
    96% (95% confidence interval, 94% to 100%). Revision TKA with use of a constrained condylar knee prosthesis had reproducible clinical success, but a complication rate of up to 9% can be expected at intermediateterm follow-up.

    48.

    Argenson JN, Flecher X, Parratte S, Aubaniac JM: Patellofemoral arthroplasty: An update. Clin Orthop Relat
    Res 2005;440:50-53.

    49.

    Hofmann AA, Goldberg T, Tanner AM, Kurtin SM:


    Treatment of infected total knee arthroplasty using an
    articulating spacer: 2- to 12-year experience. Clin Orthop Relat Res 2005;430:125-131.

    50.

    Haleem AA, Berry DJ, Hanssen AD: Mid-term to longterm followup of two-stage reimplantation for infected
    total knee arthroplasty. Clin Orthop Relat Res 2004;
    428:35-39.

    51.

    Freeman MG, Fehring TK, Odum SM, Fehring K, Griffin WL, Mason JB: Functional advantage of articulating
    versus static spacers in 2-stage revision for total knee arthroplasty infection. J Arthroplasty 2007;22(8):11161121.
    Seventy-six two-stage reimplantation procedures met
    the study inclusion criteria. There were 28 static spacers
    and 48 articulating spacers. The eradication rate was
    94.7% in the articulating group compared with 92.1%
    in the static group (P = 0.7). There were no significant
    differences in postoperative Knee Society pain scores.
    There were 28 (58%) good to excellent function scores
    in the articulating group and 10 (36%) in the static
    group (P = 0.05). Interim use of an articulating spacer
    maintains excellent infection eradication rates and may
    improve function over the use of static spacers.

    478

    52.

    Berger RA, Crossett LS, Jacobs JJ, Rubash HE: Malrotation causing patellofemoral complications after total
    knee arthroplasty. Clin Orthop Relat Res 1998;356:
    144-153.

    53.

    Vessely MB, Frick MA, Oakes D, Wenger DE, Berry DJ:


    Magnetic resonance imaging with metal suppression for
    evaluation of periprosthetic osteolysis after total knee
    arthroplasty. J Arthroplasty 2006;21(6):826-831.

    54.

    Di Cesare PE, Chang E, Preston CF, Liu CJ: Serum


    interleukin-6 as a marker of periprosthetic infection following total hip and knee arthroplasty. J Bone Joint
    Surg Am 2005;87(9):1921-1927.

    55.

    Trampuz A, Hanssen AD, Osmon DR, Mandrekar J,


    Steckelberg JM, Patel R: Synovial fluid leukocyte count
    and differential for the diagnosis of prosthetic knee infection. Am J Med 2004;117(8):556-562.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 37

    Tibial Shaft Fractures


    Brett D. Crist, MD

    Rahul Banerjee, MD

    Introduction

    Clinical Examination
    Tibia fractures may occur from direct or indirect
    trauma. Simple falls, twisting injuries, and sports injuries result in low-energy closed tibia fractures. Highenergy mechanisms of injury such as motor vehicle or
    motorcycle crashes frequently cause more severe, or
    open, tibia fractures.
    Patients with tibia fractures present with leg pain,
    swelling, deformity, and an inability to bear weight.
    Evaluation should begin with a primary survey and assessment of airway, breathing, and circulation. Details
    of the injury or accident, if available from the patient
    or emergency medical services, should be obtained to
    raise suspicion of associated injuries and/or risk of
    compartment syndrome.
    On physical examination, careful circumferential examination of the patients skin is necessary to assess for
    abrasions, ecchymosis, or open wounds. Gross defor-

    Dr. Crist has received research or institutional support


    from Synthes, KCI, Medtronic, and Pfizer. Dr. Banerjee or
    an immediate family member has received research or
    institutional support from Synthes, Smith & Nephew,
    Medtronic, Stryker, and Zimmer.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    Tibia fractures affect patients of all ages. Nonsurgical


    management is typically reserved for stable, low-energy
    fractures and requires close observation and immobilization. Unstable and high-energy fractures are typically
    managed surgically with either intramedullary nailing,
    external fixation (uniplanar and multiplanar), or plate
    fixation. Historically, surgically treated tibial shaft fractures have the benefits of faster functional return and
    lower risk of malunion. However, each surgical technique has its potential associated complications. Open
    tibial shaft fractures continue to be debilitating and
    problematic due to an increased risk of infection and
    nonunion and the need to address the associated bone
    and soft-tissue loss. Because multiple treatment options
    are available and each has advantages and disadvantages, surgeons must individualize their treatment strategy based on the patients injury, functional demands,
    and healing potential.

    mity of the extremity may be evident in the presence of


    displaced fractures. Careful neurovascular examination
    is imperative and should include documentation of motor function, sensory examination, and pulses distal to
    the injury. Examination of the ipsilateral hip, knee, and
    ankle is important to identify associated injuries.
    High-energy tibia fractures may present with concomitant vascular injuries. On examination, vascular
    injuries may manifest with signs such as diminished or
    absent pulses, decreased capillary refill, or gross bleeding. Suspected vascular compromise should prompt the
    surgeon to realign and splint the limb, and reassess the
    vascular status. In addition, if an associated vascular
    injury is suspected, ankle-brachial indices should be
    performed. Identification of vascular injury requires
    early vascular surgery consultation.
    Tibia fractures may present with associated compartment syndrome. Younger patients and patients
    with diaphyseal tibia fractures are more likely to develop compartment syndrome.1 Compartment syndrome occurs as a result of increased pressure within
    the limited space of the myofascial compartments of
    the leg. Ultimately, this increased pressure leads to vascular compromise. The anterior and deep posterior
    compartments are most susceptible to injury from associated compartment syndrome.
    Patients with tibia fractures and associated compartment syndrome may have severe pain, tense swelling of
    the leg, and pain with passive stretch of the ankle or
    toes. These so-called cardinal signs are often difficult
    to assess in patients with tibia fractures, as similar
    symptoms and signs may result from the fracture. Although the diagnosis of compartment syndrome is a
    clinical diagnosis, assessment may be aided by the measurement of intracompartmental pressures when the diagnosis is unclear or when the ability to obtain a physical examination is limited (such as in an obtunded or
    pediatric patient, or in the presence of neurologic impairment). If intracompartmental pressures are used,
    the difference between the patients diastolic blood
    pressure and the compartment pressure (delta P) should
    be calculated. Compartment pressures should not be
    measured after the induction of anesthesia because a
    spuriously low value for the diastolic blood pressure
    and a consequently high value for delta P may result.2
    Compartment syndrome is treated with fourcompartment fasciotomy of the affected leg. A delta P
    less than or equal to 30 mm Hg indicates the need for
    fasciotomy.3 It is imperative to verify release of all four
    479

    Section 4: Lower Extremity

    Table 2

    4: Lower Extremity

    Table 1

    Gustilo and Anderson Classification


    of Open Fractures

    Oestern and Tscherne Soft-Tissue Injury


    Classification of Closed Fractures

    Fracture
    Type

    Grade

    Characteristics

    Grade 0

    Minimal soft-tissue injury; typically associated


    with a simple fracture pattern secondary to an
    indirect force

    Grade 1

    Superficial abrasions or contusions apparent;


    may range from a mild to moderately severe
    fracture pattern

    Grade 2

    Include deep contaminated abrasions associated


    with localized skin or muscle contusion; severe
    fracture pattern and impending compartment
    syndrome

    Grade 3

    Extensive skin contusion or crush with significant


    underlying muscle damage, compartment
    syndrome, and severe fracture pattern

    Characteristics

    Type I

    Wounds less than 1 cm; minimal contamination


    and soft-tissue injury; simple fracture pattern

    Type II

    Wounds 1 to 10 cm; moderate comminution and


    contamination

    Type IIIA

    Minimal periosteal stripping and soft-tissue


    coverage required

    Type IIIB

    Significant periosteal stripping at the fracture


    site; soft-tissue coverage required

    Type IIIC

    Indicates an associated repairable vascular injury

    compartments because incomplete release may result in


    ongoing muscle necrosis and irreversible injury. The anterior compartment is most frequently incompletely released.4
    Radiographic examination of patients with suspected tibia fractures includes anteroposterior and lateral radiographs of the entire tibia, along with radiographs of the ipsilateral knee and the ankle to assess for
    associated injuries.
    Tibial shaft fractures are frequently associated with
    other musculoskeletal injuries. Intra-articular knee injuries (cruciate or collateral ligament injuries, meniscal
    tears, and cartilage injuries) are often unrecognized.
    Tibial shaft fractures may occur in conjunction with
    tibial plateau fractures or ankle fractures.5 There is a
    high association of spiral tibia fractures with isolated
    fractures of the posterior malleolus.6,7

    Classification
    The soft-tissue injury associated with tibial shaft fractures can be the main determinant of the patients outcome. For open fractures, the Gustilo and Anderson
    classification is typically used to communicate the
    amount of soft-tissue injury and fracture severity.8,9
    This system is mainly based on the size of the open
    wound, amount of contamination, and the fracture severity and is outlined in Table 1. This system has been
    used to determine antibiotic prophylaxis, surgical management strategies and the risk of complications such
    as infection and nonunion. The Oestern and Tscherne
    classification is used to classify the amount of softtissue injury severity associated with closed fractures in
    an effort to predict outcome and associated complications10 and is outlined in Table 2.
    Fracture classification has been used to compare patient populations from different clinical studies. The
    AO/Orthopaedic Trauma Association fracture classification is commonly used.11
    480

    Orthopaedic Knowledge Update 10

    Indications for Surgery


    Absolute indications for surgery include open fractures,
    the presence of concomitant vascular injuries or compartment syndrome, irreducible or unstable fractures,
    or failure of closed treatment. Relative indications for
    surgical treatment include fractures with concomitant
    intra-articular fractures that will require surgery, displaced fractures with an intact fibula, fractures with
    soft tissue injuries that require surgical management,
    the presence of multiple injuries, or fractures that require frequent monitoring of soft tissues that may be
    obscured in a cast.
    Nondisplaced, low-energy tibia fractures may be
    treated nonsurgically. Although no studies have defined
    the amount of displacement that precludes nonsurgical
    treatment, fractures with displacement of more than
    50% of the shaft, angulation greater than 5 to 10, rotation greater than 10, and greater than 1 cm of shortening may be best treated surgically.12

    Nonsurgical Treatment
    Nonsurgical treatment of tibial shaft fractures is best reserved for closed low-energy, isolated, nondisplaced, or
    minimally displaced fractures that may be reduced and
    immobilized effectively. Absence of an ipsilateral fibula
    fracture is a relative contraindication. Initial immobilization is best achieved with long leg splinting that allows for swelling. After reduction of swelling, the patients leg is placed into a new well-padded long leg cast.
    Physical examination should demonstrate decreased or
    minimal tenderness at the fracture site. The long leg cast
    is then replaced with a short leg patellar tendon bearing
    cast or a functional fracture brace; progressive weight
    bearing is initiated. The patellar tendon bearing cast or

    2011 American Academy of Orthopaedic Surgeons

    Chapter 37: Tibial Shaft Fractures

    functional brace may be discontinued when there is evidence of bridging callus on radiographs.
    Closed treatment with functional bracing has been
    shown to achieve high union rates with angulation and
    shortening that may be comparable to surgical treatment.12,13 With functional bracing, most fractures heal
    with less than 12 mm of shortening and less than 8 of
    angulation in either the frontal or sagittal plane. Although malunion and shortening are the primary associated complications, a small prospective randomized
    trial also revealed that patients undergoing nonsurgical
    treatment had a slower return to work, healing rate, return of knee, ankle, and hindfoot motion, and a higher
    rate of hindfoot stiffness.14 No study has commented
    on the risk of rotational malunion.

    External Fixation
    External fixation is a minimally invasive method of
    treatment that allows for relative stability of the fracture and can be used for either temporary or definitive
    management. With the success of other methods of
    treatment, however, external fixation is typically used
    for patients who cannot tolerate more extensive surgery
    because of medical or soft-tissue conditions, or osseous
    defect. Another relative indication may be a medullary
    canal too small for placement of an intramedullary nail.
    As a temporary form of fixation used during damage
    control techniques, uniplanar external fixation allows
    for relatively rapid application and stability of the extremity. It allows for easier soft-tissue evaluation and
    wound care, patient mobility, and typically more patient comfort than skeletal traction or splinting until
    definitive management can be performed. In patients
    with open fractures, this type of fixation allows for repeat dbridement of the bone ends during subsequent
    dbridements.
    Depending on the level of the tibial shaft fracture
    and any associated articular involvement, uniplanar external fixator pins should be placed in a near-far configuration on either side of the fracture to provide the
    most stable construct. Typically the pins are placed
    along the anteromedial surface of the tibia to avoid
    neurovascular or tendinous structures. If the fracture
    extends close to either the knee or ankle, caution
    should be used when placing pins to avoid penetrating
    the articular surface or joint capsule. For the knee, pins
    should be placed greater than 14 mm distal to the subchondral bone of the tibia.15 If there is any question
    about proximity to the joint or if there is articular fracture extension, joint-spanning external fixation should
    be performed.
    Because of the success of intramedullary nailing and
    patient dissatisfaction with long-term external fixator
    use, definitive uniplanar or circular external fixation
    for acute fractures is typically reserved for open tibia
    fractures that have significant soft-tissue injury or bone
    loss.

    2011 American Academy of Orthopaedic Surgeons

    Plate fixation of tibial shaft fractures may be achieved


    with either an open surgical approach with direct fracture visualization and reduction or by indirect reduction and minimally invasive percutaneous plating.
    Wound-healing problems and prominent hardware
    plague plate fixation of tibial shaft fractures; therefore,
    this technique is best reserved for specific indications
    such as tibial shaft fractures with ipsilateral articular
    fractures of the tibial plateau or pilon (Figure 1),
    periprosthetic fractures, open physes, too small of a
    medullary canal for an intramedullary nail, previous
    cruciate ligament reconstruction, fracture where external fixators are already present (Figure 1), or open fractures where the open fracture wound provides the surgical exposure.
    Open reduction and internal fixation may be achieved
    through three different surgical approaches. Anteromedial incisions and exposure of the fracture often results
    in wound-healing problems and prominent hardware;
    therefore, posteromedial or anterolateral exposure and
    plate application is preferred. Although open reduction
    and internal fixation is an alternative to intramedullary
    nailing, plating of tibial shaft fractures (particularly open
    fractures) is associated with higher rates of complications
    (19% to 30%) and worse outcomes.16
    Minimally invasive or percutaneous plating is another alternative. Medial or anteromedial plating using
    this technique is advantageous because of the subcutaneous location of the tibia; however, the use of medial
    plates may still result in symptomatic hardware, risk of
    wound breakdown, and saphenous vein and nerve injury.17 Anterolateral percutaneous plating allows for
    submuscular plate placement that decreases the risk of
    symptomatic hardware, but injury to the superficial
    peroneal nerve may occur during placement of distal
    screws.18,19 Regardless of the plate location, minimally
    invasive plating of the tibia must still follow the principles of open plating, including achieving optimal fracture reduction (alignment, length, and rotation) and
    promoting bone healing through compression for simple fracture patterns. For comminuted fractures, bridge
    plating techniques are used where indirect fracture reduction techniques are used to maintain length, overall
    alignment, and rotation. The area of fracture comminution is spanned using longer plates with screw fixation
    on either side of the zone of comminution in an effort
    to minimize disruption of the fracture blood supply.

    4: Lower Extremity

    Surgical Treatment

    Plate Fixation

    Intramedullary Nailing
    Intramedullary nailing continues to be the gold standard for treating displaced tibial shaft fractures. Despite this success, long-term follow-up shows that patients may have persistent sequelae after fracture
    healing. At 14 years, patients with isolated tibial shaft
    fractures have similar functional outcomes to population norms but approximately 73% continue to have
    moderate knee pain with activity, 42% have decreased
    ankle motion, and 35% have radiographic evidence of
    either knee or ankle arthrosis.20

    Orthopaedic Knowledge Update 10

    481

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 1

    A closed left tibial shaft fracture with ipsilateral fractures of the left tibial plateau (A) and left tibial pilon (B) is
    treated with initial plate fixation of the shaft fracture and spanning external fixation of the periarticular injuries
    with delayed open reduction and internal fixation of the plateau and pilon fractures after the soft-tissue injury
    resolved (C and D).

    Controversies that still exist with intramedullary nailing of tibia fractures include the high incidence of knee
    pain, the need for reaming, and managing proximal and
    distal metadiaphyseal fractures. Anterior knee pain is the
    most common complication associated with nailing of
    tibial shaft fractures, but no definitive reason exists for
    the up to 67% incidence.21 Iatrogenic injury during creation of the starting point and during nail insertion, nail
    prominence, quadriceps weakness, and use of a transpatellar tendon surgical approach have all been
    proposed.22-24 Relatively small prospective randomized
    controlled trials, including one with up to 8-year followup, have shown that there is no increased incidence with
    a transpatellar tendon approach.21,25 When discussing the
    risk of chronic anterior knee pain with patients, it is encouraging to note that knee pain is not usually severe and
    may continue to improve up to 8 years after surgery.22,25
    Although reaming is controversial, its benefits have
    long been thought to outweigh any disadvantages such
    as nonunion and incidence of secondary procedures.26
    The Study to Prospectively Evaluate Reamed Intramedullary Nails in Patients with Tibial Fractures (SPRINT)
    randomized 1,319 patients with open and closed tibia
    fractures to either reamed or unreamed nails and potentially challenged how substantial a difference reaming makes. At 1-year follow-up, closed fractures treated
    with reamed nails had a lower risk of autodynamization (locking bolt bending or breakage), but actual re482

    Orthopaedic Knowledge Update 10

    operation rates for bony union were not statistically


    different. There was no significant difference for open
    fractures. The authors believe that not much of a substantial effect of reaming was seen because of the
    studys rigorous design, including waiting 6 months before allowing reoperation for nonunionalthough this
    prerequisite was followed for only 55% of cases and
    equal in both reamed and unreamed groups.
    Proximal and distal metadiaphyseal tibia fractures
    can be very challenging to manage. Fractures with simple articular fracture extension can be addressed with
    simple lag screw fixation before the nailing procedure.
    Deforming forces created by the patellar tendon and iliotibial band have contributed to the incidence of
    malunion (up to 84%) of proximal metadiaphyseal
    tibia fractures.27 Both surgical techniques and nail designs have been modified to decrease the risk of
    malunion. Several authors have proposed technical
    modifications that include the semiextended position;28
    a starting point just medial to the lateral tibial spine
    and at the anterior margin of the articular surface and
    placing the guidewire parallel to the anterior cortex;29
    use of provisional fixation to maintain fracture reduction during nailing including an external fixator or
    femoral distractor,30 or a medial unicortical plate;29,31
    and blocking or Pller screws to narrow the potential
    path of the nail, which leads to improved reduction32
    (Figure 2). Nail designs with a more proximal bend33

    2011 American Academy of Orthopaedic Surgeons

    Chapter 37: Tibial Shaft Fractures

    4: Lower Extremity

    Figure 2

    Illustration showing the use of a posterior blocking screw (A) and a lateral blocking screw (B) to help maintain
    alignment of the tibia in both coronal and sagittal planes during nailing of a proximal-third tibia fracture. By
    keeping the nail against the medial (A) and anterior (B) cortices, deformity is prevented. (Reproduced with permission from Stannard J, Schmidt A, Kregor P: Surgical Treatment of Orthopaedic Trauma. New York, NY, Thieme Medical Publishers, 2007, pp 767-791.)

    and oblique locking bolt options have also minimized


    the risk of fracture malreduction during nail placement
    and improved biomechanical stability.
    Although the malunion rate is lower (up to 58%) in
    distal metadiaphyseal fractures,34 similar surgical technique modifications and nail design changes have led to
    improved alignment and biomechanical stability. Technical tricks to improve alignment during intramedullary
    nailing include ensuring that the guidewire is centered
    in the distal tibia on all fluoroscopic views; open reduction and internal fixation of the ipsilateral fibula fracture; limited open reduction; fracture reduction with
    the use of percutaneous reduction forceps, joysticks,
    femoral distractor or external fixator (Figure 3); provisional fixation with unicortical plates; and use of
    blocking screws to create a pseudocortex to help direct
    the nail and improve biomechanical stability.30,35-38 Nail
    designs with locking bolts within 3 mm of the end of
    the nail, oblique locking bolt options, and modified
    locking bolts39 have improved fixation options and biomechanical stability for intramedullary nailing of distal
    tibia fractures.

    Plating Compared With Nailing of Proximal


    and Distal Metadiaphyseal Tibia Fractures
    The desire to decrease the incidence of malunion and
    the development of percutaneous plating techniques
    have led some surgeons to turn to plating of extraarticular proximal and distal metadiaphyseal fractures.
    A recent small retrospective cohort study comparing

    2011 American Academy of Orthopaedic Surgeons

    plating and nailing of proximal fractures revealed that


    apex anterior malreduction was twice as common in
    the nail group, additional surgical techniques for reduction were used substantially more often in the nail
    group, and hardware removal was three times more
    common in the plating group.40 A meta-analysis of
    treatment of extra-articular proximal tibia fractures
    (intramedullary nail, external fixator, plating) revealed
    that nailing was associated with a lower rate of infection and a higher incidence of malunion.41
    Distal tibia fractures are challenging to treat because
    of the short segment available for nail fixation; however, the risk of surgical wound breakdown and prominent hardware has contributed to resistance in using
    plate fixation. A retrospective review of 113 open and
    closed distal tibia fractures 4 to 11 cm proximal to the
    plafond that were either nailed (76) or plated (37) revealed that the nail group had a higher risk of delayed
    or nonunion (12% versus 2.7%), especially if the fibula
    was fixed, and malunion (29% versus 5.4%). Although
    there may be a higher risk of delayed or nonunion with
    ipsilateral fibula fracture fixation, the risk of postoperative loss of the initial tibial fracture reduction is lower.38 A systematic review of retrospective studies from
    1975-2005 of extra-articular distal tibia fractures revealed that there has been no prospective trial comparing nailing with plating of these fractures; although no
    conclusions can be made, the limited number of small
    case series show that nailing leads to a higher risk of
    nonunion and malunion.42

    Orthopaedic Knowledge Update 10

    483

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 3

    Open Tibia Fractures


    Open tibial shaft fractures are the most common significant open fracture. Treatment should consist of early
    antibiotic administration, coverage of the wound with
    a sterile but nontoxic dressing, tetanus prophylaxis,
    surgical dbridement, and stabilization of the fracture.
    Open fractures are described by the GustiloAnderson classification, which classifies wounds based
    on severity, size, contamination, and associated vascular injury. The classification is useful in determining
    choice of antibiotic treatment. However, final determination of the Gustilo-Anderson grade should be performed by the treating surgeon in the operating room.
    Early administration (within 3 hours of injury) of
    the appropriate antibiotics decreases the risk of infection following open fractures.43 For Gustilo-Anderson
    type 1 or 2 open fractures, patients are given a first- or
    second-generation cephalosporin to treat the causative
    infectious organisms, which are most frequently grampositive bacteria. For type 3 open fractures, the addition of an aminoglycoside is necessary to address gram484

    Orthopaedic Knowledge Update 10

    A, Radiograph of a distal one-third


    closed tibia and ipsilateral fibula fracture. B, A femoral distractor was used
    to provisionally reduce the tibia and
    fibula fractures. Radiographs showing
    percutaneous plating of the distal fibula were obtained to aid in reduction
    of the tibia. Reamed intramedullary
    nailing was then performed with a tibial nail with very distal locking bolt options. AP (C) and lateral (D) radiographs
    show restoration of length, rotation,
    and coronal and sagittal alignment.

    negative bacteria. With soil contamination, penicillin


    should be added to cover gram-positive anaerobes. Although the duration of antibiotic treatment following
    open fractures is also controversial because no benefit
    has been shown with prolonged antibiotic administration, 24 to 72 hours of antibiotic coverage has been
    recommended following initial surgical dbridement of
    the open fracture and 24 hours after each subsequent
    dbridement until the wound is closed.44
    The timing of surgical dbridement has recently been
    debated. The previously held dogma of early dbridement within 6 hours has been disproven by numerous
    studies.43,45,46 Currently, no level I evidence exists to direct timing of dbridement. However, open fractures
    should nonetheless be treated urgently and efficiently to
    optimize patient care.
    Skillful surgical dbridement remains the most important factor in the optimal treatment of open tibia fractures. All devitalized and contaminated tissue, including
    bone, should be sharply excised from the wound. Dbridement should proceed systematically, beginning with
    the skin and progressing to the bone. Depending on the

    2011 American Academy of Orthopaedic Surgeons

    Chapter 37: Tibial Shaft Fractures

    2011 American Academy of Orthopaedic Surgeons

    type C fractures).51 NPWT may decrease the need for


    rotational or free flap reconstructive surgeries for severe open wounds; if flap coverage is required, delaying
    definitive coverage beyond 7 days substantially increases the risk of infection.52,53

    Acceleration of Fracture Healing and


    Management of Osseous Defects
    Tibial shaft fractures are a targeted area for orthobiologics. Tibial nonunions and open fractures, especially
    with bone loss, can lead to significant morbidity and
    loss of function. Although several multicenter trials are
    ongoing to evaluate the effects of different orthobiologics on tibial shaft fractures, the only data from prospective trials (level I evidence) that are currently available
    involve recombinant human bone morphogenetic
    protein-2 (rhBMP-2) and rhBMP-7.
    In the United States, the only current Food and Drug
    Administration (FDA)approved use in acute fractures
    is for rhBMP-2 in open tibia fractures treated within 14
    days of injury. The BMP-2 Evaluation in Surgery for
    Tibial Trauma (BESTT) trial revealed that open tibia
    fractures treated with an intramedullary nail and 1.5
    mg/mL of rhBMP-2 on a collagen sponge implanted at
    the time of definitive closure required fewer secondary
    procedures and had a faster time to union and lower
    rates of nonunion and infection.54 Further subgroup
    analysis of types IIIA and IIIB open fractures treated
    with rhBMP-2 had fewer bone grafting procedures and
    secondary interventions and a lower infection rate.55
    For tibial nonunions, rhBMP-7 is FDA approved as
    a humanitarian device exemption. One study prospectively compared rhBMP-7 with autogenous bone grafting for tibial nonunions; results showed similar rates of
    clinical and radiographic union.56
    Managing osseous defects in open tibia fractures,
    nonunions, and infected fractures continues to be challenging. The use of rhBMP-2 for management of osseous defects has been evaluated in a small prospective
    randomized controlled trial.57 RhBMP-2 combined
    with allograft bone graft was compared with autogenous bone grafting alone in open and closed tibia fractures without signs of infection initially managed with
    either intramedullary nailing or external fixation. Fractures with 1- to 7-cm osseous defects and at least 50%
    circumferential bone loss were included. Both groups
    had similar union rates and need for secondary interventions. Although circular wire external fixation and
    bone transport has been successful in managing acute
    and chronic osseous defects,58 the use of a two-staged
    technique incorporating the use of an antibioticimpregnated cement spacer (which leads to development of a biologic membrane) in managing large osseous defects up to 25 cm in combination fixation and
    soft-tissue coverage procedures has been successful.59
    The role that bone stimulators may play in the management of acute fracture and nonunion management is
    still a topic for debate. Although some studies support
    the use of low-intensity ultrasound in acute fractures

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    severity of the injury and level of contamination, some


    open fractures may be managed with primary closure.
    However, this is best determined by the experience of the
    treating surgeon and routine primary closure should not
    be performed. In wounds with severe contamination, serial dbridements to reassess the wound and tissue viability after 48 to 72 hours may be beneficial.
    If primary closure is not chosen, wounds should be
    dressed and left undisturbed between dbridements.
    Negative pressure wound therapy (NPWT) may be useful in the management of these wounds. Antibioticimpregnated beads may also be placed in open fracture
    wounds. The concentration of local antibiotics
    achieved with antibiotic beads far exceeds that
    achieved with intravenous antibiotics.
    Stabilization of the open fracture is essential because
    it provides an optimal environment for soft-tissue healing and prevention of infection. Primary definitive stabilization with intramedullary nailing or plating may be
    performed depending on the severity of the injury and
    the level of contamination. Definitive fixation should
    only be performed when the open fracture bed, including the soft tissues, has been thoroughly dbrided and
    is clean and viable. Immediate nailing of open tibia
    fractures has been supported in up to type IIIB fractures
    using both reamed and unreamed nails. Plating of open
    fractures is associated with a higher rate of infection.47
    External fixation provides an excellent alternative to
    nailing or plating in the face of severe injury or contamination. External fixation may be followed by definitive
    treatment (intramedullary nail or plate) once soft tissues have recovered. Conversion to an intramedullary
    nail is best performed less than 2 weeks after application of the external fixator.48,49
    If primary wound closure is not possible, alternative
    means of soft-tissue coverage must be sought. NPWT
    may be useful in decreasing the size and depth of the
    wound that will ultimately require coverage. Splitthickness skin grafts may be used to cover skin defects
    over muscle or subcutaneous tissue. For coverage of
    bone, nerves, or blood vessels, flaps may be required.
    Acute shortening of the tibia during definitive fixation
    to allow for local soft-tissue coverage has been successful in small retrospective series. Depending on the
    amount of acute shortening, bone transport or subsequent lengthening can be done, typically using external
    fixation methods.50
    Flap coverage for open tibia fractures is determined
    by the severity and location of the wound. Proximal
    wounds are best covered with rotational gastrocnemius
    flaps. Wounds in the middle third of the tibia may be
    covered with a soleus flap. Distal defects are best covered with a sural island pedicle flap or free tissue transfer. Local rotational flaps are often compromised by the
    trauma that resulted in the open tibia fracture and are
    therefore suboptimal for soft-tissue coverage. The
    Lower Extremity Assessment Project study revealed
    that there is a higher rate of wound complications requiring reoperation when rotational flaps were used instead of free flaps in open fractures with more complex
    osseous injury (AO/Orthopaedic Trauma Association

    485

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 4

    AP and lateral radiographs showing treatment of a tibial shaft fracture. A, An open tibial shaft fracture initially
    treated with reamed intramedullary nailing that eventually became an infected nonunion.) A staged exchange
    nailing was performed with interval dbridement, external fixator placement, and culture-specific antibiotic therapy. B, Three months after exchange nailing, the fracture was healed and the patient was pain free.

    and nonunions60 and electromagnetic stimulation in


    nonunions,61 comparative studies without methodological flaws are required to truly support their use.

    Tibial Malunion
    Most tibial shaft malunions result from either nonsurgical management or technical errors in surgical management. Proximal and distal metadiaphyseal fractures
    treated surgically have historically had high rates of
    malunion. Surgically treated diaphyseal fractures have
    a much lower rate of malunion unless they are managed with external fixation.
    Without restoration of the mechanical axis,
    malunion of the tibial shaft affects both the ankle and
    knee and can lead to exacerbation of ligamentous instability, and progressive pain and arthritis. Although the
    definition of malunion varies in trials, retrospective trials have shown that greater than 5 to 10 of coronal
    or sagittal plane alignment, 10 of rotation, and 1 cm
    of shortening leads to poor outcomes.62 If malunions
    486

    Orthopaedic Knowledge Update 10

    are symptomatic, full-length weight-bearing lower extremity radiographs should be used to evaluate angular
    deformity and limb-length discrepancies. A CT scan
    may be helpful to evaluate rotational deformities. Corrective osteotomies and lengthening procedures may be
    performed to address symptomatic malunions.

    Tibial Nonunion
    Nonunion of tibial shaft fractures may occur as a result
    of the injury, patient factors such as smoking or medical comorbidities (for example, diabetes), or treatment.
    Historically, there has been an absence of a wellaccepted definition of a time frame for nonunion, but
    typically a fracture that has not healed at 6 months or
    shows no progressive healing for 3 consecutive months
    is considered a nonunion.
    Other patient factors that may increase the risk of
    nonunion are poor nutrition and a history of previous
    nonunion. Many patients with a nonunion have an underlying metabolic or endocrine disorder.63 Surgeon fac-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 37: Tibial Shaft Fractures

    partment syndrome. J Orthop Trauma 2007;21(2):99103.


    In this prospective cohort study, preoperative, intraoperative, and postoperative diastolic blood pressures (DBP)
    were measured in patients undergoing intramedullary
    nailing of the tibia. Preoperative DBP correlated with
    postoperative DBP, but intraoperative DBP was significantly lower (average, 18 mm Hg lower). Therefore, reliance of intraoperative DBP for measurement of delta P
    to determine compartment syndrome may result in a
    spuriously low value and therefore in a missed diagnosis
    of compartment syndrome. Level of evidence: II.
    3.

    McQueen MM, Court-Brown CM: Compartment monitoring in tibial fractures. The pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.

    4.

    Ritenour AE, Dorlac WC, Fang R, et al: Complications


    after fasciotomy revision and delayed compartment release in combat patients. J Trauma 2008;64(2, suppl):
    S153-S161, discussion S161-S162.
    Three hundred thirty-six combat casualties from the
    wars in Iraq and Afghanistan were retrospectively reviewed to evaluate outcomes and complications of fasciotomies. The anterior compartment of the lower leg
    was most commonly missed during surgical compartment release. Patients who underwent delayed fasciotomies had twice the rate of major amputation and a
    threefold higher mortality. Level of evidence: III.

    5.

    Stuermer EK, Stuermer KM: Tibial shaft fracture and


    ankle joint injury. J Orthop Trauma 2008;22(2):107112.
    Forty-three of 214 patients with tibia fracture (20.1%)
    were found to have associated ankle joint injury including distal fibula fractures, Maissoneuve injuries, syndesmotic injuries, posterior malleolus fractures, and medial
    malleolus fractures. Level of evidence: II.

    6.

    Hou Z, Zhang Q, Zhang Y, Li S, Pan J, Wu H: A occult


    and regular combination injury: The posterior malleolar
    fracture associated with spiral tibial shaft fracture.
    J Trauma 2009;66(5):1385-1390.
    A retrospective study of 28 of 288 tibial shaft fractures
    (9.7%) had ipsilateral posterior malleolar fractures
    (PMF). None of the PMFs were identified preoperatively
    and only 10 were identified intraoperatively. Nine of the
    fractures displaced postoperatively. Thirty-four additional tibial shaft fractures were evaluated prospectively
    with CT and MRI if plain films were negative for PMF.
    Thirty out of 34 PMFs were identified3 by plain film,
    23 by CT scan, and 4 by MRI. Level of evidence: III.

    7.

    Boraiah S, Gardner MJ, Helfet DL, Lorich DG: High association of posterior malleolus fractures with spiral
    distal tibial fractures. Clin Orthop Relat Res 2008;
    466(7):1692-1698.
    Sixty-two patients with distal third tibial shaft fractures
    were retrospectively evaluated for posterior malleolar
    fractures. Twenty-four of 62 patients (39%) had associated posterior malleolus fractures. A protocol was instituted, after two fractures were missed, to obtain CT of
    the ankle on all patients with distal third tibial shaft

    Annotated References
    1.

    2.

    Park S, Ahn J, Gee AO, Kuntz AF, Esterhai JL: Compartment syndrome in tibial fractures. J Orthop Trauma
    2009;23(7):514-518.
    Four hundred fourteen patients with tibial fractures
    were retrospectively reviewed for the incidence and risk
    factors for compartment syndrome. The rate of compartment syndrome was highest for diaphyseal tibia
    fractures (8.1%). Patients who developed compartment
    syndrome were of younger age (average 27.5 years) than
    those who did not (average 39 years). Level of evidence:
    III.
    Kakar S, Firoozabadi R, McKean J, Tornetta P III: Diastolic blood pressure in patients with tibia fractures under anaesthesia: Implications for the diagnosis of com-

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    tors that may increase the risk of nonunion include distraction of the fracture site while performing
    intramedullary nailing or plating, excessive soft-tissue
    stripping with open reduction and internal fixation, or
    excessive reaming resulting in injury to the endosteal
    blood supply. In the case of open fractures, the injury
    itself may result in ultimate nonunion.
    The SPRINT trial demonstrated a lower risk of reoperation with reamed intramedullary nailing, particularly in closed tibial shaft fractures, but most of these
    events were related to autodynamization and not reoperation for bony union.26 In addition, in patients with a
    suspected nonunion, delaying reoperation for 6 months
    decreased the need for the procedure.
    Preoperative evaluation for tibial nonunions should
    include a history of the original injury and the subsequent treatment. Radiographs and a CT scan are useful
    to categorize the nature and extent of the nonunion.
    The potential for infection should be addressed by obtaining a white blood cell count with differential, erythrocyte sedimentation rate, and C-reactive protein levels.
    Screening for metabolic and endocrine disorders is also
    helpful.
    Tibial shaft nonunions, like most nonunions, may be
    broadly categorized into hypertrophic or atrophic nonunions. Hypertrophic nonunions may be treated with
    improved surgical stabilization of the fracture, whereas
    atrophic nonunions will also require biologic enhancement (through bone graft or orthobiologics) to achieve
    union.
    Tibial shaft nonunions may be treated by a variety
    of surgical methods. Exchange nailing for previously
    nailed tibial shaft fractures is effective (Figure 4). Open
    treatment with posterolateral or direct lateral (central)
    bone grafting may also achieve union.64 Ring (Ilizarov)
    external fixation provides a powerful method to treat
    nonunions but is often poorly tolerated by patients. Infected nonunions may be best treated with ring
    (Ilizarov) external fixation. Tissue culture from the
    nonunion site should be sent at the time of surgical
    treatment to determine if prolonged antibiotic therapy
    is required.

    487

    Section 4: Lower Extremity

    plating dissection revealed that the saphenous vein and


    nerve were most at risk with placement of the distal
    metaphyseal screws when inserted percutaneously.

    4: Lower Extremity

    fractures. Twenty-three patients were evaluated prospectively and 11 (48%) had posterior malleolar fractures
    and none were missed. Level of evidence: II.
    8.

    Gustilo RB, Anderson JT: Prevention of infection in the


    treatment of one thousand and twenty-five open fractures of long bones: Retrospective and prospective analyses. J Bone Joint Surg Am 1976;58(4):453-458.

    9.

    Gustilo RB, Mendoza RM, Williams DN: Problems in


    the management of type III (severe) open fractures: A
    new classification of type III open fractures. J Trauma
    1984;24(8):742-746.

    10.

    Tscherne HG: Fractures Associated with Soft Tissue Injuries. New York, NY: Springer-Verlag; 1984.

    11.

    Marsh JL, Slongo TF, Agel J, et al: Fracture and dislocation classification compendium - 2007: Orthopaedic
    Trauma Association classification, database and outcomes committee. J Orthop Trauma 2007;21(10, suppl): S1-S133.
    This supplement presents the OTA Fracture and Dislocation Classification, the revisions made since it was
    originally published in 1996, and reviews the fracture
    classification literature published since 1996.

    12.

    Sarmiento A, Latta LL: 450 closed fractures of the distal


    third of the tibia treated with a functional brace. Clin
    Orthop Relat Res 2004;428:261-271.

    13.

    Sarmiento A, Latta LL: Fractures of the middle third of


    the tibia treated with a functional brace. Clin Orthop
    Relat Res 2008;466(12):3108-3115.
    In a retrospective review, 434 closed fractures of the
    middle third of the tibial shaft were evaluated for angular deformity and final shortening. Ninety-seven percent
    of fractures healed with 8 or less of angulation in the
    mediolateral plane. Nonunion occurred in 0.9% of fractures. Mean final shortening of these fractures was 4.3
    mm. Level of evidence: IV

    14.

    488

    Hooper GJ, Keddell RG, Penny ID: Conservative management or closed nailing for tibial shaft fractures: A
    randomised prospective trial. J Bone Joint Surg Br
    1991;73(1):83-85.

    15.

    Reid JS, Van Slyke MA, Moulton MJ, Mann TA: Safe
    placement of proximal tibial transfixation wires with respect to intracapsular penetration. J Orthop Trauma
    2001;15(1):10-17.

    16.

    Bilat C, Leutenegger A, Redi T: Osteosynthesis of 245


    tibial shaft fractures: Early and late complications. Injury 1994;25(6):349-358.

    17.

    Ozsoy MH, Tuccar E, Demiryurek D, et al: Minimally


    invasive plating of the distal tibia: Do we really sacrifice
    saphenous vein and nerve? A cadaver study. J Orthop
    Trauma 2009;23(2):132-138.
    Minimally invasive plating of the distal tibia was performed on cadavers using two different precontoured
    medial distal tibia plates using a medial approach. Post-

    Orthopaedic Knowledge Update 10

    18.

    Pichler W, Grechenig W, Tesch NP, Weinberg AM, Heidari N, Clement H: The risk of iatrogenic injury to the
    deep peroneal nerve in minimally invasive osteosynthesis of the tibia with the Less Invasive Stabilisation System: A cadaver study. J Bone Joint Surg Br 2009;91(3):
    385-387.
    Minimally invasive plating of the tibia was performed
    on 18 cadavers using the Less Invasive Stabilization System through an anterolateral approach. The deep peroneal nerve was at most risk between the 11th and 13th
    holes. Because the nerve was in contact with the plate in
    all specimens, the authors recommend either not using a
    longer than 10-hole plate, or using a larger distal approach to ensure that the nerve is not injured.

    19.

    Cole PA, Zlowodzki M, Kregor PJ: Less Invasive Stabilization System (LISS) for fractures of the proximal tibia: Indications, surgical technique and preliminary results of the UMC Clinical Trial. Injury 2003;34(Suppl
    1):A16-A29.

    20.

    Lefaivre KA, Guy P, Chan H, Blachut PA: Long-term


    follow-up of tibial shaft fractures treated with intramedullary nailing. J Orthop Trauma 2008;22(8):525-529.
    A prospective cohort study was conducted in 56 patients who underwent locked intramedullary nailing for
    isolated tibial shaft fractures. Median follow-up was 14
    years. Mean normalized Short Form-36 scores demonstrated that these patients functional outcomes were
    comparable to referenced population norms. However,
    many patients experienced significant sequelae, including persistent knee pain (73.2%), swelling (33.9%), and
    restricted ankle range of motion (42.4%). Level of evidence: II.

    21.

    Vist O, Toivanen J, Paakkala T, Jrvel T, Kannus P,


    Jrvinen M: Anterior knee pain after intramedullary
    nailing of a tibial shaft fracture: An ultrasound study of
    the patellar tendons of 36 patients. J Orthop Trauma
    2005;19(5):311-316.

    22.

    Vist O, Toivanen J, Kannus P, Jrvinen M: Anterior


    knee pain and thigh muscle strength after intramedullary nailing of a tibial shaft fracture: An 8-year
    follow-up of 28 consecutive cases. J Orthop Trauma
    2007;21(3):165-171.
    Forty patients who underwent nailing for a tibial shaft
    fracture were evaluated at an average of 3.2 years.
    Twenty-eight of these patients were evaluated at 8 years.
    Anterior knee pain symptoms resolved in these patients
    between 3 to 8 years after surgery. Patients with persistent anterior knee pain at 8 years had significantly
    weaker quadriceps strength and lower functional knee
    scores. Level of evidence: IV.

    23.

    Orfaly R, Keating JE, OBrien PJ: Knee pain after tibial


    nailing: Does the entry point matter? J Bone Joint Surg
    Br 1995;77(6):976-977.

    24.

    Keating JF, Orfaly R, OBrien PJ: Knee pain after tibial


    nailing. J Orthop Trauma 1997;11(1):10-13.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 37: Tibial Shaft Fractures

    25.

    26.

    Bhandari M, Guyatt G, Tornetta P III, et al; Study to


    Prospectively Evaluate Reamed Intramedullary Nails in
    Patients with Tibial Fractures Investigators: Randomized trial of reamed and unreamed intramedullary nailing of tibial shaft fractures. J Bone Joint Surg Am 2008;
    90(12):2567-2578.
    A multicenter, blinded prospective randomized trial of
    1,226 patients with tibial shaft fractures was performed.
    Six hundred twenty-two patients were randomized to
    reamed intramedullary nailing and 604 patients were
    randomized to unreamed nailing. Reoperation for nonunion before 6 months was disallowed. At 1-year
    follow-up, only 57 patients (4.6%) required reoperation
    for nonunion. In patients with closed fractures, 45 of
    416 patients (11%) in the reamed nailing group and 68
    of 410 patients (17%) in the unreamed nailing group
    experienced a primary outcome event (relative risk,
    0.67; 95% confidence interval, 0.47 to 0.96; P = 0.03),
    suggesting that there may be an advantage to reamed intramedullary nailing in these patients due to less risk of
    screw breakage (autodynamization). In patients with
    open fractures, there was no difference between the two
    groups. Level of evidence: I.
    Cannada LK, Anglen JO, Archdeacon MT, Herscovici
    D Jr, Ostrum RF: Avoiding complications in the care of
    fractures of the tibia. J Bone Joint Surg Am 2008;90(8):
    1760-1768.
    The authors discuss surgical techniques to avoid complications in acute fracture care as well as the treatment of
    infections and nonunions.

    28.

    Tornetta P III, Collins E: Semiextended position of intramedullary nailing of the proximal tibia. Clin Orthop
    Relat Res 1996;328:185-189.

    29.

    Nork SE, Barei DP, Schildhauer TA, et al: Intramedullary nailing of proximal quarter tibial fractures. J Orthop Trauma 2006;20(8):523-528.

    30.

    Wysocki RW, Kapotas JS, Virkus WW: Intramedullary


    nailing of proximal and distal one-third tibial shaft fractures with intraoperative two-pin external fixation.
    J Trauma 2009;66(4):1135-1139.
    This retrospective case series reviewed the use of a twopin external fixator (traveling traction) used as a reduction aid during intramedullary nailing of proximal (15)
    and distal (27) extra-articular tibia fractures. Fourteen

    2011 American Academy of Orthopaedic Surgeons

    of 15 proximal and 25 of 27 distal tibia fractures healed


    with less than 5 of angulation and less than 1 cm of
    shortening. Level of evidence: IV.
    31.

    Archdeacon MT, Wyrick JD: Reduction plating for provisional fracture fixation. J Orthop Trauma 2006;20(3):
    206-211.

    32.

    Ricci WM, OBoyle M, Borrelli J, Bellabarba C, Sanders


    R: Fractures of the proximal third of the tibial shaft
    treated with intramedullary nails and blocking screws.
    J Orthop Trauma 2001;15(4):264-270.

    33.

    Henley MB, Meier M, Tencer AF: Influences of some


    design parameters on the biomechanics of the unreamed
    tibial intramedullary nail. J Orthop Trauma 1993;7(4):
    311-319.

    34.

    Vallier HA, Le TT, Bedi A: Radiographic and clinical


    comparisons of distal tibia shaft fractures (4 to 11 cm
    proximal to the plafond): Plating versus intramedullary
    nailing. J Orthop Trauma 2008;22(5):307-311.
    In this retrospective review, 111 patients with 113 distal
    tibial fractures (4 to 11 cm proximal to the tibial plafond) were treated either with an intramedullary nail
    (76) or a medial plate (37). Nine patients had delayed
    union or nonunion after nailing. One patient had a nonunion after plating. Nonunion was more common if the
    fibula was fixed at the time of tibial fixation. Angular
    malunion greater than or equal to 5 occurred in 22 patients with nails and 2 with plates. Delayed union,
    malunion, and secondary procedures were more frequent after nailing. Level of evidence: III.

    35.

    Krettek C, Miclau T, Schandelmaier P, Stephan C,


    Mhlmann U, Tscherne H: The mechanical effect of
    blocking screws (Pller screws) in stabilizing tibia
    fractures with short proximal or distal fragments after
    insertion of small-diameter intramedullary nails. J Orthop Trauma 1999;13(8):550-553.

    36.

    Tang P, Gates C, Hawes J, Vogt M, Prayson MJ: Does


    open reduction increase the chance of infection during
    intramedullary nailing of closed tibial shaft fractures?
    J Orthop Trauma 2006;20(5):317-322.

    37.

    Nork SE, Schwartz AK, Agel J, Holt SK, Schrick JL,


    Winquist RA: Intramedullary nailing of distal metaphyseal tibial fractures. J Bone Joint Surg Am 2005;
    87(6):1213-1221.

    38.

    Egol KA, Weisz R, Hiebert R, Tejwani NC, Koval KJ,


    Sanders RW: Does fibular plating improve alignment after intramedullary nailing of distal metaphyseal tibia
    fractures? J Orthop Trauma 2006;20(2):94-103.

    39.

    Horn J, Linke B, Hntzsch D, Gueorquiev B, Schwieger


    K: Angle stable interlocking screws improve construct
    stability of intramedullary nailing of distal tibia fractures: A biomechanical study. Injury 2009;40(7):767771.
    A cadaver distal third extra-articular gap model was
    created to compare conventional distal locking bolts

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    27.

    Vist O, Toivanen J, Kannus P, Jrvinen M: Anterior


    knee pain after intramedullary nailing of fractures of the
    tibial shaft: An eight-year follow-up of a prospective,
    randomized study comparing two different nailinsertion techniques. J Trauma 2008;64(6):1511-1516.
    A prospective randomized study comparing transtendinous versus paratendinous incision techniques for intramedullary nailing was conducted with 42 patients
    followed for an average of 3 years; 28 patients (14 paratendinous, 14 transtendinous) were reexamined at an
    average of 8 years after surgery. Four patients (29%) of
    each group reported anterior knee pain at 8-year followup. Lysholm, Tegner, and Iowa knee scores demonstrated no difference in the two groups. Level of evidence: II.

    489

    Section 4: Lower Extremity

    and angle stable locking bolts. Axial stiffness, maximal load to failure, and interfragmentary motion were
    measured. The angle stable group was significantly
    stiffer and had significantly less interfragmentary motion compared to the conventional group.

    4: Lower Extremity

    40.

    41.

    Bhandari M, Audige L, Ellis T, Hanson B; EvidenceBased Orthopaedic Trauma Working Group: Operative
    treatment of extra-articular proximal tibial fractures.
    J Orthop Trauma 2003;17(8):591-595.

    50.

    El-Rosasy MA: Acute shortening and re-lengthening in


    the management of bone and soft-tissue loss in complicated fractures of the tibia. J Bone Joint Surg Br 2007;
    89(1):80-88.
    Ten type III open tibia fractures within 6 weeks of injury
    and 11 established tibial nonunions with bone or softtissue loss of more than 3 cm were managed with acute
    shortening and relengthening through a tibial metaphyseal osteotomy using either an Ilizarov or monolateral
    external fixator. Average amount of bone loss addressed
    was 4.7 cm. Nine of 10 acute fractures healed without
    bone grafting. Only 1 of 10 acute fractures had a residual limb-length discrepancy. No deep infections occurred. Level of evidence: IV.

    51.

    Pollak AN, McCarthy ML, Burgess AR; The Lower Extremity Assessment Project (LEAP) Study Group: Shortterm wound complications after application of flaps for
    coverage of traumatic soft-tissue defects about the tibia.
    J Bone Joint Surg Am 2000;82A(12):1681-1691.

    52.

    Bhattacharyya T, Mehta P, Smith M, Pomahac B: Routine use of wound vacuum-assisted closure does not allow coverage delay for open tibia fractures. Plast Reconstr Surg 2008;121(4):1263-1266.
    In patients with grade IIIB open tibia fractures, the infection rate was significantly decreased if coverage occurred within 7 days even with utilization of NPWT
    (wound vacuum-assisted closure). Level of evidence: IV.

    53.

    Dedmond BT, Kortesis B, Punger K, et al: The use of


    negative-pressure wound therapy (NPWT) in the temporary treatment of soft-tissue injuries associated with
    high-energy open tibial shaft fractures. J Orthop
    Trauma 2007;21(1):11-17.
    The authors present a retrospective review of 49 patients with 50 grade III open tibia fractures treated with
    NPWT before definitive wound closure or coverage.
    There was a 30% infection rate. Seventeen patients required free tissue transfer or rotational muscle flap for
    coverage. Level of evidence: IV.

    54.

    Govender S, Csimma C, Genant HK, et al; BMP-2 Evaluation in Surgery for Tibial Trauma (BESTT) Study
    Group: Recombinant human bone morphogenetic
    protein-2 for treatment of open tibial fractures: A prospective, controlled, randomized study of four hundred
    and fifty patients. J Bone Joint Surg Am 2002;84(12):
    2123-2134.

    42.

    Zelle BA, Bhandari M, Espiritu M, Koval KJ,


    Zlowodzki M; Evidence-Based Orthopaedic Trauma
    Working Group: Treatment of distal tibia fractures
    without articular involvement: A systematic review of
    1125 fractures. J Orthop Trauma 2006;20(1):76-79.

    43.

    Patzakis MJ, Wilkins J: Factors influencing infection


    rate in open fracture wounds. Clin Orthop Relat Res
    1989;243:36-40.

    44.

    Okike K, Bhattacharyya T: Trends in the management


    of open fractures: A critical analysis. J Bone Joint Surg
    Am 2006;88(12):2739-2748.

    45.

    Harley BJ, Beaupre LA, Jones CA, Dulai SK, Weber


    DW: The effect of time to definitive treatment on the
    rate of nonunion and infection in open fractures. J Orthop Trauma 2002;16(7):484-490.

    46.

    Skaggs DL, Friend L, Alman B, et al: The effect of surgical delay on acute infection following 554 open fractures in children. J Bone Joint Surg Am 2005;87(1):812.

    47.

    Clifford RP, Beauchamp CG, Kellam JF, Webb JK, Tile


    M: Plate fixation of open fractures of the tibia. J Bone
    Joint Surg Br 1988;70(4):644-648.

    55.

    Della Rocca GJ, Crist BD: External fixation versus conversion to intramedullary nailing for definitive management of closed fractures of the femoral and tibial shaft.
    J Am Acad Orthop Surg 2006;14(10 Spec No. ):S131S135.

    Swiontkowski MF, Aro HT, Donell S, et al: Recombinant human bone morphogenetic protein-2 in open tibial fractures: A subgroup analysis of data combined
    from two prospective randomized studies. J Bone Joint
    Surg Am 2006;88(6):1258-1265.

    56.

    Friedlaender GE, Perry CR, Cole JD, et al: Osteogenic


    protein-1 (bone morphogenetic protein-7) in the treatment of tibial nonunions. J Bone Joint Surg Am 2001;
    83(pt 2, suppl 1):S151-S158.

    48.

    49.

    490

    Lindvall E, Sanders R, Dipasquale T, Herscovici D,


    Haidukewych G, Sagi C: Intramedullary nailing versus
    percutaneous locked plating of extra-articular proximal
    tibial fractures: Comparison of 56 cases. J Orthop
    Trauma 2009;23(7):485-492.
    In this retrospective review, 56 patients with extraarticular proximal tibia fractures were treated with an
    intramedullary nail (22) or percutaneous locked plating
    (34) and evaluated at an average of 3.4 years of
    follow-up (nail group) or 2.7 years of follow-up (locked
    plate group). There was no difference in final union
    rates. Implant removal in the locked plate group was
    three times greater than in the nail group. An apex anterior deformity was the most prevalent form of malreduction in both groups. Level of evidence: III.

    ing for fractures of the shaft of the femur in multiply injured patients. J Bone Joint Surg Am 2000;82(6):781788.

    Nowotarski PJ, Turen CH, Brumback RJ, Scarboro JM:


    Conversion of external fixation to intramedullary nail-

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 37: Tibial Shaft Fractures

    57.

    58.

    Jones AL, Bucholz RW, Bosse MJ, et al; BMP-2 Evaluation in Surgery for Tibial Trauma-Allograft (BESTTALL) Study Group: Recombinant human BMP-2 and allograft compared with autogenous bone graft for
    reconstruction of diaphyseal tibial fractures with cortical defects. A randomized, controlled trial. J Bone Joint
    Surg Am 2006;88(7):1431-1441.

    59.

    Masquelet AC: Muscle reconstruction in reconstructive


    surgery: Soft tissue repair and long bone reconstruction.
    Langenbecks Arch Surg 2003;388(5):344-346.

    60.

    Busse JW, Kaur J, Mollon B, et al: Low intensity pulsed


    ultrasonography for fractures: Systematic review of randomised controlled trials. BMJ 2009;338:b351.
    A systematic review of 13 randomized trials examining
    the efficacy of low-intensity pulsed ultrasound for fractures suggests that the evidence is moderate to very low
    in quality and provides conflicting results. Level of evidence: II.

    61.

    Mollon B, da Silva V, Busse JW, Einhorn TA, Bhandari


    M: Electrical stimulation for long-bone fracture-healing:
    A meta-analysis of randomized controlled trials. J Bone
    Joint Surg Am 2008;90(11):2322-2330.

    2011 American Academy of Orthopaedic Surgeons

    62.

    Schmidt A, Finkemeier CG, Tornetta P: Treatment of


    closed tibia fractures, in: Tornetta P, ed: Instructional
    Course Lectures Trauma. Rosemont, IL, American
    Academy of Orthopaedic Surgeons, 2006, 215229.

    63.

    Brinker MR, OConnor DP, Monla YT, Earthman TP:


    Metabolic and endocrine abnormalities in patients with
    nonunions. J Orthop Trauma 2007;21(8):557-570.
    Thirty-seven patients with nonunions were referred to
    endocrinologists and evaluated. Eighty-four percent of
    patients had one or more new diagnoses of metabolic or
    endocrine abnormalities. The most common newly diagnosed abnormality was vitamin D deficiency. Eight patients underwent no surgical intervention for nonunion,
    but achieved bony union following the diagnosis and
    treatment of a new metabolic or endocrine abnormality.
    Level of evidence: IV.

    64.

    Ryzewicz M, Morgan SJ, Linford E, Thwing JI, de Resende GV, Smith WR: Central bone grafting for nonunion of fractures of the tibia: A retrospective series.
    J Bone Joint Surg Br 2009;91(4):522-529.
    In a retrospective cohort study, 23 out of 24 tibial nonunions united after undergoing autogenous bone grafting through lateral approach and anterior to the fibula
    and interosseous membrane. A tibiofibular synostosis
    was created upon union. These 24 patients were compared to a cohort of 20 tibial nonunions treated with
    posterolateral bone grafting procedures. The central
    bone graft patients healed faster and required fewer procedures to achieve union. Level of evidence: III.

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    Rozbruch SR, Pugsley JS, Fragomen AT, Ilizarov S: Repair of tibial nonunions and bone defects with the Taylor Spatial Frame. J Orthop Trauma 2008;22(2):88-95.
    A retrospective review of 38 tibial nonunions treated
    with the Taylor Spatial Frame is presented. Seventy-one
    percent achieved bony union after initial treatment. Infection correlated with initial failure of treatment and
    persistent nonunion. Functional outcome inversely correlated with the number of previous surgeries. Level of
    evidence: IV.

    A meta-analysis of randomized controlled trials investigating the efficacy of electromagnetic stimulation on delayed unions or nonunions suggested no significant impact of this modality. Level of evidence: II.

    491

    Chapter 38

    Ankle Fractures
    Matt Graves, MD

    Ankle Fractures

    Initial Evaluation
    Clinical
    The patient history focuses on the mechanism and timing of injury, as these provide clues to associated injuries and progression of swelling. Specific findings in the
    history noted to have an adverse effect on outcome include advanced age, osteoporosis, diabetes mellitus, peripheral vascular disease, female sex, and high American Society of Anesthesiologists (ASA) class.2-4 The
    effect of obesity is controversial, as it has had differing
    effects depending on the study.5,6 Social factors such as
    smoking, alcohol use, and lower levels of education
    have been noted as independent predictors of lower
    physical function postoperatively.7 The presence of
    these findings should not prevent surgical treatment of
    unstable, displaced ankle fractures but instead should
    (1) allow for a more candid preoperative discussion regarding potential complications and outcome, (2) encourage more careful soft-tissue handling and attention

    Dr. Graves or an immediate family member is a member


    of a speakers bureau or has made paid presentations
    on behalf of Synthes or is a paid consultant for product
    development and has received research or institutional
    support from Synthes.

    2011 American Academy of Orthopaedic Surgeons

    4: Lower Extremity

    Ankle fractures are among the most common injuries


    treated by an orthopaedic surgeon.1 As with other fractures, the treatment goal is expedient return to optimal
    function in the absence of complications. This goal typically requires an anatomic reduction of the ankle mortise with maintenance of ankle joint stability during
    early, active mobilization. With nondisplaced, stable
    fractures, function can be achieved nonsurgically. With
    displaced, unstable fractures, surgical treatment is necessary. It logically follows that a clear understanding of
    displacement and stability is required. More than 50
    years after the popularization of surgical treatment, the
    understanding of these concepts is still being refined.
    Over the past 5 years, understanding has improved significantly. These changes will be covered as they relate
    to the clinical and radiographic evaluation, currently
    used classification systems, recent modifications of surgical treatment, and the complications and expected
    outcomes of treatment.

    to construct stability, and (3) encourage treatment of


    modifiable risk factors during the perioperative period.
    The physical examination should include a neurovascular examination of the leg and focus on the soft tissue
    in line with proposed surgical incisions. Dislocations
    and subluxations should be reduced expediently to take
    pressure off of the skin and neurovascular bundle and
    prevent point loading of articular cartilage. This can be
    accomplished by using intra-articular analgesic injections, intravenous narcotics, or conscious sedation. A
    recent study compared the efficacy of an intra-articular
    block to conscious sedation for the closed reduction of
    ankle fracture-dislocations.8 The intra-articular lidocaine block provided a similar degree of analgesia that
    was adequate for reduction, and a decreased time to
    reach the reduced, splinted position.
    Radiographic
    Plain radiographs are the standard imaging modality
    for the evaluation of ankle fractures. Quality imaging is
    essential and consists of the AP, mortise, and lateral radiographs. Each view provides insight into the pathoanatomy of the injury complex. Classic studies have
    shown that reproducible radiographic measurements
    can be used to quantify the extent of injury and help
    predict clinical outcome.9,10
    The AP view is defined by placing the long axis of
    the foot in the true vertical position. In addition to
    viewing the cortical margins of the malleoli and the talus, it is necessary to evaluate the relationship between
    the talus and the distal tibial subchondral surface. The
    tibiotalar joint space should be symmetric with no signs
    of talar tilt. Markers for syndesmotic injury include the
    tibiofibular overlap and the tibiofibular clear space
    (Figure 1, A).
    The mortise view is defined by internally rotating the
    leg so that the medial and lateral malleoli are parallel to
    the tabletop. This typically requires approximately 10
    of internal rotation of the fifth metatarsal with respect
    to the vertical position.11 This rotation is required because the coronal plane of the ankle joint is externally
    rotated with respect to the coronal plane of the knee
    joint. It provides the true AP view of the tibiotalar articulation. In addition to evaluating cortical margins
    and the tibiotalar joint space, specific radiographic parameters should be noted (Figure 1, B). The tibiofibular
    overlap is also used in this view to evaluate syndesmotic injury. The medial clear space is considered to be
    representative of the status of the deep deltoid liga-

    Orthopaedic Knowledge Update 10

    493

    Section 4: Lower Extremity

    4: Lower Extremity

    Figure 1

    Standard trauma series for evaluation of ankle pathology. A, AP view. The tibiofibular overlap is measured 1 cm
    above the plafond. It is the distance between the lateral edge of the Chaput fragment of the distal tibia and the
    medial border of the fibula. The tibiofibular clear space is measured at the same level and is the distance between
    the depth of the incisura fibularis and the medial border of the fibula. It reflects the posterior aspect of the distal
    tibiofibular relationship. B, Mortise view. The medial clear space is the distance between the lateral border of the
    medial malleolus and the medial border of the talus at the level of the talar dome. The Shenton line of the ankle
    is noted by following the subchondral bone of the distal tibial articular surface across the syndesmotic space to the
    small spike of the fibula. The dime sign is the unbroken curve between the lateral part of the articular surface of
    the talus and the distal fibular peroneal tendon recess. C, Lateral view. Outlines of the medial malleolus (black),
    lateral malleolus (red), and posterior malleolus (green) are noted.

    ment. Markers for fibular length include the talocrural


    angle, the Shenton line of the ankle, and the dime
    sign.12,13
    The lateral view is defined by placing the radiographic beam perpendicular to the long axis of the ankle joint (Figure 1, C). It provides for evaluation of the
    cortical margins of the malleoli, with improved visualization of the posterior malleolus. The tibiotalar joint
    space should be symmetric with no signs of talar subluxation. The relationship of the posterior border of
    the distal fibula to the tibia provides information regarding syndesmotic competency. Associated or occult
    injuries are also noted, including fractures of the lateral
    process of the talus, posterior tubercle of the talus, and
    anterior process of the calcaneus.
    The indications for additional imaging modalities
    such as CT and MRI are unclear. CT has provided for
    an improved understanding of posterior malleolar fracture patterns, articular impaction, and syndesmotic
    reduction.14-17 MRI has been used to evaluate the competency of the syndesmosis and deep deltoid ligament,
    as well as to better view osteochondral talar lesions associated with ankle fractures.18-20

    Classification
    Danis and Weber/AO
    The Danis and Weber/AO classification of malleolar
    fractures focuses on the height of the fibular fracture
    (Figure 2). The rationale is based on the relationship
    between the height of the fibula fracture and the associated damage to the tibiofibular ligaments. The higher
    the fibula fracture, the more extensive the damage to
    the syndesmosis, and thus the greater degree of ankle
    joint instability. A recently published study has sup494

    Orthopaedic Knowledge Update 10

    ported the reproducibility of this classification system,


    revealing substantial interobserver and intraobserver
    agreement using an AP and lateral view of the ankle.21
    Although this classification system still is commonly
    used, some have taken issue with prioritizing the fibula
    in evaluation of ankle joint stability, as many recent
    studies have convincingly established the primacy of
    the deep deltoid and medial malleolus in determining
    ankle joint stability.22 In addition to this, an MRI study
    has recently questioned the relationship of the level of
    fibula fracture to the integrity of the interosseous membrane.18
    Lauge-Hansen
    The Lauge-Hansen classification system is an extensive
    mechanistic system based on a cadaver study that attempted to improve the understanding of ankle fracture
    patterns.23 The first word in the classification system
    refers to the position of the foot at the time of injury;
    the second word refers to the direction of the deforming force (Figure 2). The system is imperfect. All ankle
    fractures do not fit neatly into the different classes. The
    proposed mechanism of injury has been refuted and the
    interobserver and intraobserver reliability have been
    questioned; nevertheless, the system is still commonly
    used.24,25 Much of the recent literature devoted to ankle
    fractures has used the Lauge-Hansen system; recent
    treatment advances will therefore be described with respect to this system.

    Treatment Advances
    Supination-Eversion
    Supination-eversion (also called supination-external rotation) ankle fractures are the most common type seen

    2011 American Academy of Orthopaedic Surgeons

    Chapter 38: Ankle Fractures

    4: Lower Extremity

    Figure 2

    The Danis and Weber and Lauge-Hansen classification systems of ankle fractures. (Reproduced with permission from
    Carr JB, Trafton PG: Malleolar fractures and soft tissue injuries of the ankle, in Browner BD, Jupiter JB, Levine AM,
    Trafton PG: Skeletal Trauma, ed 2. Philadelphia, PA, WB Saunders, 1998, pp 2327-2404.)

    clinically, accounting for nearly 70% of all malleolar


    fractures. The fibular fracture pattern is oblique and
    oriented from posterosuperior to anteroinferior, typically at the level of the syndesmotic ligaments (Weber
    B). If there is no associated medial injury, the ankle
    mortise is thought to be stable, with closed treatment
    leading to successful long-term outcomes.26 If there is
    an associated medial malleolar fracture, the ankle mortise is thought to be unstable, and surgical fixation is
    the treatment of choice.
    Recent literature has centered on the determination
    of instability in the absence of a medial malleolar fracture. Historically, clinical signs and symptoms have
    been used as a correlate for deep deltoid instability. The
    presence of these findings, in addition to a radiograph
    revealing the typical fibular fracture pattern, led to surgical management. More recently, findings such as medial tenderness, medial swelling, and medial ecchymosis

    2011 American Academy of Orthopaedic Surgeons

    have been identified as inaccurate predictors of instability.27,28 These soft-tissue findings can be present secondary to superficial deltoid injury in the absence of deep
    deltoid compromise. Because of this, radiographic
    stress examinations have been used to more accurately
    demonstrate dynamic instability that is not apparent on
    static radiographs. With the applied stress, a mortise
    radiographic view is used and the medial clear space is
    evaluated for widening. This widening represents talar
    subluxation and is evidence of deep deltoid instability
    (Figure 3). Both the gravity stress view and the manual
    stress view have been proposed for differentiating between supination-eversion type II and ligamentous
    supination-eversion type IV fractures.27-29 Although
    both views seem to be reliable, the gravity stress view
    requires less radiation exposure for the surgeon and has
    been perceived as more comfortable for the patient.30
    Most recently, the assumption that a positive ankle

    Orthopaedic Knowledge Update 10

    495

    Section 4: Lower Extremity

    stabilize the ankle mortise. In the absence of a medial


    malleolar fracture, evidence of deep deltoid incompetence can be reached through stress views by examining
    the medial clear space. If instability is present, surgical
    treatment is recommended. Syndesmotic stability
    should always be examined via a stress examination
    while visualizing the tibiofibular clear space and tibiofibular overlap after fixing other components of the injury.

    4: Lower Extremity

    Figure 3

    Evaluation of the medial clear space in the presence of an isolated fibular fracture. A, Mortise
    view of ankle fracture without stress. B, Mortise
    view of ankle fracture with stress. Widening of
    the medial clear space reveals a nonfunctional
    deep deltoid ligament and ankle joint
    instability.

    stress test represents a complete deep deltoid transection has been questioned.20 In this study, MRI was used
    as a decision tool in the treatment of ankle fractures.
    Patients with a positive stress test after an isolated Weber B lateral malleolus fracture were further evaluated
    using MRI to determine the status of the deep deltoid.
    If the deep deltoid is partially intact, the extremity was
    placed in a walking boot and weight bearing with ambulation was allowed as tolerated. At short-term
    follow-up, there was no evidence of residual medial
    clear space widening, posttraumatic arthrosis, or poor
    outcomes in this group. Further work will be necessary
    to clearly define the role of MRI as a decision-making
    tool in the treatment of ankle fractures.
    Controversy also exists as to the ideal type of lateral
    malleolar fixation in this fracture pattern. Lag screw
    fixation has been efficacious in noncomminuted
    oblique fractures in patients younger than 50 years,
    when the fracture was long enough to accept two lag
    screws at least 1 cm apart.31 Smaller incisions and
    fewer reports of hardware prominence were noted.
    More commonly, the implant decision is between the
    dorsal antiglide plate and the lateral neutralization
    plate. Although dorsal plating provides the potential
    advantages of improved biomechanical strength, less
    soft-tissue dissection, less palpable hardware, and longer screw placement, it provides the potential disadvantage of peroneal tendon irritation.32,33 Lateral neutralization plating provides the potential advantage of
    avoidance of the peroneal tendons. To date, no clinical
    study comparing the two techniques has statistically
    shown one to be superior.34
    To summarize, isolated oblique Weber B lateral malleolar fractures can be treated nonsurgically with the
    expectation of a good outcome. When this form of fibula fracture is associated with a medial malleolar fracture, surgical treatment is recommended to reduce and
    496

    Orthopaedic Knowledge Update 10

    Supination-Adduction
    Supination-adduction ankle fractures are characterized
    by a transverse, tension-based fibula fracture below the
    level of the syndesmotic ligaments (Weber A level) with
    an associated vertical medial malleolar fracture. Because the medial-sided injury is compression based, articular impaction is often present at the anteromedial
    corner of the tibial plafond. Evidence of this associated
    marginal impaction was noted in early descriptions of
    the Weber A fracture, and highlighted in a more recent
    case series of supination-adduction ankle fractures.16
    Radiographic visualization of this impaction is noted
    at the medial gutter on the AP and/or mortise view and
    at the anterior aspect of the plafond on the lateral view.
    Although cortical reduction reads are often used to ensure articular reduction in malleolar fractures, the associated impaction present in these injuries makes this
    technique less than ideal. Because of this, an anteromedial approach that allows direct visualization of the articular surface is a logical choice with this fracture pattern. Reduction of the articular surface with possible
    grafting of the impaction defect is possible. Stabilization of this medial reduction can take many forms. A
    recent biomechanical study revealed that a properly applied buttress plate offers a significant mechanical advantage over screw-only constructs. This advantage
    must be weighed against the disadvantages of greater
    soft-tissue dissection and more prominent hardware.35
    Pronation-Abduction
    Pronation-abduction fractures are characterized by a
    tension-based medial-sided injury (deltoid disruption
    and/or transverse medial malleolar fracture) in association with a compression-based, comminuted Weber B
    fibula fracture. More severe pronation-abduction injuries often present with transverse medial tension failure
    soft tissue injuries with extrusion of the plafond. As in
    the supination-adduction variant of ankle fractures, the
    compression gutter should be evaluated for plafond impaction. In the pronation-abduction pattern, the compression gutter is the anterolateral corner of the tibial
    plafond. Because of the primacy of the medial side of
    the ankle in controlling talar displacementand the
    simple transverse fracture noted on the medial side
    with this patternit is logical to fix the medial malleolus first if a fracture is present. Through the pull of the
    deep deltoid, the talus typically returns to its anatomic
    position in the mortise and indirectly reduces the fibula
    via the intact lateral ligamentous complex. Extraperiosteal plating is then possible, decreasing the risk of

    2011 American Academy of Orthopaedic Surgeons

    Chapter 38: Ankle Fractures

    fibular nonunion associated with excessive soft-tissue


    dissection.36 If length is not adequately restored indirectly through the pull of the lateral ligamentous complex, direct manipulation of the distal fragment and a
    length-stable fibular construct is required. A stress examination of the syndesmosis is then completed, with
    fixation recommended if instability is noted upon visualization of the distal tibiofibular clear space and overlap.

    Specific Fracture Components


    Requiring Further Delineation
    Distal Tibiofibular Syndesmosis
    The distal tibiofibular syndesmosis is a fibrous articulation connecting the tibia and fibula that consists of five
    parts: (1) interosseous membrane, (2) interosseous ligament, (3) anterior inferior tibiofibular ligament, (4)
    posterior inferior tibiofibular ligament, and (5) inferior
    transverse tibiofibular ligament. It functions to resist
    external rotation, axial translation, and lateral translation of the talus. The mechanism of injury is typically
    severe external rotation of the ankle and foot relative
    to the position of the tibia. Clinical signs and symptoms of injury include ecchymosis proximal to the ankle joint, pain over the anterior inferior tibiofibular ligament, pain created while squeezing the tibia and fibula
    together (squeeze test), and pain with an external rotation stress test. Classic radiographic signs of injury on
    the AP view include a tibiofibular clear space of greater
    than 5 mm and a tibiofibular overlap of less than 10
    mm. On the mortise radiograph, a tibiofibular overlap
    of less than 1 mm is suggested to be pathologic.10 These
    numbers have been questioned in multiple studies, as
    there is considerable variability in the absolute values
    among uninjured patients as well as variability within
    the same patient based on radiographic positioning.
    Radiographic subtleties can be clarified with stress
    views. Standard stress mechanisms include an external
    rotation stress view or directly manipulating the fibula
    intraoperatively (after fixation) via a clamp.
    If instability is present, surgical treatment is recommended. Obtaining and maintaining an accurate reduction improves Short Musculoskeletal Functional Assess-

    2011 American Academy of Orthopaedic Surgeons

    4: Lower Extremity

    Pronation-External Rotation
    Pronation-external rotation injuries are the most unstable of all ankle fracture patterns. Pathoanatomy begins
    on the medial side with a deltoid disruption and/or a
    medial malleolar fracture. After disrupting the anterior
    inferior tibiofibular ligament, a Weber C fibula fracture
    takes the form of a spiral or oblique pattern. Posterior
    malleolar injuries are occasionally noted. A syndesmotic disruption is present until proven otherwise and
    should be addressed if any instability is present. Treatment requires an anatomic reduction of the malleolar
    fractures and the syndesmotic disruption. Outcomes
    are generally not as good as with other malleolar fracture patterns. These deficiencies are likely related to
    problems with the distal tibiofibular syndesmosis. This
    specific injury component requires further discussion.

    ment Index scores.37 The understanding of what


    constitutes an accurate reduction is changing. A recent
    study using axial CT to evaluate reduction after standard fixation techniques noted that radiographic measurements did not accurately reflect the status of the
    syndesmotic reduction.17 Alternative techniques such as
    open visualization of the syndesmosis and radiographic
    imaging in multiple planes have been described to improve reduction.38,39 Assuming an accurate reduction
    has been established, there is little consensus as to what
    is necessary to maintain that reduction. There is general
    agreement that weight bearing should be delayed and
    syndesmotic fixation should remain in place for at least
    3 months. There is no general agreement on the use of
    3.5- or 4.5-mm screws, one screw or two, tricortical
    screws or quadricortical screws, or screw removal over
    leaving the screw in place.
    Posterior Malleolus
    The posterior malleolus has three important functions:
    resisting posterior translation of the talus, enhancing
    syndesmotic stability through the attachment of the
    posterior inferior tibiofibular and inferior transverse
    tibiofibular ligaments, and distributing weight-bearing
    forces by increasing the surface area of the ankle joint.
    The classic indication for fixation is based on size.
    Measurements are made on the lateral radiograph, with
    fragments greater than 25% of the articular surface requiring surgical treatment.40 This indication has been
    questioned, as posterior malleolar fracture patterns are
    variable and rarely oriented purely in the coronal
    plane. A recent CT study clarified the typical pathoanatomy of the posterior malleolus and divided fracture patterns into three basic types (Figure 4). Because
    of fracture pattern variability, the authors encouraged
    preoperative CT to assist with surgical planning.
    Clearer surgical indications revolve around the function
    of the posterior malleolus. Dynamic intraoperative
    stress radiographs allow testing of posterior talar translation and syndesmotic stability after the remainder of
    the osseous ankle pathology has been stabilized. Decision making based on distributing weight-bearing
    forces is more complicated. Biomechanical studies reveal changes in peak pressure distribution with larger
    fragments that could potentially lead to posttraumatic
    arthrosis, but guidelines for treatment based on these
    studies are lacking. If surgical stabilization is chosen,
    visualization of the reduction can be enhanced radiographically via the external rotation lateral view and
    clinically via a posterolateral approach exploiting the
    interval between the flexor hallucis longus and the peroneal tendons.41 Occasionally an adjunctive posteromedial approach is helpful.15
    When a posterior malleolar fracture is combined
    with a lateral malleolar fracture, the order of fixation
    should be considered. Advantages of fixing the lateral
    malleolus before the posterior malleolus include indirectly improving the reduction of the posterior malleolus via the posterior inferior tibiofibular ligament attachment, and allowing for dynamic intraoperative

    Orthopaedic Knowledge Update 10

    497

    Chapter 38: Ankle Fractures

    Primary fracture lines are outlined, creating common fragments in complete articular fractures.
    A is the anterolateral or Chaput fragment. M
    denotes the medial malleolar fragment. P is the
    posterior malleolar or Volkmann fragment. The
    size of the common fragments varies and additional articular pieces are created via secondary
    fracture lines. Reproduced from Topliss CJ, Jackson M, Atkins RM: Anatomy of pilon fractures
    of the distal tibia. J Bone Joint Surg
    2005;87:692-697.

    Postoperative care varies in that nonweight-bearing


    status is typically prolonged, and protected weight
    bearing takes a longer course.45

    4: Lower Extremity

    Figure 5

    neck, acetabulum, and spine. The lower extremity


    should be evaluated for neurologic or vascular compromise and signs of compartment syndrome. Recent evidence suggests that abnormalities of the arterial tree of
    the distal leg are noted in a significant percentage of
    high-energy tibial plafond fractures.47 Despite this finding, the routine use of CT angiograms is not currently
    recommended. Specific attention should be placed on
    the soft-tissue envelope surrounding the ankle joint.
    Energy is manifested via swelling, abrasions, ecchymosis, fracture blister formation, and open wounds. Subluxations and dislocations should be urgently reduced
    in the emergency department. The initial reduction
    should be maintained with the use of a well-padded
    splint to alleviate pressure on the skin from displaced
    fragments and decrease the secondary injury created by
    fragment instability.
    Initial radiographic evaluation includes AP, mortise,
    and lateral views of the ankle. High-quality radiographs provide clear evidence of the pattern of instability and the requisite forces that must be negated with
    the fixation construct, but are typically inadequate to
    provide a clear understanding of the articular injury.
    Because of this, additional imaging studies are common. CT provides useful information that often alters
    surgical decision making.48 The timing of CT is variable
    and depends on the injury characteristics and the treatment plan. In complex articular injuries with axial instability, the information provided from CT scans is
    most useful after the ligamentotaxis provided by spanning external fixation.

    Classification
    Tibial Plafond Fractures
    Although ankle fractures typically occur from lower energy rotational mechanisms, have minor articular damage, are surrounded by a reasonable soft-tissue envelope, and have a low complication rate with surgical
    treatment, tibial plafond fractures are very different.
    The difference is related to the energy and direction of
    the mechanism of injury. Tibial plafond fractures typically occur from higher energy mechanisms with a
    component of axial load, have significant articular
    damage in the weight-bearing zone, are surrounded by
    more compromised soft-tissue envelopes, and present a
    historically high complication rate with surgical treatment. Because of these differences, tibial plafond fractures must be approached with an understanding of the
    small margin for error and a great respect for the complication profile.

    Emergency Department Evaluation: Clinical


    and Radiographic
    Clinical evaluation begins with a search for associated
    systemic injuries. The level of energy associated with
    these injury mechanisms demands a thorough patient
    evaluation. Associated musculoskeletal injuries include
    those created by axial load, such as fractures of the calcaneus, tibial plateau, supracondylar femur, femoral

    2011 American Academy of Orthopaedic Surgeons

    Ruedi and Allgwer System and the AO/OTA System


    Multiple classification systems have been developed for
    tibial plafond fractures. The two most widely used are
    the Ruedi and Allgwer system and the AO/OTA system. The Ruedi and Allgwer system differentiates pilon fractures based on the presence of articular displacement and the degree of articular comminution.
    The AO/OTA system is first based on the degree of
    continuity of the articular surface to the tibial shaft,
    creating a division between extra-articular, partial articular, and complete articular fractures. Further subdivisions relate to the degree of fragmentation noted in the
    metaphyseal and articular regions. Problems have been
    noted with interobserver agreement beyond the initial
    division of the classification system.49
    Articular Surface
    Although the previously mentioned classification systems differentiate between pilon fractures based on the
    degree of articular comminution, they do not denote
    the commonly encountered articular fracture lines. Although the articular fracture pattern varies from case to
    case, typical fragments and primary fracture lines are
    present (Figure 5). The primary fracture line begins at
    the anterolateral portion of the articular surface at the
    level of the distal tibiofibular joint. This fracture line
    extends medially and splits near the central portion of

    Orthopaedic Knowledge Update 10

    499

    Section 4: Lower Extremity

    the plafond, exiting anteriorly and posteriorly. This creates three typical fragments in complete articular fractures: a medial malleolar fragment, a posterior malleolar (Volkmann) fragment, and an anterolateral joint
    (Chaput) fragment. Variability in the size of these fragments and further articular comminution is created via
    secondary fracture lines. In addition to noting the size
    and position of the typical articular fragments, care
    should be taken to evaluate articular impaction. Impaction occurs in both complete articular and partial articular fractures. In partial articular fractures, the talus
    acts as a pestle during axial loading, impinging on the
    leading edge of the intact articular surface before escaping through the fractured fragments.

    Evolution of Treatment
    4: Lower Extremity

    Immediate Open Reduction and Internal Fixation


    Because of the inconsistent and often poor outcomes
    associated with closed treatment of these complex injuries, other treatment options were evaluated. With the
    advent of improved instrumentation and surgical technique, a classic study described the fundamental principles of surgical management. These principles included
    reconstruction of the fibula, primarily in simple fibular
    fracture patterns and secondarily in complex fibular
    fracture patterns; anatomic reconstruction of the tibial
    articular surface; cancellous grafting of defects resulting
    from the reduction of impacted pieces; and plate osteosynthesis via the medial aspect of the tibia. These principles required atraumatic surgical technique and allowed for early, active pain-free mobilization.
    Following these principles led to remarkable results,
    with 75% of the patients in the series being pain free
    with good functional outcomes.50
    Multiple series of patients treated with immediate
    open reduction and internal fixation (ORIF) in the
    United States showed equally remarkable but very different results.51-53 Wound dehiscence, postsurgical infections, and hardware failure were commonly noted after
    ORIF of Ruedi and Allgwer type III fractures. It was
    postulated that the difference in results was related to
    the energy associated with the injury and the experience of the operating surgeons. Most patients in the
    Swiss series50 were injured during lower energy skiing
    accidents, whereas most in the North American
    series51-53 were injured via higher energy mechanisms
    such as falls from heights, motor vehicle collisions, and
    motorcycle crashes. The system of health care also differed with fewer, more experienced surgeons treating
    pilon fractures in the Swiss series. This high complication rate led to a change in management techniques and
    management principles. If an anatomic reduction and
    stable fixation without soft-tissue compromise could
    not be predicted based on the injury pattern, alternative
    methods of treatment were chosen. The complication
    profile began to drive surgical decision making.
    External Fixation With/Without Limited ORIF
    With the goal of preventing major complications, external fixation began to replace ORIF as the definitive
    500

    Orthopaedic Knowledge Update 10

    treatment modality for complex pilon fractures.54,55


    Avoiding or limiting surgical approaches logically limited wound complications; it also limited the surgeons
    ability to directly see the articular surface and achieve
    an anatomic reduction. Another compromise included
    the inability to allow for postoperative motion with
    joint-spanning, nonhinged frames. Further experience
    with the technique led to improved radiographic reductions. Alternative frame types (joint-spanning articulated frames and hybrid frames that did not span the
    joint) were popularized because they allowed for earlier
    ankle motion.56 Despite the improvements, many surgeons still thought that the technique did not consistently allow for the same quality of reduction that
    could be achieved with direct visualization through an
    open approach. Different management strategies were
    developed in an attempt to limit the compromises created by avoiding open approaches.
    Staged ORIF
    Staged surgical management strategies were developed
    to maximize the advantages of an open approach while
    minimizing the disadvantages.57,58 Temporizing jointspanning external fixation in axially unstable fractures
    decreased the secondary soft-tissue trauma created by
    fragment instability. Additionally it allowed for improved initial pain control via increased stability, improved provisional reductions via ligamentotaxis, and
    improved soft-tissue evaluation by eliminating the need
    for splinting. After the initial stage of treatment, time
    was allowed for restoration of healthy soft tissue. Although not preventing the need for careful soft-tissue
    handling, the delay provided a larger margin of error
    for the definitive surgical treatment.
    Currently, open approaches are described for anterolateral, anteromedial, medial, posteromedial, posterolateral, and lateral access. The choice of approach is related to many factors, including articular fracture
    pattern, metadiaphyseal fracture pattern, direction of
    talar displacement, soft-tissue quality, necessity of fibular fixation, and surgeon preference. If multiple approaches are used, maximizing the interval between the
    approaches is ideal. Despite this recommendation, incisions may be safely placed less than 7 cm apart if careful attention is given to soft-tissue technique and surgical timing.59 Plate osteosynthesis through open
    approaches in a delayed fashion has substantially decreased wound healing complications and secondary
    surgical infections (Figure 6).

    Complications and Determinants of Outcome


    High-energy pilon fracture management has been
    fraught with complications. The injured soft-tissue envelope and traumatic surgical soft-tissue handling have
    led to wound-healing complications and subsequently
    deep infections. Comminuted metaphyseal areas with
    limited inherent stability and marginal muscle coverage
    have led to malunions and nonunions. Severe articular
    cartilage damage and unsuccessful articular reconstructive efforts have led to posttraumatic arthritis. The

    2011 American Academy of Orthopaedic Surgeons

    Chapter 38: Ankle Fractures

    4: Lower Extremity

    Figure 6

    Staged management using initial spanning external fixation and fibular fixation followed by an interval for softtissue recovery before definitive treatment. A and B, Injury AP and lateral radiographs. C and D, AP and lateral
    radiographs following the first stage of management. E and F, Six-month follow-up radiographs after the definitive surgical treatment.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    501

    Section 4: Lower Extremity

    4: Lower Extremity

    damage to the soft-tissue envelope created by the initial


    injury, surgical intervention, and joint immobilization
    has led to postoperative scarring and stiffness. The limited soft-tissue envelope and bulky implants have led to
    hardware prominence.
    Changes in treatment techniques and implant design
    have decreased but not eliminated the incidence of
    complications. Staged management, improved softtissue handling, less extensile approaches, indirect reduction techniques, definitive external fixation, and
    lower profile plates have all likely played a role. Honest
    assessments of individual interest and capabilities as
    well as improvements in referral networks will likely
    continue to decrease the incidence of complications.
    Outcome instruments vary greatly and both clinicianbased and patient-reported outcome instruments have
    been used to describe function after pilon fracture
    treatment. General health-related instruments have revealed that patients with pilon fractures continue to experience physical and psychosocial impairment long after the initial injury.60-63 Patient-specific and fracturespecific variables are linked to the overall outcome.
    Preexisting medical comorbidities, male sex, workrelated injuries, lower income levels, and lower education levels are noted to negatively affect scores.60,62,63
    The severity of the injury and the quality of the reduction have been correlated with the development of arthrosis, but not always with the clinical outcome.60,63
    Despite the high incidence of posttraumatic ankle arthritis, the rate of ankle arthrodesis remains low and
    patients continue to improve for many years after the
    index procedure.63 Optimizing outcome requires
    achieving the best possible reduction in the absence of
    postoperative complications, with attention also placed
    on the recognition of and assistance with patientspecific variables.

    cussed. Open injuries, diabetes, and peripheral vascular


    disease were strong risk factors for short-term complications. Level of evidence: II.
    5.

    Bstman OM: Body-weight related to loss of reduction


    of fractures of the distal tibia and ankle. J Bone Joint
    Surg Br 1995;77(1):101-103.

    6.

    Strauss EJ, Frank JB, Walsh M, Koval KJ, Egol KA:


    Does obesity influence the outcome after the operative
    treatment of ankle fractures? J Bone Joint Surg Br 2007;
    89(6):794-798.
    The authors present a retrospective review evaluating
    the number of comorbidities, incidence of complications, time to fracture union, fracture type, and level of
    function between obese and nonobese patients with ankle fractures. At 2 years after surgery, obesity did not
    seem to have an effect on the incidence of complications, time to fracture union, or level of function.

    7.

    Bhandari M, Sprague S, Hanson B, et al: Health-related


    quality of life following operative treatment of unstable
    ankle fractures: A prospective observational study. J Orthop Trauma 2004;18(6):338-345.

    8.

    White BJ, Walsh M, Egol KA, Tejwani NC: Intraarticular block compared with conscious sedation for
    closed reduction of ankle fracture-dislocations: A prospective randomized trial. J Bone Joint Surg Am 2008;
    90(4):731-734.
    The authors discuss a prospective, randomized trial
    comparing conscious sedation and intra-articular block
    for analgesia and the ability to allow for ankle fracture
    reduction and application of a splint. No difference in
    analgesia or allowance for reduction was noted. The
    intra-articular block allowed for a shorter average time
    for reduction and splinting. Level of evidence: I.

    9.

    Joy G, Patzakis MJ, Harvey JP Jr: Precise evaluation of


    the reduction of severe ankle fractures. J Bone Joint
    Surg Am 1974;56(5):979-993.

    10.

    Pettrone FA, Gail M, Pee D, Fitzpatrick T, Van Herpe


    LB: Quantitative criteria for prediction of the results after displaced fracture of the ankle. J Bone Joint Surg Am
    1983;65(5):667-677.

    11.

    Goergen TG, Danzig LA, Resnick D, Owen CA: Roentgenographic evaluation of the tibiotalar joint. J Bone
    Joint Surg Am 1977;59(7):874-877.

    12.

    Weber BG, Simpson LA: Corrective lengthening osteotomy of the fibula. Clin Orthop Relat Res 1985;199:6167.

    13.

    Sarkisian JS, Cody GW: Closed treatment of ankle fractures: A new criterion for evaluation - a review of 250
    cases. J Trauma 1976;16(4):323-326.

    14.

    Haraguchi N, Haruyama H, Toga H, Kato F: Pathoanatomy of posterior malleolar fractures of the ankle.
    J Bone Joint Surg Am 2006;88(5):1085-1092.

    Annotated References

    502

    1.

    Court-Brown CM, McBirnie J, Wilson G: Adult ankle


    fracturesan increasing problem? Acta Orthop Scand
    1998;69(1):43-47.

    2.

    Ganesh SP, Pietrobon R, Ceclio WA, Pan D, Lightdale


    N, Nunley JA: The impact of diabetes on patient outcomes after ankle fracture. J Bone Joint Surg Am 2005;
    87(8):1712-1718.

    3.

    Egol KA, Tejwani NC, Walsh MG, Capla EL, Koval KJ:
    Predictors of short-term functional outcome following
    ankle fracture surgery. J Bone Joint Surg Am 2006;
    88(5):974-979.

    4.

    SooHoo NF, Krenek L, Eagan MJ, Gurbani B, Ko CY,


    Zingmond DS: Complication rates following open reduction and internal fixation of ankle fractures. J Bone
    Joint Surg Am 2009;91(5):1042-1049.
    Californias discharge database was queried for patients
    who had undergone ORIF of an ankle fracture over a
    10-year period with complications reviewed and dis-

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 38: Ankle Fractures

    Weber M: Trimalleolar fractures with impaction of the


    posteromedial tibial plafond: Implications for talar stability. Foot Ankle Int 2004;25(10):716-727.

    23.

    Lauge-Hansen N: Fractures of the ankle. II. Combined


    experimental-surgical and experimental-roentgenologic
    investigations. Arch Surg 1950;60(5):957-985.

    16.

    McConnell T, Tornetta P III: Marginal plafond impaction in association with supination-adduction ankle
    fractures: A report of eight cases. J Orthop Trauma
    2001;15(6):447-449.

    24.

    Michelson J, Solocoff D, Waldman B, Kendell K, Ahn


    U: Ankle fractures: The Lauge-Hansen classification revisited. Clin Orthop Relat Res 1997;345:198-205.

    25.
    17.

    Gardner MJ, Demetrakopoulos D, Briggs SM, Helfet


    DL, Lorich DG: Malreduction of the tibiofibular syndesmosis in ankle fractures. Foot Ankle Int 2006;
    27(10):788-792.

    Gardner MJ, Demetrakopoulos D, Briggs SM, Helfet


    DL, Lorich DG: The ability of the Lauge-Hansen classification to predict ligament injury and mechanism in ankle fractures: An MRI study. J Orthop Trauma 2006;
    20(4):267-272.

    18.

    Nielson JH, Gardner MJ, Peterson MG, et al: Radiographic measurements do not predict syndesmotic injury in ankle fractures: An MRI study. Clin Orthop
    Relat Res 2005;436:216-221.

    26.

    Kristensen KD, Hansen T: Closed treatment of ankle


    fractures. Stage II supination-eversion fractures followed for 20 years. Acta Orthop Scand 1985;56(2):
    107-109.

    19.

    Boraiah S, Paul O, Parker RJ, Miller AN, Hentel KD,


    Lorich DG: Osteochondral lesions of talus associated
    with ankle fractures. Foot Ankle Int 2009;30(6):481485.

    27.

    McConnell T, Creevy W, Tornetta P III: Stress examination of supination external rotation-type fibular fractures. J Bone Joint Surg Am 2004;86(10):2171-2178.

    28.

    Egol KA, Amirtharajah M, Tejwani NC, Capla EL,


    Koval KJ: Ankle stress test for predicting the need for
    surgical fixation of isolated fibular fractures. J Bone
    Joint Surg Am 2004;86(11):2393-2398.

    29.

    Michelson JD, Varner KE, Checcone M: Diagnosing deltoid injury in ankle fractures: the gravity stress view.
    Clin Orthop Relat Res 2001;387:178-182.

    30.

    Schock HJ, Pinzur M, Manion L, Stover M: The use of


    gravity or manual-stress radiographs in the assessment
    of supination-external rotation fractures of the ankle.
    J Bone Joint Surg Br 2007;89(8):1055-1059.
    Gravity and manual stress tests were compared in
    supination-external rotation ankle fractures. Gravity
    stress was determined to be as reliable and perceived as
    more comfortable than manual stress.

    31.

    Tornetta P III, Creevy W: Lag screw only fixation of the


    lateral malleolus. J Orthop Trauma 2001;15(2):119121.

    32.

    Weber M, Krause F: Peroneal tendon lesions caused by


    antiglide plates used for fixation of lateral malleolar
    fractures: The effect of plate and screw position. Foot
    Ankle Int 2005;26(4):281-285.

    33.

    Schaffer JJ, Manoli A II: The antiglide plate for distal


    fibular fixation: A biomechanical comparison with fixation with a lateral plate. J Bone Joint Surg Am 1987;
    69(4):596-604.

    34.

    Lamontagne J, Blachut PA, Broekhuyse HM, OBrien


    PJ, Meek RN: Surgical treatment of a displaced lateral
    malleolus fracture: The antiglide technique versus lateral plate fixation. J Orthop Trauma 2002;16(7):498502.

    35.

    Dumigan RM, Bronson DG, Early JS: Analysis of fixation methods for vertical shear fractures of the medial

    In this retrospective case series, the incidence and effect


    of osteochondral lesions of the talus in ankle fractures
    that were surgically treated were evaluated. All patients
    were assessed preoperatively by MRI and functional
    outcome was measured at a minimum of 6 months using
    Foot and Ankle Outcome Scoring. Osteochondral lesions were noted in 17% of cases but showed no statistically significant effect on outcome. Level of evidence:
    IV.
    20.

    Koval KJ, Egol KA, Cheung Y, Goodwin DW, Spratt


    KF: Does a positive ankle stress test indicate the need
    for operative treatment after lateral malleolus fracture?
    A preliminary report. J Orthop Trauma 2007;21(7):
    449-455.
    The authors present a retrospective review of patients
    who had a positive ankle stress test after an isolated Weber B lateral malleolar fracture. An MRI was ordered to
    evaluate the status of the deep deltoid ligament. If the
    deep deltoid was partially torn, patients were treated
    nonsurgically. At a minimum 12-month follow-up, all
    fractures had united without evidence of medial clear
    space widening or posttraumatic arthritis.

    21.

    22.

    Malek IA, Machani B, Mevcha AM, Hyder NH: Interobserver reliability and intra-observer reproducibility of
    the Weber classification of ankle fractures. J Bone Joint
    Surg Br 2006;88(9):1204-1206.
    Michelson JD, Magid D, McHale K: Clinical utility of a
    stability-based ankle fracture classification system. J Orthop Trauma 2007;21(5):307-315.
    To test the hypothesis that ankle fracture prognosis is
    dependent on initial biomechanical stability, an alternative classification system created using stability-based
    treatment criteria was developed on the basis of a structured analysis of the ankle fracture literature. Results
    supported the hypothesis that a stability-based ankle
    classification system could be prognostic.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    15.

    503

    Section 4: Lower Extremity

    posttraumatic ankle arthritis after ankle related fractures were analyzed in a retrospective cohort study.
    Fracture type and severity, occurrence of complications,
    and patient-related factors were associated with the latency time between injury and the development of arthritis.

    malleolus. J Orthop Trauma 2006;20(10):687-691.


    36.

    4: Lower Extremity

    37.

    504

    Siegel J, Tornetta P III: Extraperiosteal plating of


    pronation-abduction ankle fractures. J Bone Joint Surg
    Am 2007;89(2):276-281.
    A retrospective review of consecutive patient series managed with extraperiosteal plating of fibular fractures in
    pronation-abduction type injuries is presented. Extraperiosteal plating was found to be an effective method of
    stabilization that led to predictable union. Level of evidence: IV.
    Weening B, Bhandari M: Predictors of functional outcome following transsyndesmotic screw fixation of ankle fractures. J Orthop Trauma 2005;19(2):102-108.

    38.

    Candal-Couto JJ, Burrow D, Bromage S, Briggs PJ: Instability of the tibio-fibular syndesmosis: Have we been
    pulling in the wrong direction? Injury 2004;35(8):814818.

    39.

    Miller AN, Carroll EA, Parker RJ, Boraiah S, Helfet


    DL, Lorich DG: Direct visualization for syndesmotic
    stabilization of ankle fractures. Foot Ankle Int 2009;
    30(5):419-426.
    An established protocol for treatment of ankle fractures
    with syndesmotic injury was evaluated retrospectively.
    Patients who underwent stabilization of the syndesmosis
    with direct visualization were compared with historic
    control subjects who underwent indirect fluoroscopic
    syndesmotic visualization. Postoperative CT scans were
    obtained in all patients. Based on the definition of an
    anatomic syndesmotic reduction, malreductions were
    significantly decreased in the direct visualization group.
    Level of evidence: III.

    40.

    Hartford JM, Gorczyca JT, McNamara JL, Mayor MB:


    Tibiotalar contact area: Contribution of posterior malleolus and deltoid ligament. Clin Orthop Relat Res
    1995;320:182-187.

    41.

    DeCoster TA: External rotation-lateral view of the ankle in the assessment of the posterior malleolus. Foot
    Ankle Int 2000;21(2):158.

    42.

    Herscovici D Jr , Scaduto JM, Infante A: Conservative


    treatment of isolated fractures of the medial malleolus.
    J Bone Joint Surg Br 2007;89(1):89-93.
    Patients who had nonsurgical treatment of isolated medial malleolar fractures were evaluated retrospectively.
    High rates of union and good functional results were
    noted with nonsurgical treatment.

    45.

    Wukich DK, Kline AJ: The management of ankle fractures in patients with diabetes. J Bone Joint Surg Am
    2008;90(7):1570-1578.
    This article discusses treatment options for ankle fractures in patients with diabetes, along with complications
    associated with diabetes.

    46.

    Chaudhary SB, Liporace FA, Gandhi A, Donley BG,


    Pinzur MS, Lin SS: Complications of ankle fracture in
    patients with diabetes. J Am Acad Orthop Surg 2008;
    16(3):159-170.
    The authors discuss issues related to open or closed
    treatment of ankle fractures in patients with diabetes.

    47.

    LeBus GF, Collinge C: Vascular abnormalities as assessed with CT angiography in high-energy tibial plafond fractures. J Orthop Trauma 2008;22(1):16-22.
    CT angiography was added to a routine staged treatment protocol for ORIF of tibial plafond fractures. In
    more than half of high-energy tibial plafond fractures,
    CT angiography identified significant abnormalities of
    the arterial tree of the distal leg.

    48.

    Tornetta P III, Gorup J: Axial computed tomography of


    pilon fractures. Clin Orthop Relat Res 1996;323:273276.

    49.

    Swiontkowski MF, Sands AK, Agel J, Diab M, Schwappach JR, Kreder HJ: Interobserver variation in the AO/
    OTA fracture classification system for pilon fractures: Is
    there a problem? J Orthop Trauma 1997;11(7):467470.

    50.

    Ruedi T: Fractures of the lower end of the tibia into the


    ankle joint: Results 9 years after open reduction and internal fixation. Injury 1973;5(2):130-134.

    51.

    Dillin L, Slabaugh P: Delayed wound healing, infection,


    and nonunion following open reduction and internal
    fixation of tibial plafond fractures. J Trauma 1986;
    26(12):1116-1119.

    52.

    McFerran MA, Smith SW, Boulas HJ, Schwartz HS:


    Complications encountered in the treatment of pilon
    fractures. J Orthop Trauma 1992;6(2):195-200.

    43.

    Mont MA, Sedlin ED, Weiner LS, Miller AR: Postoperative radiographs as predictors of clinical outcome in
    unstable ankle fractures. J Orthop Trauma 1992;6(3):
    352-357.

    53.

    Teeny SM, Wiss DA: Open reduction and internal fixation of tibial plafond fractures: Variables contributing to
    poor results and complications. Clin Orthop Relat Res
    1993;292:108-117.

    44.

    Horisberger M, Valderrabano V, Hintermann B: Posttraumatic ankle osteoarthritis after ankle-related fractures. J Orthop Trauma 2009;23(1):60-67.
    The etiologies, pathomechanisms, and predisposing factors that lead to the development and progression of

    54.

    Bonar SK, Marsh JL: Unilateral external fixation for severe pilon fractures. Foot Ankle 1993;14(2):57-64.

    55.

    Bone L, Stegemann P, McNamara K, Seibel R: External


    fixation of severely comminuted and open tibial pilon

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 38: Ankle Fractures

    fond fractures. With careful attention to soft- tissue


    management and surgical timing, incisions for tibial plafond fractures can be placed less than 7 cm apart.

    fractures. Clin Orthop Relat Res 1993;292:101-107.


    56.

    Tornetta P III, Weiner L, Bergman M, et al: Pilon fractures: Treatment with combined internal and external
    fixation. J Orthop Trauma 1993;7(6):489-496.
    Patterson MJ, Cole JD: Two-staged delayed open reduction and internal fixation of severe pilon fractures. J Orthop Trauma 1999;13(2):85-91.

    58.

    Sirkin M, Sanders R, DiPasquale T, Herscovici D Jr: A


    staged protocol for soft tissue management in the treatment of complex pilon fractures. J Orthop Trauma
    1999;13(2):78-84.

    59.

    Howard JL, Agel J, Barei DP, Benirschke SK, Nork SE:


    A prospective study evaluating incision placement and
    wound healing for tibial plafond fractures. J Orthop
    Trauma 2008;22(5):299-305, discussion 305-306.
    The authors of a prospective observational cohort study
    tested the validity of the recommendation that a 7-cm
    skin bridge represents the minimum safe distance between surgical incisions in the treatment of tibial pla-

    2011 American Academy of Orthopaedic Surgeons

    Williams TM, Nepola JV, DeCoster TA, Hurwitz SR,


    Dirschl DR, Marsh JL: Factors affecting outcome in tibial plafond fractures. Clin Orthop Relat Res 2004;423:
    93-98.

    61.

    Harris AM, Patterson BM, Sontich JK, Vallier HA: Results and outcomes after operative treatment of highenergy tibial plafond fractures. Foot Ankle Int 2006;
    27(4):256-265.

    62.

    Pollak AN, McCarthy ML, Bess RS, Agel J, Swiontkowski MF: Outcomes after treatment of high-energy
    tibial plafond fractures. J Bone Joint Surg Am 2003;
    85(10):1893-1900.

    63.

    Marsh JL, Weigel DP, Dirschl DR: Tibial plafond fractures. How do these ankles function over time? J Bone
    Joint Surg Am 2003;85(2):287-295.

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    57.

    60.

    505

    Chapter 39

    Foot Trauma
    Brad J. Yoo, MD

    Eric Giza, MD

    Introduction

    Dr. Yoo or an immediate family member has received research or institutional support from the AO and Smith &
    Nephew. Dr. Giza or an immediate family member serves
    as a paid consultant to or is an employee of Arthrex and
    has received research or institutional support from the
    Orthopaedic Scientific Research Foundation.

    2011 American Academy of Orthopaedic Surgeons

    4: Lower Extremity

    The human foot is a complex assembly of irregularly


    shaped bones interwoven with stout ligaments and
    muscle-tendon units. It represents a defining characteristic of the human species, enabling erect bipedal motion and releasing the upper extremities from the responsibilities of locomotion. The foot must be durable
    enough to withstand seemingly endless repetitive loads
    of up to seven times body weight. As further testament
    to its incredible design, the foot exhibits contradictory
    motion within the span of a single gait cycle. One moment, the foot is a rigid platform, serving as an effective
    lever to propel the body forward. Immediately afterward, the foot becomes flexible, yielding under the
    bodys weight, dispersing load, and conforming to uneven walking surfaces.
    The foots versatile behavior is made possible
    through the intimate interactions of more than 28
    asymmetrically-shaped bones and 31 articulations. The
    hindfoot, being most proximal to the ankle, consists of
    the talus and calcaneus. These two bones comprise
    most of the diarthrodial subtalar joint, which enables
    hindfoot supination and pronation. The midfoot consists of the navicular bone, three keystone-shaped cuneiforms, and the trapezoidal cuboid. These bones articulate via flat, relatively immobile rigid joints that form a
    Roman arch in the transverse plane. Like water under
    an arch, the space created by the arcade of the midfoot
    bones allows neurovascular and tendinous structures to
    pass underneath without being compressed by the
    bodys weight. Most distally, the forefoot is composed
    of the metatarsals and phalanges. Motion via diarthrodial joints occurs at the metatarsophalangeal and interphalangeal articulations.
    Flexibility is obtained through the ankle, subtalar,
    talonavicular, and metatarsophalaneal joints. To a
    lesser extent, the calcaneocuboid and the flat tarsometatarsal articulations of the fourth and fifth digits
    also require some mobility to allow for normal foot

    mechanics. Other articulations, such as the naviculocuneiform joints or the tarsometatarsal joints of the first,
    second, and third columns, demand rigidity and often
    cause painful symptoms when instability is induced
    from fracture or ligament injury.
    From a functional standpoint, the foot may be compared to a three-legged stool. The calcaneus, the great
    hallux, and the lesser metatarsal heads comprise each
    of the legs while the talus represents the seat. The tripod has stability only when the position of each of its
    legs are in their correct anatomic relationships. Shortening of the foots medial column will create a cavus
    deformity. Shortening of the foots lateral column will
    create a planovalgus deformity. The calcaneus, when
    fractured, will shorten and angulate. All components of
    the foot must be spatially oriented in their proper position in order for the foot to function properly. This crucial concept must be kept close in mind while reconstructing fractures of the foot. Advances in fracture
    fixation and the recognition of the importance of an
    anatomic reduction have helped to dramatically improve functional outcomes following injury.

    Initial Evaluation
    The foot remains a commonly overlooked aspect of the
    secondary musculoskeletal survey. Metatarsal and foot
    phalanx fractures remain as one of the most frequently
    unnoticed fractures during the initial evaluation. A high
    level of suspicion is the first step toward an accurate diagnosis and prevention of missed injuries. Evaluation
    begins with a detailed history of the traumatic event.
    The mechanism, magnitude, duration, and location of
    the traumatic event will raise the index of suspicion,
    prompt the examiner to inquire further, and aid in the
    diagnosis. A complete review of systems should include
    additional mitigating factors that may impact treatment. Identifying the presence of diabetes mellitus, previous bony or soft tissue injury, or existing arthritic
    conditions is helpful. The ambulatory status of the patient should be documented. Questions regarding current or previous nicotine use should not be neglected,
    as a positive history may influence surgical decision
    making. Occupational status and patient expectations
    are additional important pieces of information.
    Patients frequently are vague with reports of foot
    pain. If the patient is cooperative during the interview,
    it is helpful to obtain specific information regarding the

    Orthopaedic Knowledge Update 10

    507

    Section 4: Lower Extremity

    4: Lower Extremity

    point of maximal pain. Pain localized at the medial


    midfoot will increase the suspicion for a Lisfranc injury
    and simultaneously decrease concern for a lateral talar
    process or calcaneus fracture. Both feet and ankles
    should be completely exposed and visually inspected
    for swelling, ecchymoses, and deformity. Puncture
    wounds or lacerations should increase vigilance for the
    presence of open fractures. The web spaces are often
    overlooked and should be individually examined for
    skin injury, along with the posterior heel. Open fractures should be treated with sterile gauze dressing and
    the prompt administration of a first-generation cephalosporin and tetanus toxoid. It is generally not advisable to probe wounds or attempt dbridement in the
    emergency department, especially if a formal inspection
    and surgical dbridement are planned during surgical
    treatment. Formal wound cultures typically are not
    helpful unless obtained after thorough dbridement and
    irrigation in a sterile environment. A detailed neurovascular examination must be performed. Vascular assessment is still possible if the patient is not awake. A cursory examination is not sufficient because subtle
    dysesthesias are frequently present despite the patient
    reporting intact sensation.1 These sensory disturbances can frequently result in postinjury neuropathic
    pain. All sensory nerves to the foot should be examined, including the deep peroneal, superficial peroneal,
    medial plantar, lateral plantar, sural, and saphenous
    nerves. Motor function also should be assessed. The
    dorsalis pedis and posterior tibial arteries should be
    palpated and the quality, cadence, and amplitude of the
    pulses documented. Ankle-brachial indices are objective
    measurements to evaluate the vascular competency of
    the limb compared with the contralateral side.
    High-quality radiographs are obtained, preferably
    without the area being obscured by articles of clothing
    or plaster. It is crucial that orthogonal radiographs with
    true AP, oblique, and lateral projections include the
    joint above and the joint below the suspected injury.
    Based on plain radiographic findings, a CT scan may
    be obtained. Upon completion of the assessment, the
    foot and ankle are placed into a well-padded, durable
    splint to improve pain control and allow easy softtissue inspection if warranted.
    Skin blistering has a correlation with the degree of
    soft-tissue shearing at the time of trauma.2 Blisters may
    emerge immediately or over the course of hours, sometimes days. Two main subtypes of fracture blister have
    been identified (serous or hemorrhagic), based on the
    depth of dermal-epidermal injury. Proponents of the
    deroofing of blister skin argue that epithelialization of
    the blister bed is hastened with this technique. Those
    against deroofing of blisters argue that the intact blister
    skin serves as biologic dressing that keeps the blister
    bed sterile. Deroofing or application of silver-based
    topical ointments have been shown to confer no statistical difference in patient outcomes.3 Surgery should be
    delayed until blister beds have been re-epithelialized,
    and incisions across unepithelialized or hemorrhagic
    blister beds should be avoided.3
    Compartment syndrome of the foot is a frequently
    508

    Orthopaedic Knowledge Update 10

    overlooked clinical entity. Suspicion should be especially heightened in the presence of a high-energy
    crushing event; however, isolated compartment syndromes of the foot without fracture have been reported. Some authors suggest that compartment syndrome develops in up to 10% of calcaneal fractures.4
    The presence of an open injury does not preclude compartment syndrome, as small fascial defects may not be
    sufficient to significantly alter compartment volume.5 A
    missed compartment syndrome results in treatable
    curly toes, and is associated with well-documented
    disabling sequelae such as toe clawing, stiffness, aching,
    weakness and atrophy, sensory disturbances, and fixed
    deformities of the forefoot.6 Compartment syndrome is
    clinically challenging to diagnose because foot trauma
    is an especially painful event, and often patients are experiencing considerable discomfort even at rest. Despite
    this nebulous presentation, patients with compartment
    syndrome frequently describe a severe, relentless, burning pain involving the entire foot. The skin often is
    shiny and taut. Toe abduction and adduction specifically provoke compartments within the foot and help
    confirm the diagnosis. In one series, up to 85% of patients with foot compartment syndrome experienced
    pain with passive motion, making this the most sensitive clinical finding.7 If pathologic pain, swelling,
    numbness, or vascular status worsen, the patient
    should be reassessed and invasive pressure monitoring
    performed if necessary. All nine foot compartments
    should be measured. The medial compartment is confluent with the deep posterior compartment of the leg.
    The calcaneal compartment is especially susceptible to
    involvement with calcaneal fractures. This compartment contains the quadratus plantae, the lateral plantar
    nerve, and occasionally the medial plantar nerve. This
    frequently overlooked compartment must be recognized as a possible offending factor, especially in the
    setting of a calcaneus fracture.8 Surgical release is performed by way of a dorsal medial and dorsal lateral incision to decompress the four interossei and the deeper
    adductor compartment. A medial longitudinal incision
    will release the medial, calcaneal, superficial, and lateral compartments. Negative pressure dressings may
    aid with postoperative wound care, and delayed closure
    is performed in a staged manner as is typical for compartment syndromes elsewhere in the body.

    Calcaneus Fractures
    With the development of internal fixation principles the
    patient with calcaneus fracture is no longer incapacitated. Despite these advances, the definitive treatment
    of calcaneus fractures and the indications for surgical
    intervention remain controversial.9-11

    Mechanism of Injury and


    Fracture Characteristics
    Calcaneus fractures result from a complex interaction
    of axial, angulatory, and torsional loads. The injury

    2011 American Academy of Orthopaedic Surgeons

    Chapter 39: Foot Trauma

    2011 American Academy of Orthopaedic Surgeons

    Imaging
    All patients with suspected calcaneus fractures should
    undergo a plain radiographic evaluation including
    high-quality AP, oblique, and lateral projections of the
    foot. The diagnosis is most evident on the lateral projection, which will demonstrate the degree of calcaneal
    compression quantified by the Bohler angle. The degree
    of height loss has prognostic implications, with a
    smaller Bohler angle correlating with poorer function
    outcomes.17 Shortening of the calcaneus and degree of
    involvement of the posterior facet may also be appreciated with a lateral radiograph. The AP foot radiograph
    examines for anterior process fracture lines commonly
    oriented in the sagittal plane. A separate Harris axial
    heel view will depict the amount of varus tuberosity angulation, lateral wall displacement, and lateral tuberosity displacement. The degree of fibular abutment is also
    appreciated on this radiograph. Because calcaneal fractures are typically involved with high-energy events, additional imaging is warranted for concomitant injuries
    including the ipsilateral ankle, knee, or lumbar spine.
    CT is frequently performed primarily before surgery.
    Each fracture line and fragment are clearly discernable.
    Axial sections define the size of the sustentacular fragment, extension to the calcaneocuboid facet, and the
    status of the posterior facet. Reformats in the lateral
    and coronal planes parallel the findings in the lateral
    and Harris axial views, respectively. Three-dimensional
    reformats may help the surgeon crystallize these multiple sequences as a readily comprehensible modeled simulation.
    Classifications of CT are widely accepted, helping in
    preoperative identification of those patterns associated
    with poorer outcomes or more technically challenging
    surgery. The most common, the Sanders classification,
    uses the coronal plane reformats to identify the widest
    portion of the talar inferior facet. The number and location of posterior facet fracture lines have been demonstrated to correlate with outcomes following surgical
    fixation, with poorer outcome measures associated
    with more comminuted patterns.17,18

    4: Lower Extremity

    mechanism can be likened to an axe cleaving a block of


    wood. The most lateral portion of the talar lateral process acts as the axe, with the critical angle of Gissane
    serving as the strike point. This latter region is more
    clearly defined as the dense cortical bone on the lateral
    superior calcaneal surface, just anterior to the posterior
    facet. The resulting fracture line travels anterolaterally
    and posteromedially. The anterolateral fracture exit
    point typically is at the critical angle of Gissane, but
    frequently may be located as anterior as the calcaneocuboid facet. The posteromedial fracture line exit point
    is posterior to the sustentaculum. As a result, two main
    fragments are created by the primary fracture line. The
    posterior fragment consists of the posterolateral tuberosity and portions of the posterior facet. The anterior
    fragment consists of the anterior process, the middle
    facet, and typically the most medial regions of the posterior facet.12 Depending on the magnitude of injury,
    additional fracture lines may emanate from the strike
    point. These secondary fracture lines split the anterior
    process in the sagittal plane. Posterior-directed secondary fracture lines may cleave the posterior facet in a
    predominantly sagittal plane, creating a joint depression fracture pattern. In this scenario, a variable portion of the superolateral posterior facet is rotated distally and caudally into the trabeculae sparse region
    known as the neutral triangle. Both elevation and rotation of this fragment are required to properly reduce
    the posterior facet. The posterior-directed secondary
    fracture line may similarly travel in the coronal plane,
    cleaving the tuberosity in half when viewed from the
    lateral projection. A tongue-type injury can be identified by the presence of an intact cephalad tuberosity
    cortex that is confluent with portions of the posterior
    facet.13 In this setting, tuberosity displacement is further exacerbated by the attachment of the
    gastrocnemius-soleus complex.
    With the primary and secondary fracture lines thus
    formed, the calcaneus adopts a typical posture of vertical height loss, widening with lateral wall expulsion,
    length loss when viewed from the lateral projection, and
    varus positioning of the heel. There is commonly a separate medial sustentacular fragment of varying size, also
    termed the constant fragment because of the tendency
    of discovering this fragment in its correct anatomic relationship with the talus due to the competency of the
    talocalcaneal interosseous ligament. This fragment may
    be used as the starting point for reconstructive efforts.
    The pathologic posturing of the fractured calcaneus also
    causes the talus to rest in a more horizontal position,
    which eventually will result in tibiotalar impingement
    and the inability to dorsiflex the ankle.
    If the energy absorbed is extreme, open fractures
    may result. The caudal extent of the sustentaculum is
    frequently the offender, piercing the medial soft tissues.
    A severe eversion moment of the foot at the time of axial load may precipitate further tension failure of the
    medial soft tissues. As expected, more severe open fractures are associated with high rates of osteomyelitis and
    wound complications.14-16 These injury patterns should
    be approached with great caution.

    Decision Making for Treatment


    Optimal treatment of calcaneus fractures remains controversial and varies according to each individual fracture and patient. Nonsurgical treatment is indicated for
    patients with nondisplaced fractures, those unable to
    tolerate surgery, and those unable to walk. Nonsurgical
    treatment should be considered for patients with documented psychiatric, organic brain, or substance abuse
    disorders because they may not comply with a postoperative weight-bearing protocol. Factors that affect the
    local microcirculation and threaten wound healing
    should be considered in the decision to treat surgically.
    Relative contraindications include a history of smoking, diabetes mellitus, or peripheral vascular disease.
    Improved outcomes following surgical fixation are
    associated with smoking cessation, age younger than
    40 years, and a simple fracture pattern found on CT.
    Surgically treated patients who have poor physiologic

    Orthopaedic Knowledge Update 10

    509

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 1

    Intraoperative posterior facet reduction through


    a lateral extensile approach.

    status, a heavy physical workload, workers compensation claims, comminuted fracture patterns, and those
    who smoke do not demonstrate statistically different
    functional outcome scores than those treated nonsurgically.18 Women, males younger than 40 years, those patients with a light physical workload, or those with
    simple articular fracture patterns have a better prognosis with surgical intervention. Recent literature suggests
    that despite comminution of the posterior facet, open
    surgical treatment to restore calcaneal morphology will
    facilitate later fusion procedures. Patients treated with
    staged fusion had improved long-term functional outcome scores compared with patients initially treated
    without surgery and then with staged calcaneal osteotomy and fusion.19

    Surgical Treatment
    Most displaced intra-articular calcaneal fractures are
    treated with direct visualization and open reduction
    and internal fixation. Once the decision for surgical
    treatment has been made, the foot must achieve softtissue quiescence before incisions, which is indicated by
    the disappearance of turgidity from the lateral calcaneal soft tissue and the appearance of fine skin wrinkles. Generalized swelling should not be confused with
    the pathologically widened foot due to tuberosity displacement and angulation. Extreme tuberosity displacement can affect skin perfusion directly over the medial
    sustentaculum. Full-thickness ulcerations can result
    from this pressure-induced necrosis. Fracture blisters
    may be deroofed and treated with a dry bandage until
    epithelialization. Although typically on the medial side,
    some blisters may appear laterally. Planned incisions
    should avoid blister beds, especially hemorrhagic blisters. Incisions that cross these types of blister beds have
    demonstrated an increased risk of postoperative wound
    complications.3 A perisurgical sciatic nerve blockade,
    an analgesic technique, has been correlated with a significant decrease in the amount of postoperative nar510

    Orthopaedic Knowledge Update 10

    Figure 2

    Intraoperative Harris radiograph confirms restoration of heel alignment as well as length and
    position of screw fixation.

    cotics required to achieve pain control and is a safe intervention because postoperative foot compartment
    syndrome in this setting is rare.20
    Surgical intervention is typically performed as a lateral extensile approach.16 The developed flap is nourished by branches of the lateral calcaneal artery. Injury
    to this feeding vessel during exposure may compromise
    the viability of the flap and increase the risk of apical
    flap necrosis.21 Exposure of the lateral aspect of the calcaneus allows for direct reduction of the anterior process, the posterior facet, and the tuberosity (Figure 1).
    Key elements in the reduction are anatomic congruity
    of articular surfaces, especially the posterior facet; medialization and compression of the calcaneal tuberosity;
    restoration of calcaneal height (Bohler angle); and ensuring the three talocalcaneal articulations are aligned
    anatomically with respect to each other, thus enabling
    subtalar motion. Appropriate valgus positioning of the
    tuberosity may be confirmed with the use of Harris radiographs (Figure 2). The reduction may be held and
    compressed by any number of prefashioned calcaneal
    plates. Without these plates, effective internal fixation
    may be accomplished with a series of strategically
    placed small fragment plates. Screws may be directed
    toward regions with the highest bone density available:
    the sustentaculum, the subchondral region of the posterior facet, the superior anterior process, and the calcaneal tuberosity deep to the Achilles insertion. If screw
    purchase is ineffective or severe osteopenia is present, a
    locked implant may be considered. The clinical ramifications of using a mechanically stronger locked implant
    remains unclear and warrants further investigation.13
    The use of bone graft or bone graft substitutes continues to be a source of debate when treating calcaneus

    2011 American Academy of Orthopaedic Surgeons

    Chapter 39: Foot Trauma

    4: Lower Extremity

    Figure 3

    Displaced tongue-type fracture (A) with skin at risk over the posterior heel. Percutaneous fixation of the displaced
    tuberosity fragment (B).

    fractures. The graft functions as a supplement to internal fixation, supporting the elevated posterior facet
    from below and as an osteoconductive matrix to facilitate bony ingrowth. In this regard, autograft bone has
    not been shown to improve functional outcome. Allograft bone may be used largely as scaffolding, with
    little supportive power. In contrast, injectable calcium
    phosphate cement as a fixation adjunct has been shown
    to permit early weight bearing without loss of the articular reduction. Though early weight bearing may be
    possible with these fractures, the literature does not
    demonstrate superior outcome scores with respect to
    the use of bone graft substitutes compared with allograft or no graft at all.
    Wound closure is a crucial element in surgical treatment. The flap periosteum is annealed to the periosteum of the calcaneus. Placement of accurate sutures is
    crucial and is aided by the passage of all the sutures before knot-tying. A tension-free closure is then performed using a modified Allgwer-Donati mattress suture. This technique has the least impact upon
    cutaneous blow flow compared with simple, vertical
    mattress, or horizontal mattress configurations.22 A
    well-padded splint is applied with the ankle in neutral
    position to prevent equinus posture. After wound healing has been documented, the foot is placed in a removable orthosis and subtalar motion is initiated under the
    supervision of a physical therapist. Weight bearing may
    be initiated at the surgeons discretion, typically once
    bony consolidation has occurred (between 6 to 12
    weeks).
    Results of Surgical Treatment
    An investigation performed by the Evidence-based Orthopaedic Trauma Group examined the difference between surgically and nonsurgically treated calcaneal
    fractures. Level II data, two meta-analyses, and one
    economic analysis abstract determined no statistical
    difference existed with respect to pain and functional

    2011 American Academy of Orthopaedic Surgeons

    outcome.17 Surgical treatment was considered superior


    to nonsurgical treatment concerning return to work
    and the ability to wear shoes of the same size before injury. When data were separated for subgroup analysis,
    a potential benefit was identified for women and young
    males, those patients with a single, simple displaced
    intra-articular fracture, and patients with light physical
    occupations. Arthrodesis rates were significantly reduced compared with nonsurgical treatment. From an
    economic perspective, surgical treatment was less costly
    than nonsurgical care. Potential benefits for nonsurgical treatment were seen in patients older than 50 years,
    those receiving workers compensation, and those with
    demanding physical occupations. It was concluded that
    large, randomized, controlled trials are required to validate the conclusions generated by the subgroup analysis.17

    Fractures Involving the Calcaneal Tuberosity


    Depending on the nature of the axial load, a fracture
    line may allow cephalad and rotational migration of
    the calcaneal tuberosity. The fracture fragment may be
    purely extra-articular or involve extension into the posterior facet, a tongue type-fracture. Chronic tightness
    of the gastrocnemius-soleus complex may contribute to
    this pattern. Whether intra-articular or extra-articular,
    the displaced tuberosity segment is pulled proximally
    by the gastrocnemius-soleus tendon with a variable degree of rotation. This fracture pattern has the potential
    of tenting the posterior heel skin, leading to soft-tissue
    compromise. If this fracture is left without intervention,
    skin necrosis and subsequent open fracture status may
    result. A recent study evaluating 139 patients with
    tongue type fractures revealed that 21% of patients had
    some degree of posterior skin compromise at presentation. The authors concluded that early recognition of
    the threatened posterior skin and emergent treatment

    Orthopaedic Knowledge Update 10

    511

    Section 4: Lower Extremity

    with percutaneous fixation effectively minimized progression to soft-tissue compromise23 (Figure 3).

    Talus Fractures

    4: Lower Extremity

    The talus articulates with the tibia, fibula, calcaneus,


    and navicular, and 60% of its surface is covered in cartilage. Talar body cartilage is thickest on the medial
    side and ranges from 0.8 to 2.0 mm on average. It thins
    at the proximal and distal portions of the curved dome.
    The talar radius of curvature is flattest in the center and
    matches the radius of curvature and cartilage thickness
    of the medial and lateral edges of the femoral trochlea.
    The talus serves as a link to transmit load to the foot
    and absorbs up to six times body weight with each
    step. A recent study of 25 tali identified consistent sets
    of lamellae of the talus, including vertical plates from
    the posterior two thirds of the lateral part of the trochlear surface onto the posterior facet, and sagittal plates
    from the medial body extending through the neck in
    continuity with curved plates of the head.22 Although
    the talus has no tendinous attachments, the unique
    bony architecture affords pronation-supination and
    dorsiflexion-plantar flexion through multiple facets and
    multiple ligament attachments. The body of the talus
    and the neck are not coaxial, with an average medial
    angulation of 24.23 Varus malposition of the talus by 2
    mm can prevent hindfoot eversion by locking the transverse tarsal joints, which leads to forefoot adduction.24
    Branches of the peroneal, posterior tibial, and anterior tibial arteries supply the talus, with most of the
    vascular supply from an anastomosis at the inferior talar neck. The extraosseous contributions of the surrounding arteries and tarsal canal are particularly important for healing. The artery of the tarsal canal, a
    branch of the posterior tibial artery, is considered the
    primary blood supply contributing to the lateral two
    thirds of the body.25
    An anteromedial approach (between the tibialis anterior and posterior) and an anterolateral approach
    (lateral to the peroneus tertius) are often combined
    with a posterolateral approach (between the peroneal
    and Achilles tendons) to gain adequate exposure of the
    fracture. Understanding of the blood supply is important when considering exposure of the talus, and a medial or lateral malleloar osteotomy can improve visualization while minimizing soft-tissue dissection and
    disruption of the bloody supply.26
    Plain AP, lateral, and oblique radiographs of the ankle as well as a Canale view (foot internally rotated 15
    with the beam tilted 15 cephalad) are appropriate in
    the initial evaluation of a talus fracture. CT can add
    valuable information about fracture pattern and
    amount of preoperative comminution, and has been
    found to be the most accurate method to measure postoperative malunion and rotation.24 A cadaver study
    demonstrated that posteromedial fractures of the talus
    could be reliably identified on plain radiographs by implementing a 30 external rotation view.27
    512

    Orthopaedic Knowledge Update 10

    Talar Neck Fractures


    Fractures of the talar neck occur after dorsiflexion of
    the ankle. The pattern of comminution and articular involvement depends on the deforming force and position
    of the limb at the time of injury. The Hawkins classification continues to be the standard preoperative grading system that correlates with postoperative osteonecrosis of the talar body.28,29 It has been suggested that
    delay in fixation of the fracture does not adversely affect outcome as much as the initial degree of displacement and association with an open injury.30 Initial
    treatment includes reduction of the fracture, if displaced, via knee flexion, ankle plantar flexion, and ankle distraction. The reduced fracture should be placed
    in a well-padded splint with careful monitoring of the
    soft tissues. Open fractures require emergent surgical
    treatment.
    Type I are nondisplaced, whereas type II are displaced fractures where the body stays reduced in the
    ankle mortise and the subtalar joint is dislocated. Type
    III fractures involve talar neck displacement with dislocation of both the ankle and subtalar joints. Type IV
    fractures are type III with a corresponding talonavicular dislocation.
    Hawkins type I fractures can be treated nonsurgically but require strict adherence to no weight bearing
    and recurrent radiographs to ensure that displacement
    does not develop. Displaced fractures (types II through
    IV) require open fixation to restore talus anatomy and
    function. Union has been reported in 88% of fractures.30 Fixation of the fracture depends on the fracture
    pattern and presence of comminution, which commonly occurs in the medial neck. Spanning plates are
    frequently necessary to maintain talar neck length and
    may be used as an adjunct to screw fixation.31 Posterior
    to anterior screw fixation has improved strength over
    anterior screws alone.32 However, posterior fixation
    can be technically difficult and adds another potential
    insult to the tenuous blood supply of the talus when
    combined with anteromedial/lateral incisions. A recent
    cadaver study demonstrated that a mini-blade plate
    combined with an anterior screw provided equivalent
    stability to posterior fixation.33 Patients may begin
    range of motion if stable fixation was obtained postoperatively; however, strict adherence to no weight bearing is necessary until radiographic union is confirmed.
    Functional outcomes following talar neck fractures
    vary and depend on the development of complications
    such as osteonecrosis, malunion, and arthritis of the
    tibiotalar and talocalcaneal joints. Posttraumatic arthritis is more common than osteonecrosis30,34,35 (Figure 4).
    In one study of 70 patients, approximately half required secondary reconstructive procedures 10 years
    following fixation of talar neck fractures.36 Rates of osteonecrosis range from 10% to 20% for Hawkins type
    I fractures, 20% to 50% for type II, and 60% to 100%
    for type III. A positive Hawkins sign is characterized by
    radiolucency of the subchondral bone in the talar body
    on mortise radiographs and represents localized osteopenia as bone resorption occurs during the revascu-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 39: Foot Trauma

    Figure 4

    Displaced talar neck fracture (arrow) (A) that underwent open reduction and internal fixation and complete healing (B). Five years postoperatively, the patient complained of subtalar discomfort; a sagittal CT demonstrates progressive degenerative change (C).

    Talar Body Fractures


    Fractures of the talar body are uncommon and account
    for 13% to 23% of talus fractures. An anatomic reduction and fixation is necessary to lessen the potential for
    posttraumatic arthritis, which has been reported in
    88% of patients.37 Body fractures are often the result of
    high-energy trauma and cause caudal compression
    when the hindfoot is supinated or pronated.38 Fracture
    patterns include coronal and sagittal split as well as articular crush. Specialized radiographs, such as a 30 external rotation view,27 and CT are needed to identify
    the fracture pattern so that proper exposure can be
    planned via a medial, lateral, or posterior malleolar osteotomy.39 Fixation with cannulated, headless screws
    can allow for solid fixation of the fracture fragments
    below the articular surface.
    One study reported the retrospective results of 19
    patients with displaced fractures of the talar body
    treated by internal fixation with an average follow-up
    of 26 months.38 Results were excellent in four patients,
    good in six, fair in four, and poor in five. Complications included superficial wound problems, delayed
    union or malunion, and osteonecrosis in seven patients.
    It was concluded that talar body crush fractures and
    fractures associated with open injuries or talar neck
    fractures have a less favorable outcome.38

    Lateral Process and Posteromedial Fractures


    The lateral process of the talus forms the talofibular
    joint on its superolateral margin and the most lateral
    portion of the posterior subtalar facet on its inferolateral margin. Fractures of the lateral process of the talus
    most commonly occur from forced dorsiflexion and axial loading with eversion. According to one study, lateral process fractures represent 10.4% of all talus fractures at a level I trauma center.40 The awareness of this

    2011 American Academy of Orthopaedic Surgeons

    4: Lower Extremity

    larization and remodeling process. The prognostic reliability of the Hawkins sign was evaluated in 41
    patients with displaced talar fractures, and was found
    to have a sensitivity of 100% and a specificity of
    58%.35 It most commonly appears between 6 and 9
    weeks after fixation.35

    fracture type has grown along with the popularity of


    snowboarding, as it comprises 34% of ankle fractures
    in snowboarders. Type I involves a nonarticular fragment, type II involves the talofibular and subtalar
    joints, and type III involves comminution. The fracture
    can often be a source of chronic pain and is commonly
    misdiagnosed as an ankle sprain. The long-term sequelae of lateral process fractures include malunion,
    nonunion, and degenerative subtalar arthritis. CT is often necessary to visualize the entire fragment, but the
    fracture can sometimes be seen on an AP ankle radiograph. Nonsurgical treatment with limited weight bearing is recommended for nondisplaced fractures; however, surgical intervention with open reduction and
    internal fixation or excision of the fragment is suggested for displaced or large fractures.
    One study evaluated the clinical and radiologic outcome after unilateral fracture of the lateral process of
    the talus in 23 snowboarders with a mean follow-up of
    3.5 years treated either surgically or nonsurgically.41
    Subtalar osteoarthritis was present in 45% of patients;
    outcome after fracture of the lateral process of the talus
    in snowboarders is favorable with early diagnosis and
    prompt treatment.
    Posteromedial fractures are often associated with
    high-energy trauma and medial subtalar dislocations.
    CT or an external rotation radiograph is usually
    needed to identify the amount of displacement.27
    Larger, displaced fragments require fixation via a direct
    posterior or medial malleolus osteotomy in order restore the articulations of the ankle and subtalar joint.

    Subtalar Dislocations
    Subtalar dislocations often result from high-energy injuries with the medial or lateral clinical appearance of
    the foot demonstrating the direction of the dislocation.
    Medial dislocation is more common and occurs via
    plantar flexion and inversion. Prevention of reduction
    results from buttonholing through the extensor digitorum brevis. Lateral dislocation occurs with plantar
    flexion and eversion, and prevention of reduction results from buttonholing through the medial talonavicular capsule and dorsal subluxation of the posterior
    tibial tendon. Plain radiographs will reveal the disloca-

    Orthopaedic Knowledge Update 10

    513

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 5

    Radiograph showing a medial column plate for


    temporary stabilization of navicular dislocations.

    tion, and early closed reduction is advised. Postreduction CT is advised to ensure joint congruency and to
    evaluate for subtalar debris or osteochondral injury. Up
    to 89% of patients will develop radiographic signs of
    subtalar arthritis.42

    Fractures of the Tarsal Navicular


    The tarsal navicular is a rectangular bone that articulates with the talar head, calcaneus, cuboid, and each
    cuneiform. On the concave side exists a synovial ball
    and socket joint with the talar head. This articulation is
    a major component of subtalar motion. This mobile region is contrasted by the relatively immobile planar
    naviculocuneiform articulations, a rigid complex that
    forms the midfoot arch. Fractures of the navicular may
    either be intra-articular body fractures, ligamentous
    avulsion fractures, or chronic stress fractures.
    Acute fractures of the tarsal navicular body commonly occur after axial loading injuries to the medial
    column of the forefoot. Variable amounts of navicular
    articular impaction may be seen. Untreated subluxation
    and instability leads to abnormal contact stresses and
    the subsequent propensity for posttraumatic arthritis.
    Isolated talonavicular arthrosis is a particularly difficult
    condition to treat, as attempts at solitary fusion of this
    articulation are associated with high rates of nonunion.
    The resultant arthrodesis, if successful, significantly
    limits subtalar motion and imparts increased stress
    upon adjacent joints.
    Navicular body fractures have been classified into
    three types. Type 1 fractures exist in the coronal plane,
    without resulting angulation of the forefoot. In type 2
    514

    Orthopaedic Knowledge Update 10

    fractures, the fracture line is from dorsolateral to


    plantar-medial and the forefoot is displaced medially. In
    type 3 injuries, there is sagittal plane comminution and
    the forefoot is displaced laterally. In type 3 fractures,
    which are increasingly observed following high-speed
    motor vehicle accidents, the head of the talus is forced
    in a plantar-lateral direction, resulting in talonavicular
    subluxation and instability. There is often impaction
    and comminution of the plantar-lateral navicular body,
    which contributes to further instability and joint incongruity. This classification system separates simpler patterns from more complex types. As expected, simpler
    fracture patterns and those patterns where anatomic reduction was possible were associated with high clinical
    outcome scores.43
    If the patient is an acceptable surgical candidate, surgical fixation of displaced intra-articular navicular
    body fractures is indicated. Surgical goals include restoration of a congruous talonavicular articular surface
    and permission of early subtalar motion, if possible.
    Nondisplaced navicular fracture may be treated in a
    nonweight-bearing cast for 6 to 8 weeks. Simple fracture patterns may be treated with lag screw or plate fixation, confirming the articular reduction visually and
    radiographically. Temporary joint distraction with the
    use of an external fixator will permit better visualization of the articular surface. It is important to avoid exposing the complete cephalad surface of the navicular
    body for concern of jeopardizing the blood supply.
    Type 3 fractures are challenging to treat surgically. As
    mentioned previously, there is often joint impaction
    plantarly, which must be disimpacted to reestablish the
    normal arcade of the talar facet. The normal curvature
    of the tarsal navicular must not only be restored from a
    medial to lateral dimension, but also from a dorsal to
    plantar dimension. Unfortunately, the plantar-lateral
    comminution present in these injuries can be difficult to
    see. Often, the fragmentation is so extensive that internal fixation is impossible. Despite these surgical challenges, the instability must be addressed if the talar
    head remains persistently subluxated. In these instances, a temporary medial column plate may be applied. An 8- to 10-hole, 2.7-mm reconstruction plate
    with fixation points in the first metatarsal, cuneiforms,
    and talar head creates a medial column scaffold. Once
    appropriately reduced, screw fixation will permit a durable construct while bony and soft-tissue healing occurs44 (Figure 5). Plate removal is typically possible after 3 to 4 months. Another option for these challenging
    injuries is a transarticular screw across the talonavicular articulation to maintain the reduction. This screw
    must be removed once bony healing has occurred to allow some talonavicular motion.
    Avulsion fractures of the navicular body are also
    common, representing up to half of all navicular fractures.45 Fractures involving the dorsal lip result from
    foot eversion and pull of the deltoid ligament attachments. Injury to the medial or plantar navicular results
    from the attachments of the posterior tibial tendon or
    the spring ligament. Nonsurgical treatment typically results in excellent functional results. The foot is placed

    2011 American Academy of Orthopaedic Surgeons

    Chapter 39: Foot Trauma

    Fractures of the Cuboid


    The cuboid represents a key element in the lateral column of the foot. It is the only bone in the foot that articulates with both the tarsometarsal joint (Lisfranc
    complex) as well as the midtarsal joint (Chopart joint).
    The cuboid also connects the lateral column to the
    transverse plantar arch, thus providing rigid inherent
    stability to the foot. Fractures of the cuboid typically
    result from an axial load or abduction moment of the
    forefoot. The injury may be subtle and is often difficult
    to detect with plain radiographs alone. A slight break
    in the cuboid cortical line or double density of the calcaneal facet may be the only finding. When evaluating
    for cuboid fractures, it is essential to consider the foot
    as two separate but linked medial and lateral columns.
    Like the pelvic ring, injury to one column frequently
    creates injury to the other. For example, compression of
    the cuboid is accompanied by tension failure of the medial column, typically through capsuloligamentous
    structures. Though the only radiographically evident
    injury is a cuboid fracture, there may be global ligamentous instability of the forefoot, which predisposes
    to lateral subluxation or frank midfoot dislocation.
    The diagnosis of a cuboid fracture requires a high index of suspicion. Lateral swelling or tenderness should
    prompt a careful physical examination as well as highquality views of the foot. Loss of cuboid height and
    intra-articular involvement of the calcaneal facet is best
    appreciated on the oblique view. Articular impaction
    may also be appreciated on the lateral view. CT will
    help clarify each individual fracture line to aid in preoperative assessment. Currently, no consensus exists regarding surgical indications of these fractures. Nondisplaced fractures of the cuboid may be closely observed
    in a nonweight-bearing short leg cast for evidence of
    early fracture displacement. If no displacement occurs,
    treatment should continue until the fracture is healed in
    approximately 6 to 8 weeks. Extra-articular fractures
    that result in forefoot deformity should be considered
    for surgical treatment. Loss of lateral column height

    2011 American Academy of Orthopaedic Surgeons

    with accompanying medial capsuloligamentous incompetence allows the foot to assume a pathologic
    planovalgus position and creates the potential for longterm disability. This so-called nutcracker injury can be
    treated with a lateral distraction frame to regain the appropriate cuboid height, followed by bone grafting and
    internal fixation to secure the reduction. Depending on
    the quality of the fixation, the distraction frame may be
    left in place as additional support for the lateral column lengthening. It is important to avoid overdistraction of the lateral column, as this may create a paradoxical cavus foot. Preoperative planning using the
    contralateral limb as a template will prevent this surgical error. Displaced intra-articular fractures should also
    be considered for surgical fixation. The calcaneocuboid
    joint is a mobile planar synovial joint and articular incongruity results in abnormal contact force distribution, joint irritation, and subsequent arthrosis. In addition, distal impaction of the articular facet results in an
    osseous defect into which the calcaneal anterior process
    may subside, effectively creating dynamic lateral column instability. Progressive weight bearing may occur
    once fracture consolidation has been achieved, typically
    at 6 to 8 weeks.

    4: Lower Extremity

    in a rigid shoe for 3 to 6 weeks. Larger fragments associated with the posterior tibial tendon insertion may
    undergo reduction and internal fixation if significant
    retraction and subsequent concern for healing exists.
    Stress fractures of the tarsal navicular are insidious
    conditions that are often initially overlooked. The fracture line is characteristic, oriented in the sagittal plane
    in the central third of the bone.9 This overuse injury
    frequently seen in athletes may be exacerbated by preexisting foot deformities such as cavovarus posture.
    The diagnosis may be confirmed with the use of either
    technetium bone scan or CT. Initial treatment is strict
    adherence to no weight bearing in a short leg cast for 6
    to 8 weeks. Progressive weight bearing is permitted
    once the patient is clinically symptom free. Patients
    who do not respond to nonsurgical treatment are candidates for lag screw fixation, which should be augmented with autogenous grafting.

    Tarsometatarsal Injuries
    Injury to the tarsometatarsal joints (Lisfranc injuries)
    represents approximately 0.2% of all fractures; however, the injuries are missed in approximately 20% to
    30% of multitrauma patients, so the actual incidence
    may be underestimated.46 The proximal intermetatarsal
    ligaments create a strong connection in the midfoot,
    but are absent between the first and second metatarsals. The plantar ligaments between the base of the second metatarsal and the medial cuneiform are the strongest component of the Lisfranc ligament. The inherent
    stability of the tarsometatarsal joints creates a rigid lever arm of the medial column of the foot during pushoff in the gait cycle, and is maintained through an anatomic Roman arch in the coronal plane and recessed
    base of the second metatarsal in the axial plane. A recent study comparing preoperative MRI to intraoperative findings of Lisfranc injuries identified the important role of the intercuneiform ligaments for midfoot
    stability.47 Normal tarsometatarsal joints allow for only
    2 to 4 mm of motion in the first tarsometatarsal joint
    and no motion in the second and third joints, while the
    fourth and fifth tarsometatarsal joints allow up to 10
    of plantar flexion and dorsiflexion.46
    Trauma often results from direct crushing or indirect
    axial loading combined with a twisting mechanism. Patients will report pain with weight bearing and midfoot
    rotation. Patients with more subtle or purely ligamentous injuries have midfoot pain when the second metatarsal is depressed and elevated. Care must be taken to
    examine for a compartment syndrome or neurovascular
    injury and to document decreased dorsal sensation. AP,
    lateral, and oblique radiographs will often reveal a
    fleck sign at the base of the second metatarsal, which

    Orthopaedic Knowledge Update 10

    515

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 6

    AP (A) and lateral (B) foot radiographs demonstrating a fleck sign (arrows) of the base of the second metatarsal in a
    patient with an unstable Lisfranc fracture-dislocation.

    represents the plantar attachment of Lisfranc ligament


    (Figure 6). For injuries associated with lower energy
    trauma, weight-bearing or simulated weight-bearing AP
    views of the bilateral feet are needed to evaluate for
    widening. MRI is helpful to delineate the involvement
    of the ligament complex in cases where the plain radiographs are negative with a positive clinical examination.47 CT can be useful in patients with comminution
    to better define the extent of injury. Various classification schemes have been proposed and are based on the
    presence of a lateral column disruption or the divergence of the lateral and medial columns.48
    Surgical intervention is recommended for any displaced injury and outcomes demonstrate that improved
    function is associated with anatomic reduction and
    minimal delay in treatment.48,49 Anatomic restoration
    of the second tarsometatarsal articulation should be
    performed first and secured with Kirschner wires. Care
    must be taken to then assess the remaining tarsometatarsal joints and intercuneiform joints for instability.
    Fixation of the first and third tarsometatarsal joints as
    well as the intercuneiform joints can be performed with
    screws or bridging plates. In the absence of communition and shortening of the lateral column, the fourth
    and fifth tarsometatarsal joints can be pinned. Removal
    of hardware is recommended 8 to 16 weeks after initial
    surgery. Disruption of the articular surface with multiple passes of wires and drills may be associated with
    late arthritis, and one recent cadaver study demon516

    Orthopaedic Knowledge Update 10

    strated a significant increase in articular damage with


    multiple repositioning of the guidewire during fixation.50 Another cadaver study demonstrated that a
    suture-button fixation device has similar stability to
    screw fixation for Lisfranc injuries.51 To date, there
    have been no clinical studies that investigate the use of
    the suture-endobutton compared with traditional screw
    fixation.
    Even with immediate fixation, 25% to 50% of patients can develop chronic midfoot pain and posttraumatic arthritis requiring subsequent procedures.52 A
    prospective, randomized study of 41 patients comparing open reduction and internal fixation to primary fusion of tarsometatarsal fracture-dislocations found a
    statistical improvement in American Orthopaedic Foot
    and Ankle Society scores and return to function in the
    primary arthrodesis group.53 Another prospective study
    compared the results of 22 patients treated with delayed fusion after nonsurgical treatment to those of 22
    patients who had immediate open reduction and internal fixation and found improved functional results with
    early surgical treatment.54

    Fifth Metatarsal Fractures


    Fractures of the fifth metatarsal are classified by anatomic location of the fracture. Classification of proximal fractures includes proximal tubercle fractures in-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 39: Foot Trauma

    4: Lower Extremity

    Figure 7

    Oblique radiographs of the foot of a professional American football player with a stress fracture of the fifth metatarsal (arrow) before (A) and after (B) intramedullary fixation with a 5.5-mm screw and calcaneal bone grafting.

    volving the metatarsocuneiform joint (type I), Jones


    fractures
    involving
    the
    proximal
    watershed
    metaphyseal-diaphyseal region (type II), and diaphyseal
    stress fractures (type III).55 The blood supply to the
    proximal fifth metatarsal is composed of metaphyseal
    arteries that enter at the base of the fifth metatarsal and
    a nutrient artery that enters at the proximal diaphysis.
    This perfusion pattern has a correlation to the risk of
    delayed union or nonunion due to an avascular zone
    created by the watershed area. One study reviewed 21
    type II proximal fifth metatarsal fractures that underwent open reduction and internal fixation and found
    that 18 of 21 patients had clinical and radiographic evidence of a varus hindfoot.56
    For all foot fractures, AP, lateral, and oblique radiographs should be obtained. Type I fractures can initially
    be treated with protected weight bearing in a removable boot, with increasing activity as tolerated by pain.
    Type II and III fractures should be treated with 6 to 8
    weeks of no weight bearing until signs of radiographic
    union have occurred. One prospective study of 52 fifth
    metatarsal proximal avulsion fractures treated with a
    stiff-soled shoe demonstrated that patients returned to
    work after an average of 22 days, but full recovery
    could take at least 6 months.57 A univariate and regression analysis on the factors predicting outcome of fifth
    metatarsal avulsion fractures performed on 38 patients
    showed that prolonged absence of weight bearing was

    2011 American Academy of Orthopaedic Surgeons

    associated with stiffness and a poor global outcome.58


    In individuals with high physical demands, or those
    with a type II delayed union or nonunion, open reduction and internal fixation of the fifth metatarsal is warranted. Percutaneous or limited open reduction and internal fixation with a solid or cannulated screw can be
    performed under fluoroscopy (Figure 7). Full fracture
    healing can take up 12 weeks.59 One study investigated
    the fixation of proximal fifth metatarsal fractures using
    5.5-mm screws and compared them to a retrospective
    group of patients whose fractures were fixed with
    4.5-mm screws. More of the 4.5-mm screws experienced bending, whereas more of the 5.5-mm screws
    penetrated the cortex distally; however, no clinical difference was noted between the screws.60 Another study
    followed 14 athletes for an average of 42 months after
    open reduction and internal fixation of a proximal fifth
    metatarsal fracture; 13 patients returned to the same
    level of activity and good to excellent results were
    achieved in all patients.61

    Metatarsophalangeal Dislocations
    Due to the thick plantar ligamentous attachments,
    metatarsophalangeal dislocations are uncommon and
    usually the result of high-energy injuries. Treatment includes closed reduction and assessment of stability un-

    Orthopaedic Knowledge Update 10

    517

    Section 4: Lower Extremity

    der fluoroscopy to confirm stability and cast or boot


    immobilization to prevent dorsiflexion of the toes for 4
    to 6 weeks. First metatarsophalangeal dislocation can
    be classified into type I, where the plantar plate buttonholes over the first metatarsal head proximal to the sesamoids; type IIA, where the intersesamoid ligament
    ruptures and the plantar plate buttonholes with separation of the sesamoids; and type IIB, where the sesamoid
    fractures in a transverse direction. Irreducible dislocations or proximal migration of the plantar plate and
    sesamoids warrant surgical intervention and repair.

    Treatment of fracture blisters with silver sulfadiazine


    (Silvadene) promoted epithelialization and reduced softtissue complications in nondiabetic patients with fracture blisters. Hemorrhagic blisters involve a higher risk
    of complications than serous blisters, presumably because hemorrhagic blisters represent a more severe tissue disruption.
    4.

    Myerson M, Manoli A: Compartment syndromes of the


    foot after calcaneal fractures. Clin Orthop Relat Res
    1993;290:142-150.

    5.

    Matsen FA III: Compartmental syndrome: An unified


    concept. Clin Orthop Relat Res 1975;113:8-14.

    6.

    Fulkerson E, Razi A, Tejwani N: Review: acute compartment syndrome of the foot. Foot Ankle Int 2003;
    24(2):180-187.

    7.

    Myerson M: Diagnosis and treatment of compartment


    syndrome of the foot. Orthopedics 1990;13(7):711-717.

    8.

    Manoli A II, Weber TG: Fasciotomy of the foot: An anatomical study with special reference to release of the
    calcaneal compartment. Foot Ankle 1990;10(5):267275.

    9.

    Miric A, Patterson BM: Pathoanatomy of intra-articular


    fractures of the calcaneus. J Bone Joint Surg Am 1998;
    80(2):207-212.

    10.

    Heier KA, Infante AF, Walling AK, et al: Open fractures


    of the calcaneus: Soft-tissue injury determines outcome.
    J Bone Joint Surg Am 2003;85(12):2276-2282.

    11.

    Berry GK, Stevens DG, Kreder HJ, et al: Open fractures


    of the calcaneus: A review of treatment and outcome.
    J Orthop Trauma 2004;18(4):202-206.

    12.

    Benirschke SK, Kramer PA: Wound healing complications in closed and open calcaneal fractures. J Orthop
    Trauma 2004;18(1):1-6.

    13.

    Gardner MJ, Nork SE, Barei DP, Kramer PA, Sangeorzan BJ, Benirschke SK: Secondary soft tissue compromise in tongue-type calcaneus fractures. J Orthop
    Trauma 2008;22(7):439-445.
    A high incidence of wound complications (21%) exists
    with displaced tongue-type calcaneus fractures. Urgent
    closed reduction, plantar flexion splinting, and wound
    observation are essential.

    14.

    Buckley R, Tough S, McCormack R, et al: Operative


    compared with nonoperative treatment of displaced
    intra-articular calcaneal fractures: A prospective, randomized, controlled multicenter trial. J Bone Joint Surg
    Am 2002;84(10):1733-1744.

    15.

    Sanders R: Displaced intra-articular fractures of the calcaneus. J Bone Joint Surg Am 2000;82(2):225-250.

    16.

    Radnay CS, Clare MP, Sanders RW: Subtalar fusion after displaced intra-articular calcaneal fractures: Does

    Metatarsal Fractures

    4: Lower Extremity

    The metatarsals have dense proximal ligamentous attachments as well as strong distal intermetatarsal ligaments at the level of the metatarsal neck. Therefore,
    isolated metatarsal fractures do not displace because of
    soft-tissue connections. Multiple metatarsal fractures
    are usually the result of direct trauma from a crush or
    fall, whereas isolated fractures of the fifth metatarsal
    usually occur from torsion creating an oblique fracture.
    Nondisplaced or minimally displaced lesser metatarsal shaft and neck fractures can often be treated in a
    cam walker boot with frequent early follow-up to ensure that displacement does not occur. Isolated fractures often heal uneventfully, but multiple fractures can
    displace. Metatarsal neck fractures that heal in plantar
    flexion of the metatarsal head can create metatarsophalangeal overload, metatarsalgia, and hammering of the
    lesser toes. A single dorsal incision can be used for the
    second, third, and fourth metatarsals, and fixation can
    be accomplished with Kirschner wires of dorsal plating.
    Surgical intervention is usually indicated for first metatarsal fractures due to the higher loads transmitted
    through the first ray for the medial column. Complications include malunion, nonunion, and synostosis,
    which can lead to alteration in gait from a change in
    the biomechanics of the weight-bearing surface of the
    foot. A review of 23 open metatarsal fractures in 10 patients with clinical follow-up of 6 to 122 months
    (mean, 53 months) found that injuries with minimal
    soft-tissue damage had improved outcomes compared
    to those with Gustilo type IIIB injuries.62

    Annotated References
    1.

    518

    Trepman E, Nihal A, Pinzur MS: Current topics review:


    Charcot neuroarthropathy of the foot and ankle. Foot
    Ankle Int 2005;26(1):46-63.

    2.

    Giordano CP, Scott D, Koval KJ, Kummer F, Atik T,


    Desai P: Fracture blister formation: A laboratory study.
    J Trauma 1995;38(6):907-909.

    3.

    Strauss EJ, Petrucelli G, Bong M, Koval KJ, Egol KA:


    Blisters associated with lower-extremity fracture: Results of a prospective treatment protocol. J Orthop
    Trauma 2006;20(9):618-622.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 39: Foot Trauma

    initial operative treatment matter? J Bone Joint Surg


    Am 2009;91(3):541-546.
    Improved functional outcome and fewer wound complications were associated with subtalar fusion for symptomatic posttraumatic subtalar arthritis after initial open
    reduction and internal fixation for displaced intraarticular calcaneus fractures compared with subtalar arthrodesis for the treatment secondary to calcaneal
    malunion following initial nonsurgical management.
    Level of evidence: III.
    17.

    Cooper J, Benirschke S, Sangeorzan B, Bernards C, Edwards W: Sciatic nerve blockade improves early postoperative analgesia after open repair of calcaneus fractures. J Orthop Trauma 2004;18(4):197-201.
    Borrelli J Jr, Lashgari C: Vascularity of the lateral calcaneal flap: A cadaveric injection study. J Orthop Trauma
    1999;13(2):73-77.

    19.

    Richter M, Gosling T, Zech S, et al: A comparison of


    plates with and without locking screws in a calcaneal
    fracture model. Foot Ankle Int 2005;26(4):309-319.

    20.

    Schildhauer TA, Bauer TW, Josten C, Muhr G: Open reduction and augmentation of internal fixation with an
    injectable skeletal cement for the treatment of complex
    calcaneal fractures. J Orthop Trauma 2000;14(5):309317.

    21.

    Sagi HC, Papp S, Dipasquale T: The effect of suture pattern and tension on cutaneous blood flow as assessed by
    laser Doppler flowmetry in a pig model. J Orthop
    Trauma 2008;22(3):171-175.
    As tension was increased across a porcine wound
    model, the modified Allgwer-Donati suture configuration had the least effect on cutaneous blood flow compared with sutures made in a simple, vertical mattress,
    or horizontal mattress fashion.

    22.

    23.

    24.

    Athavale SA, Joshi SD, Joshi SS: Internal architecture of


    the talus. Foot Ankle Int 2008;29(1):82-86.
    Twenty-five pairs of dry adult human tali were sectioned
    in various planes and dissected grossly to study the internal architecture of the talus. Two sets of lamellae
    were observed in the body of the talus. One set was descending from the posterior two thirds of the lateral
    part of trochlear surface onto the posterior calcaneal
    facet of the talus. These lamellae were in the form of
    vertical perforated interconnected plates. The second set
    of trabeculae originated from the medial part of the
    trochlear surface and the anterior third of the lateral
    part.
    Sarrafian S: Osteology, in Anatomy of the Foot and Ankle. Philadelphia, PA, JB Lippincott, 1983, pp 40-80.
    Chan G, Sanders DW, Yuan X, Jenkinson RJ, Willits K:
    Clinical accuracy of imaging techniques for talar neck
    malunion. J Orthop Trauma 2008;22(6):415-418.
    Eight cadaveric tali were evaluated to compare the ability of plain radiographs, CT, and radiostereometric
    analysis (RSA) to detect changes in talus fracture frag-

    2011 American Academy of Orthopaedic Surgeons

    25.

    Mulfinger GL, Trueta J: The blood supply of the talus.


    J Bone Joint Surg Br 1970;52(1):160-167.

    26.

    Ziran BH, Abidi NA, Scheel MJ: Medial malleolar osteotomy for exposure of complex talar body fractures.
    J Orthop Trauma 2001;15(7):513-518.

    27.

    Ebraheim NA, Karkare N, Gehling DJ, Liu J, Ervin D,


    Werner CM: Use of a 30-degree external rotation view
    for posteromedial tubercle fractures of the talus. J Orthop Trauma 2007;21(8):579-582.

    4: Lower Extremity

    18.

    ment position and alignment. The fragments were then


    displaced and rotated to create a varus and supination
    deformity, and screw fixation was repeated in nonanatomic alignment. Displacement and rotation were directly measured. The most accurate imaging technique
    to measure displacement in talar neck malunion is CT
    scan. RSA was less useful as an imaging technique in
    this study.

    The investigators evaluated the use of the 30 external


    rotation view for the diagnosis of fractures of the posteromedial tubercle of the talus using cadaver specimens. On the 30 external rotation view of the ankle, all
    fractures of the posteromedial tubercle of the talus were
    revealed. In contrast, the fracture was visualized in only
    two cases using the standard lateral radiograph of the
    ankle, and not once in the anteroposterior or mortise
    views.
    28.

    Hawkins LG: Fractures of the neck of the talus. J Bone


    Joint Surg Am 1970;52(5):991-1002.

    29.

    Canale ST, Kelly FB Jr: Fractures of the neck of the talus: Long-term evaluation of seventy-one cases. J Bone
    Joint Surg Am 1978;60(2):143-156.

    30.

    Lindvall E, Haidukewych G, DiPasquale T, Herscovici


    D Jr, Sanders R: Open reduction and stable fixation of
    isolated, displaced talar neck and body fractures. J Bone
    Joint Surg Am 2004;86(10):2229-2234.

    31.

    Fleuriau Chateau PB, Brokaw DS, Jelen BA, Scheid DK,


    Weber TG: Plate fixation of talar neck fractures: Preliminary review of a new technique in twenty-three patients. J Orthop Trauma 2002;16(4):213-219.

    32.

    Swanson TV, Bray TJ, Holmes GB Jr: Fractures of the


    talar neck: A mechanical study of fixation. J Bone Joint
    Surg Am 1992;74(4):544-551.

    33.

    Attiah M, Sanders DW, Valdivia G, et al: Comminuted


    talar neck fractures: A mechanical comparison of fixation techniques. J Orthop Trauma 2007;21(1):47-51.
    Thirty human cadaver tali were osteotomized across the
    talar neck. The specimens were randomized to one of
    three fixation groups: three anterior-to-posterior screws,
    two cannulated screws inserted from posterior to anterior, and one screw from anterior to posterior and a medially applied blade plate. No statistically significant difference was found between the fixation methods, even
    when variations in age and sex were considered.

    Orthopaedic Knowledge Update 10

    519

    4: Lower Extremity

    Section 4: Lower Extremity

    34.

    Vallier HA, Nork SE, Barei DP, Benirschke SK, Sangeorzan BJ: Talar neck fractures: Results and outcomes.
    J Bone Joint Surg Am 2004;86(8):1616-1624.

    35.

    Tezval M, Dumont C, Strmer KM: Prognostic reliability of the Hawkins sign in fractures of the talus. J Orthop Trauma 2007;21(8):538-543.
    In a retrospective study of the prognostic reliability of
    the Hawkins sign, 31 patients with displaced, surgical
    talar fractures were followed for more than 36 months.
    The Hawkins sign was absent in the five patients who
    developed osteonecrosis of the talus. In the remaining
    26 patients who did not develop osteonecrosis, a positive (full) Hawkins sign was observed 11 times, a partially positive Hawkins sign 4 times, and a negative
    Hawkins sign 11 times. The Hawkins sign thus showed
    a sensitivity of 100% and a specificity of 57.7%. Therefore, the Hawkins sign is a good indicator of talus vascularity following fracture.

    36.

    37.

    Vallier HA, Nork SE, Benirschke SK, Sangeorzan BJ:


    Surgical treatment of talar body fractures. J Bone Joint
    Surg Am 2004;86(Pt 2, suppl 1)180-192.

    38.

    Ebraheim NA, Patil V, Owens C, Kandimalla Y: Clinical outcome of fractures of the talar body. Int Orthop
    2008;32(6):773-777.
    Nineteen patients with talar body fractures were studied
    retrospectively to assess outcome after surgical treatment with an average follow-up of 26 months. Talar injuries are serious because they can compromise motion
    of the foot and ankle and result in severe disability.
    Crush fractures of the talar body and those associated
    with open injuries and talar neck fractures are associated with a less favorable outcome.

    39.

    40.

    41.

    520

    Sanders DW, Busam M, Hattwick E, Edwards JR,


    McAndrew MP, Johnson KD: Functional outcomes following displaced talar neck fractures. J Orthop Trauma
    2004;18(5):265-270.

    Muir D, Saltzman CL, Tochigi Y, Amendola N: Talar


    dome access for osteochondral lesions. Am J Sports
    Med 2006;34(9):1457-1463.
    Langer P, DiGiovanni C: Incidence and pattern types of
    fractures of the lateral process of the talus. Am J Orthop (Belle Mead NJ) 2008;37(5):257-258.
    A retrospective review at a level I trauma center over 3
    years identified the respective incidence and variation in
    fracture configuration of all isolated lateral process injuries. The incidence was 10.4%. The fractures were most
    commonly single large fragments closely followed in frequency by nonarticular chip patterns.
    von Knoch F, Reckord U, von Knoch M, Sommer C:
    Fracture of the lateral process of the talus in snowboarders. J Bone Joint Surg Br 2007;89(6):772-777.
    The authors present a study of the clinical and radiologic outcome after unilateral fracture of the lateral process of the talus in 23 snowboarders with a mean
    follow-up of 3.5 years. The outcome after fracture of
    the lateral process of the talus in snowboarders is favor-

    Orthopaedic Knowledge Update 10

    able provided an early diagnosis is made and adequate


    treatment, which is related to the degree of displacement
    and associated injuries, is undertaken.
    42.

    Bibbo C, Anderson RB, Davis WH: Injury characteristics and the clinical outcome of subtalar dislocations: A
    clinical and radiographic analysis of 25 cases. Foot Ankle Int 2003;24(2):158-163.

    43.

    Sangeorzan BJ, Benirschke SK, Mosca V, Mayo KA,


    Hansen ST Jr: Displaced intra-articular fractures of the
    tarsal navicular. J Bone Joint Surg Am 1989;71(10):
    1504-1510.

    44.

    Schildhauer TA, Nork SE, Sangeorzan BJ: Temporary


    bridge plating of the medial column in severe midfoot
    injuries. J Orthop Trauma 2003;17(7):513-520.

    45.

    Eichenholtz SN, Levine DB: Fractures of the tarsal navicular bone. Clin Orthop Relat Res 1964;34:142-157.

    46.

    Desmond EA, Chou LB: Current concepts review: Lisfranc injuries. Foot Ankle Int 2006;27(8):653-660.

    47.

    Raikin SM, Elias I, Dheer S, Besser MP, Morrison WB,


    Zoga AC: Prediction of midfoot instability in the subtle
    Lisfranc injury: Comparison of magnetic resonance imaging with intraoperative findings. J Bone Joint Surg
    Am 2009;91(4):892-899.
    MRIs of 21 feet in 20 patients were evaluated with regard to the integrity of the dorsal and plantar bundles of
    the Lisfranc ligament, the plantar tarsal-metatarsal ligaments, and the medial-middle cuneiform ligament.
    Nineteen (90%) of the 21 Lisfranc joint complexes were
    correctly classified on MRI; therefore, MRI is accurate
    for detecting traumatic injury of the Lisfranc ligament
    and for predicting Lisfranc joint complex instability.

    48.

    Myerson MS, Fisher RT, Burgess AR, Kenzora JE: Fracture dislocations of the tarsometatarsal joints: End results correlated with pathology and treatment. Foot Ankle 1986;6(5):225-242.

    49.

    Calder JD, Whitehouse SL, Saxby TS: Results of isolated Lisfranc injuries and the effect of compensation
    claims. J Bone Joint Surg Br 2004;86(4):527-530.

    50.

    Gaines RJ, Wright G, Stewart J: Injury to the tarsometatarsal joint complex during fixation of Lisfranc fracture
    dislocations: An anatomic study. J Trauma 2009;66(4):
    1125-1128.
    The purpose of this study was to determine whether the
    involved joint surface area increased with repositioning
    of the guidewire before screw placement. Nine matched
    pairs of cadaver feet were dissected after cannulated
    screws were placed after a single pass across the joint
    for right feet and two passes across the joint for left feet.
    The mean injury area for the first metatarsal (MT1) was
    0.106 cm2 for one pass and 0.168 cm2 for two passes of
    the guidewire before screw advancement (P = 0.003)
    The mean injury area for the second metatarsal (MT2)
    was 0.123 and 0.178 cm2 for one and two passes, respectively (P = 0.018). The authors concluded that

    2011 American Academy of Orthopaedic Surgeons

    Chapter 39: Foot Trauma

    changing the placement of the guidewire across the midfoot significantly increased the joint surface affected by
    screw placement.
    51.

    Raikin SM, Slenker N, Ratigan B: The association of a


    varus hindfoot and fracture of the fifth metatarsal
    metaphyseal-diaphyseal junction: The Jones fracture.
    Am J Sports Med 2008;36(7):1367-1372.
    The objective of the study was to assess the utility of
    MRI for the diagnosis of an injury to the Lisfranc and
    adjacent ligaments in 21 patients and to determine
    whether conventional MRI is a reliable diagnostic tool,
    with manual stress radiographic evaluation with the patient under anesthesia and surgical findings being used
    as a reference standard. The authors found that intraoperatively, 17 unstable and 4 stable Lisfranc joints were
    identified. The strongest predictor of instability was disruption of the plantar ligament between the first cuneiform and the bases of the second and third metatarsals.
    Nineteen (90%) of the 21 Lisfranc joint complexes were
    correctly classified on MRI. They concluded that MRI is
    accurate for detecting traumatic injury of the Lisfranc
    ligament and for predicting Lisfranc joint complex instability when the plantar Lisfranc ligament bundle is
    used as a predictor.

    57.

    Egol K, Walsh M, Rosenblatt K, Capla E, Koval KJ:


    Avulsion fractures of the fifth metatarsal base: A prospective outcome study. Foot Ankle Int 2007;28(5):581583.
    Fifty-two patients who sustained an avulsion fracture of
    the fifth metatarsal base and presented to the outpatient
    clinic of the hospital system were followed prospectively
    with a standardized protocol. An average of 22 days
    were lost from work, and although patients can be expected to return to their preinjury level of function, recovery may take 6 months or longer.

    58.

    Vorlat P, Achtergael W, Haentjens P: Predictors of outcome of non-displaced fractures of the base of the fifth
    metatarsal. Int Orthop 2007;31(1):5-10.
    The purpose of this study was to identify those factors
    that influence the outcome after nonsurgical treatment
    of undisplaced fractures of the fifth metatarsal on 38
    patients who were treated with plaster and periods of
    no weight bearing (NWB). The most significant predictor of poor functional outcome was longer NWB, which
    was strongly associated with worse global outcome, discomfort, and reported stiffness. The authors concluded
    that NWB should be kept to a minimum for acute avulsions of the tuberosity of the fifth metatarsal.

    59.

    Clapper MF, OBrien TJ, Lyons PM: Fractures of the


    fifth metatarsal: Analysis of a fracture registry. Clin Orthop Relat Res 1995;315:238-241.

    60.

    Porter DA, Rund AM, Dobslaw R, Duncan M: Comparison of 4.5- and 5.5-mm cannulated stainless steel
    screws for fifth metatarsal Jones fracture fixation. Foot
    Ankle Int 2009;30(1):27-33.

    61.

    Leumann A, Pagenstert G, Fuhr P, Hintermann B,


    Valderrabano V: Intramedullary screw fixation in proximal fifth-metatarsal fractures in sports: Clinical and
    biomechanical analysis. Arch Orthop Trauma Surg
    2008;128(12):1425-1430.
    Fourteen active patients with fifth metatarsal fracture
    were followed for an average of 42 months with clini-

    Panchbhavi VK, Vallurupalli S, Yang J, Andersen CR:


    Screw fixation compared with suture-button fixation of
    isolated Lisfranc ligament injuries. J Bone Joint Surg
    Am 2009;91(5):1143-1148.
    This cadaver study of 14 paired specimens was performed to compare the stability provided by a suture
    button with that provided by a screw when used to stabilize the diastasis associated with Lisfranc ligament injury. The authors found no significant difference in displacement between specimens fixed with the suture
    button and those fixed with the screw.

    52.

    Kuo RS, Tejwani NC, Digiovanni CW, et al: Outcome


    after open reduction and internal fixation of Lisfranc
    joint injuries. J Bone Joint Surg Am 2000;82(11):16091618.

    53.

    Coetzee JC, Ly TV: Treatment of primarily ligamentous


    Lisfranc joint injuries: Primary arthrodesis compared
    with open reduction and internal fixation. Surgical technique. J Bone Joint Surg Am 2007;89(suppl 2 pt 1):
    122-127.
    Forty-one patients with an isolated acute or subacute
    primarily ligamentous Lisfranc joint injury were enrolled in a prospective, randomized clinical trial comparing primary arthrodesis with traditional open reduction and internal fixation. The patients were followed
    for an average of 42.5 months. The patients who had
    been treated with a primary arthrodesis estimated that
    their postoperative level of activities was 92% of their
    preinjury level, whereas the open reduction group estimated that their postoperative level was only 65% of
    their preoperative level. A primary stable arthrodesis of
    the medial two or three rays appears to have a better
    short- and medium-term outcome than open reduction
    and internal fixation of ligamentous Lisfranc joint injuries.

    54.

    Rammelt S, Schneiders W, Schikore H, Holch M, Heineck J, Zwipp H: Primary open reduction and fixation
    compared with delayed corrective arthrodesis in the
    treatment of tarsometatarsal (Lisfranc) fracture dislocation. J Bone Joint Surg Br 2008;90(11):1499-1506.
    This comparative cohort study conducted over a period
    of 5 years compared primary open reduction and internal fixation in 22 patients with secondary corrective arthrodesis in 22 patients who presented with painful
    malunion at a mean of 22 months after injury. It was
    concluded that primary treatment by open reduction
    and internal fixation of tarsometatarsal fracturedislocations leads to improved functional results, earlier
    return to work, and greater patient satisfaction than secondary corrective arthrodesis.

    55.

    Torg JS, Balduini FC, Zelko RR, Pavlov H, Peff TC,


    Das M: Fractures of the base of the fifth metatarsal distal to the tuberosity: Classification and guidelines for
    non-surgical and surgical management. J Bone Joint
    Surg Am 1984;66(2):209-214.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    56.

    521

    Section 4: Lower Extremity

    cal, radiologic, and biomechanical evaluation. Thirteen


    of 14 patients were highly satisfied and returned to full
    activity.
    Hoxie S, Turner NS III, Strickland J, Jacofsky D: Clinical course of open metatarsal fractures. Orthopedics
    2007;30(8):662-665.

    4: Lower Extremity

    62.

    This case series examined the outcome of 10 patients


    with open metatarsal fractures. Six sustained Gustilo
    grade I or II injuries, and all healed without the need for
    additional soft-tissue coverage. Four patients with
    Gustilo grade IIIB developed complications and all eventually required amputation. Level of evidence: IV.

    522

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 40

    Foot and Ankle Reconstruction


    Mark D. Perry, MD

    Arthur Manoli II, MD

    Introduction

    Arthritis and Malposition


    A broad area of reconstruction is related to arthritis/
    malalignment. This involves arthrosis resulting from
    cartilage injury or incongruent surfaces. Ankle stability
    is provided by a combination of bony architecture and
    ligament integrity. Either bone loss or joint subluxation
    results in malalignment of the foot or ankle. Issues regarding the medial column of the foot are traditionally
    treated with arthrodesis because this is the more rigid
    and stable column. Issues involving the lateral aspect of
    the foot tend to focus on joint preservation to help
    maintain mobility.

    4: Lower Extremity

    Foot and ankle reconstruction is taking an increasingly


    more important role as patient expectations, survivability of injuries, and patient demands increase overall.
    The goal of surgery, whether because of elective, acquired, or traumatic issues, is to align the foot in a neutral position without pain on weight bearing and provide the mobility and support desired. More than $3
    billion a year is spent on the treatment of posttraumatic
    arthritis.1 This chapter will focus on the traditional
    treatments used in reconstructing the foot and ankle
    secondary to arthritis, malalignment, or tendon issues
    with emphasis on emerging treatments.

    stability needs to be achieved. A stable syndesmosis can


    be achieved by restoring the proper anatomy between
    the fibula and the tibia incisura2 (Figure 1). When the
    syndesmosis can be reconstructed, there is adequate
    restoration of function. When the mortise cannot be
    held with stability, such as fractures of the Chaput tubercle or comminution resulting in the loss of the anterolateral aspect of the distal tibia, then treatment with
    syndesmosis fusion can be attempted.

    Ankle
    Traumatic arthritis of the tibiotalar joint occurs as a
    result of articular injuries resulting from rotational injuries about the ankle, typically valgus impaction fractures (Figure 2). These injuries also occur as directimpact loading through the tibiotalar joint (pilon
    fractures) or as a result of osteochondral injuries of the
    talar dome. Treatment options for ankle arthritis are resection, arthroplasty, and arthrodesis.
    Resection
    Tibiotalar joints with significant bony impingement
    may require excision of the protruding bone (Figure 3).
    Ligament realignment and calcaneal osteotomy may
    provide symptomatic relief in ankles with mild arthritis
    but mechanical overloading secondary to talar tilt.3
    Fresh osteochondral total ankle allograft transplantation is not currently a feasible treatment option.4

    Anatomic Areas of Injury

    Syndesmosis
    Injury to the syndesmosis is treated with a realignment
    procedure. To hold the ankle mortise in position, a
    combination of bony stability as well as ligamentous

    Dr. Perry or an immediate family member serves as a


    board member, owner, officer, or committee member of
    the American Academy of Orthopaedic Surgeons resolutions committee. Dr. Manoli or an immediate family
    member has received royalties from DJ Orthopaedics; is
    a member of a speakers bureau or has made paid presentations on behalf of Stryker and Synthes; and serves
    as a board member, owner, officer, or committee member of the Michigan Orthopaedic Society.

    2011 American Academy of Orthopaedic Surgeons

    Figure 1

    Intraoperative photograph showing unrecognized syndesmotic injury with interposed soft


    tissue.

    Orthopaedic Knowledge Update 10

    523

    4: Lower Extremity

    Section 4: Lower Extremity

    Figure 3

    Figure 2

    AP radiograph showing loss of lateral tibiotalar


    joint space after a valgus impaction fracture.

    Figure 4

    AP radiograph showing failed total ankle arthroplasty in a patient with severe bilateral pain.

    Arthroplasty
    Appropriate patient selection is critically important for
    good outcomes of total ankle athroplasty5 (Figure 4).
    Proponents of ankle arthroplasty cite preservation of
    the subtalar joint as a benefit to arthroplasty. However,
    more recent ankle replacement designs are incorporating fixation into the calcaneus through the subtalar
    joint.6 Ankle replacement must be performed with bony
    alignment and soft-tissue tensions restored to normal.
    The deltoid ligament may need its length shortened to
    restore soft-tissue balance. Arthroplasties placed in a
    varus or valgus position will fail.7 At 2-year follow-up
    524

    Orthopaedic Knowledge Update 10

    Lateral radiograph showing blocking lesion to


    dorsiflexion.

    of Hintegra prosthesis (Integra Life Sciences, Plainsboro, NJ) placement, there was no difference in results
    for patients with severe varus deformity compared to
    control subjects.8 Varus deformity correction was accomplished by a medial release and, if necessary, a lateral plication of tissues.
    Although the concept of total ankle replacement is
    simple, in actuality the results depend on implant design and surgical expertise. Currently there are more
    than 10 different implants available for use in Europe,
    with an increasing number in the United States. Each
    design has specific and unique consequences that may
    result in the need for revision.
    It is anticipated that over the next few years as indications and techniques are refined, total ankle replacement will also become as reliable as knee replacement.9 Proprioception does not significantly change
    after total ankle arthroplasty.10 The motion achieved after total ankle replacement is similar to preoperative
    range of motion. However, the improvement of a measured 5 resulted in a clinically greater perception of
    motion, perhaps because of the additional motion being pain free.11
    In a 2009 study of the Scandinavian Total Ankle Replacement (STAR; Small Bone Innovations, New York,
    NY), there was a 50% decrease in secondary minor
    and major surgeries when comparing surgeons who
    performed an average of 16 versus 43 total ankle replacements. Component size was adapted to smaller
    implants as the learning curve was refined. The overall reoperation rate in this series was 11%.12
    A third-generation total ankle implant demonstrated
    good pain relief and improved function with a 95%
    survival rate at 6 years. However, this implant was
    withdrawn by the manufacturer because of significant
    osteolysis issues.13
    It is difficult to make a broad statement that total
    ankle replacement is preferable to arthrodesis. It is possible that each implant design will have different short-,
    medium-, and long-term function and survivorship

    2011 American Academy of Orthopaedic Surgeons

    Chapter 40: Foot and Ankle Reconstruction

    with different necessary secondary surgeries (such as


    syndesmotic fusion). The learning curve for these procedures is not insignificant. Although total ankle replacement may be a powerful tool in the treatment of
    ankle arthritis, many factors must be considered before
    treatment of tibiotalar arthritis.

    Hindfoot and Midfoot


    Painful arthritis of the hindfoot and midfoot is treated
    with fusion of the symptomatic joints. The results of
    subtalar fusion are better after failed surgical treatment
    than in nonsurgically treated intra-articular calcaneal
    fractures21 because of the restoration of bone morphology. Talonavicular arthritis as a result of a trauma requires fusion. Similar to the lateral column of the foot,
    the talonavicular joint provides significant sagittal and
    coronal plane motion to the foot. However, there is no
    alternative to a talonavicular fusion or a talonavicular
    cuneiform fusion where there is significant talonavicular arthritis. Incorporation of a subtalar fusion with an
    isolated talonavicular fusion can increase fusion rates,
    although this results in even more restrictive foot motion. Midfoot posttraumatic arthritis occurs as a result
    of fractures of the cuneiforms as a sequelae of injury to
    the tarsometatarsal joints. The first, second, and third
    tarsometatarsal joints are treated collectively by arthrodesis to eliminate arthritic pain to the medial column of
    the midfoot with no significant functional limitations.
    Fusions between the tarsal navicular and intercuneiform joints provide effective, asymptomatic support to
    a previously arthritic medial column of the midfoot.
    The lateral tarsometatarsal joints, the fourth and
    fifth metatarsals, and their articulation to the cuboid
    are qualitatively different from the first, second, and

    2011 American Academy of Orthopaedic Surgeons

    Figure 5

    4: Lower Extremity

    Arthrodesis
    The traditional attitudes concerning the role of arthrodesis are being challenged. The functional results of arthrodesis in general have been an elimination of painful
    ambulation with known limitations in mobility. The
    outcomes, however, with resultant loss of joint motion
    are resulting in the design of procedures and techniques
    to salvage joint motion. Whether significant differences
    in outcomes are seen is unclear.14
    Although a salvage procedure, ankle arthrodesis currently has broader surgical indications and remains the
    primary treatment of ankle arthritis.15 Shoe wear with
    an appropriate rocker bottom and increased subtalar
    joint motion provide restorative aspects of gait after arthrodesis.15 Arthrodesis of the tibiotalar joint can be
    successfully treated with compression screws,16 external
    frames,17 or plates used in combination. Plate fixation
    has been shown to increase stability.18 Failed arthrodesis can be treated with arthroplasty19 if there is intrinsic
    coronal plane stability, which can be facilitated by
    wider talar components. Repeat arthrodesis is warranted if failure was the result of poor fixation technique or other correctable issues. Failed arthroplasty
    can be treated with arthrodesis;20 however, significant
    replacement bone stock and rigid fixation are required.

    Arthroscopic view showing dense and billowing


    soft tissue that occupies the ankle joint space.

    third medial tarsometatarsal joints. This relatively rigid


    column of the midfoot requires significant mobility.
    Tarsometatarsal arthrodesis relieves the symptoms of
    arthritis but provides an undesirable rigid foot. This
    condition can be resolved with either tissue arthroplasty or joint arthroplasty.22

    Os Trigonum
    Fractures of the os trigonum occur in the region of incomplete coalescence of the posterior talus ossicle to
    the rest of the talar body. This posteromedial region of
    the talar body is where the flexor hallucis longus slides
    into the groove. This area is impinged in maximal plantar flexion and also may have symptoms with flexor
    hallucis longus gliding. Removal of the os trigonum
    will eliminate the acute symptoms.

    Treatment of Foot and Ankle Pain


    Patients who have continued pain after routine ankle
    fractures or twisting injuries will often have symptomatic impingement in the anterolateral or anteromedial
    aspect of the tibiotalar joint. Arthroscopy in this setting
    reveals significant areas of fibrosis and fibrous bands
    that impinge during normal ankle joint motion (Figure
    5). Arthroscopy also can be used to remove cartilage
    from the distal tibia and talus as mentioned for arthroscopically assisted arthrodesis. Therapeutic indications for subtalar arthroscopy include arthrodesis23 and
    minimally invasive calcaneal reconstruction.

    Osteochondral Lesions
    Cartilage lesions of the talus can be more accurately described as osteochondral lesions (OCLs). Osteochondritis dissecans is a subtype of OCL. The current classification system uses the four-stage Berndt and Harty
    1959 classification system.24 Stage I is an intact carti-

    Orthopaedic Knowledge Update 10

    525

    Section 4: Lower Extremity

    4: Lower Extremity

    treated with one core (Figure 6). Large defects are


    treated with multiple transplantations or plugs. Reproduction of a smooth articular surface is technically
    challenging and may result in an organ pipe arrangement of cartilage plugs. Sometimes this results in a
    catching sensation for large lesions. Osteochondral allograft transplantation using either fresh osteochondral
    allografts or fresh-frozen grafts has been described. Allograft has a risk of resorption and fragmentation of
    the graft. Autologous chondrocyte implantation is a
    technique in which autologous chondrocytes are cultured and injected into the prepared lesion. Although
    this hyaline-like cartilage regeneration is a possible
    treatment method, there is considerable cost, and additional surgical procedures are necessary. Although interarticular hyaluronic acid derivative injections are
    used in the treatment of knee arthritis, treatment of
    compromised ankle joint cartilage currently is not standard practice but may prove to be a useful adjunctive
    therapy.24
    Figure 6

    Intraoperative photograph showing talar dome


    preparation after a medial malleolar osteotomy.
    (Courtesy of Al Pearsall, MD, Mobile, AL.)

    Major Acquired Deformities

    Hallux Valgus
    lage lesion with a bone injury. Stage II and III lesions
    are nondisplaced cartilage injuries that are incomplete
    (stage II) or complete (stage III). Stage IV is a detached
    OCL. Clinically these injuries present as ankle joint effusions with periarticular tenderness. Nonsurgical
    treatment consists of rest and ice with temporary reduction of weight bearing.
    The most common areas of OCLs are the central
    medial aspect followed by the central lateral talus. Central medial lesions tend to be the largest. Injuries that
    do not penetrate the subchondral bone have no stimulus for healing. Therefore, initial treatment is aimed at
    revascularizing the bony defect. The healing response
    induces a fibrocartilage, not hyaline cartilage. For intact cartilage, retrograde drilling provides revascularization of the bone without introducing chondral injury. Microfracture and microdrilling similarly seek to
    stimulate fibrocartilage development for stage II and III
    lesions. For lesions with small cartilage damage (less
    than 6 mm), microfracture/microdrilling is the preferred treatment of chondral injuries. When chondral
    injury is greater than 15 mm, the efficacy of
    microfracture/microdrilling is questionable.
    Tissue transplantation becomes the treatment modality for larger chondral injuries of the talus or failed
    microfracture. Most of the talar dome is accessible
    without a medial malleolar osteotomy. If required,
    three-screw fixation of the osteotomy is preferable to
    two-screw fixation to prevent proximal migration.
    Most authors consider osteochondral autograft tissue
    transplantation to be a salvage procedure unless the lesion is larger than 6 mm in diameter.
    In the osteochondral autologous transfer system, the
    tissue is taken from the nonweight-bearing aspect of
    the ipsilateral distal femur. Often the lesion can be
    526

    Orthopaedic Knowledge Update 10

    Hallux valgus, the main deformity of the forefoot, has


    more than 130 described procedures.25-32 More than
    80% of patients have family history and bilaterality,
    with surgery improving quality of life.33,34 The classification of bunions and their subsequent treatment is
    based on the intermetatarsal angle (IMA; normal <9)
    and the hallux valgus angle (HVA; normal <15). Other
    considerations are the distal metatarsal articular angle
    (normal <10) and the hallux interphalangeal angle
    (normal <10).
    Nonsurgical treatment of symptomatic bunions is a
    shoe with a soft leather upper and a high and wide toe
    box to accommodate the foot. The current position of
    the American Orthopaedic Foot and Ankle Society asserts that cosmesis is not a valid surgical indication.
    Bunion deformities are classified according to HVA and
    IMA as mild (HVA <30, IMA <13), moderate (HVA
    <40, IMA >13), or severe (HVA >40, IMA >20).
    Moderate to severe bunion deformities require proximal intervention using either arthrodesis of the first
    tarsometatarsal joint or a proximal osteotomy. Working proximally allows significant correction of the increased IMA. The Lapidus procedure also addresses hypermobility of the first ray (the first tarsometatarsal
    joint). In addition to being an effective primary procedure, the Lapidus procedure has been shown to be a
    good salvage procedure for failed hallux valgus surgeries.35 Once the tarsometatarsal fusion is established, recurrence of the deformity is unlikely.36
    Distal soft-tissue releases and tightenings will need
    to be done to improve the HVA. The medial capsulorrhapy is enhanced with a suture anchor closure. Softtissue procedures that release the adductor may result
    in an iatrogenic adduction deformity of the great toe
    (hallux varus).

    2011 American Academy of Orthopaedic Surgeons

    Chapter 40: Foot and Ankle Reconstruction

    For moderate hallux valgus deformities an osteotomy closer to the metatarsophalangeal joint is performed. The standard osteotomy is a chevron where
    the metatarsal head is slid laterally and held in position
    by fixation. The plantar osteotomy should be proximal
    to the joint capsule.37 If first metatarsophalangeal joint
    arthritis is present, a fusion alone may decrease the
    IMA in patients with moderate disease.38 Lesser bunion
    deformities may be treated with distal soft-tissue releases. However, it is more likely that the bunion will
    respond to nonsurgical intervention for these minor deformities.

    Pes Planus

    2011 American Academy of Orthopaedic Surgeons

    4: Lower Extremity

    Peritalar subluxations are responsible for two main


    types of deformities. The dorsilateral peritalar subluxation is most recognized because of the adult-acquired
    flatfoot. This condition results in abduction of the forefoot and the development of a hindfoot valgus deformity (Figure 7). There is a spectrum of tendon involvement that begins as a tendinitis of the posterior tibial
    tendon and ends with an incompetent and painful tendon with significant tendinosis, lack of tendon excursion, and fixed deformity of the subtalar, talonavicular,
    and calcaneocuboid joints. A tenolysis may be appropriate early treatment; later during the course of the
    disease when the deformity is not reducible and an arthrosis has occurred, a triple arthrodesis is appropriate
    treatment.
    Adult acquired flatfoot deformity is most often
    caused by posterior tibial tendon dysfunction. Stage I is
    characterized by early degeneration of the tendon with
    medial focal pain or a peritendinitis. Stage II is distinguished by a passively correctable deformity. Stage IIA
    is defined to be less than 30% of the talar head and
    coverage on the standing AP radiograph. Stage IIB is
    associated with more deformity. Initial nonsurgical
    treatment is with nonsteroidal anti-inflammatory drugs
    and immobilization, although this treatment has not
    been shown to prevent or decrease the progression of
    deformity. Stage III is a fixed valgus deformity of the
    hindfoot. In stage IV, a valgus deformity of the tibiotalar joint has formed.39
    Surgical treatment of stage I involves a tenosynovectomy and tendon repair for intrasubstance or longitudinal tears. Stage II has more surgical options. A calcaneal medial slide and tendon transfer are performed for
    stage IIA deformity. For stage IIB deformity, lateral column lengthening is often required.
    The reconstruction of a stage IIB adult acquired flatfoot deformity requires multiple significant surgeries at
    different locations throughout the foot. Temporary fixation of the osteotomies and arthrodesis allow better
    control of the final alignment.40 There is concern that
    the addition of a lateral column lengthening increases
    lateral pressure. Increased lateral pressure was not the
    result of excessive lengthening of the lateral column
    when fluoroscopy was used to assess the reduction of
    the talonavicular joint.41 The increase in lateral pressure may be negated/improved by a medial tarsometa-

    Figure 7

    Clinical photograph showing right heel valgus


    deformity displaying too many toes.

    tarsal arthrodesis or medial cuneiform osteotomy.42


    Tarsometatarsal arthrodesis may also correct resulting
    supination deformity occurring after lateral column
    lengthening.

    Subtle Cavus Foot


    A plantar-medial peritalar subluxation results in a subtle cavus foot, which is radiographically determined by
    the Meary angle, which must be greater than zero. The
    angle is formed by a line drawn through the talus and
    by another line directed down the first metatarsal on a
    lateral weight-bearing radiograph. The subtle cavus
    foot is supinated with a varus heel, resulting in an inflexible, stiff foot. If the deformity is not passively correctable, osteotomies are required to provide a normal
    plantigrade foot. A heel slide is performed to incur
    hindfoot valgus and a closing wedge osteotomy is performed on the dorsal surface of the first metatarsal to
    provide a predictable correction with resolution of
    symptoms.

    Minor Acquired Deformities


    Progressive deformities are a result of an inbalance of
    foot invertors and evertors. Similarly, an imbalance between the intrinsic muscles and the long dorsiflexors
    and plantar flexors results in claw toe deformities.

    Orthopaedic Knowledge Update 10

    527

    Section 4: Lower Extremity

    an avascular condition (Figure 8). Treatment initially


    consists of unloading the sesamoid using offloading
    splints and stretching of the gastrocnemius-soleus complex. If the medial sesamoid is involved, downward
    shaving of the sesamoid may be appropriate for symptom relief. Conditions involving the lateral sesamoid
    that are unresponsive to nonsurgical treatment may require resection, and frequently can be confused with a
    bipartite sesamoid. Sesamoiditis, however, tends to be
    associated with more stellate sesamoids and is more indicative of nonhealing.

    4: Lower Extremity

    Tendinopathy

    Figure 8

    Radiograph showing right foot lateral sesamoid


    disruption (arrow) with the left side as
    comparison.

    These conditions are common in tall patients or those


    with neurovascular issues. The denervation of the small
    nerves of the foot intrinsics results in overpull of the
    longus muscles. Nonsurgical management consists of a
    sling to hold the proximal phalanx parallel to the
    ground. Surgical management is reserved for painful
    deformities at the distal tips of the toes or proximal interphalangeal joint symptoms or ulcerations from the
    shoe rubbing against the toes. After surgery the toe
    should be straight and not interfere with other toes.
    The metatarsophalangeal joint will have appropriate
    passive plantar flexion and dorsiflexion, accomplished
    through a combination of tendon transfers and bony
    resection.
    Crossover toe is caused by a traumatic injury to the
    metatarsophalangeal joint capsule, with development
    of fibrosis and contractures causing the toe to deviate
    into another toe.43 This condition typically will cause
    impingement of the second toe onto the great toe. Because of the absence of a flexion contracture, bone
    shortening does not need to be performed. Instead, a
    dorsal capsulotomy and a tendon transfer of the brevis
    over the dorsum of the proximal phalanx holds the toe
    in the reduced position.
    Sesamoiditis is a painful condition of the sesamoids
    at the level of the first metatarsophalangeal joint and is
    the result of overpressure similar to a metatarsalgia or
    528

    Orthopaedic Knowledge Update 10

    Peroneal tendinopathy results from either acute trauma


    or microtrauma as opposed to a watershed vascular
    area of the posterior tibial tendon. The peroneal tendons frequently develop with longitudinal splits to the
    brevis (Figure 9) or the longus. When seen early, primary repair of the tendons have good functional outcomes. A predisposing factor for tears of the brevis is
    the presence of space-occupying lesions in the fibular
    groove at the tip of the lateral malleolus. The brevis
    muscle, which protrudes distally onto the tendon, needs
    to be resected such that the retrofibular groove is clear.
    Acute injuries to the peroneal tendon frequently involve
    a rupture of the superior peroneal retinaculum that can
    often be seen on plain radiographs as an avulsion of the
    lateral malleolus. Subluxating or dislocating peroneal
    tendons have been described following calcaneal fractures or other lower extremity trauma. Multiple Kirschner wires can percutaneously hold the reduced tendons.44
    The peroneus brevis tendon is an important structure in defining forefoot anatomy. If torn beyond repair, tenodesis may be done by sacrificing the longus or
    secondary repair involving autograft or allograft tendon. Primary repair and tubularization are indicated
    for tears involving less than 50% of the tendon, and tenodesis is indicated for tears involving more than 50%
    of the tendon.45
    Lateral ankle pain may also present secondary to an
    accessory peroneal tendon, which is often poorly visualized on MRI. The most common is the peroneus tertius, which runs in the anterior compartment of the leg.
    Other accessory peroneal tendons, however, run behind
    the fibula in the retinaculum and attach to either tendons or the calcaneus itself (Figure 10).
    The region of the Achilles tendon has several areas
    of pathology: between the tendon and the cortex of the
    calcaneus (bursitis), tendinitis, or tendinosis in the distal tendon. Initially for tendinitis or retrocalcaneal bursitis, nonsurgical treatment consisting of stretching
    with focus on the gastrocnemius tendon, or possibly a
    release of the tendon46 and modalities to control inflammation has been successful.47 With persistent pain
    due to tendinosis, a posterior midline incision48 is recommended to detach the Achilles tendon insertion, dbride diseased tendon and bursae,49 and reattach the
    Achilles tendon.50

    2011 American Academy of Orthopaedic Surgeons

    Chapter 40: Foot and Ankle Reconstruction

    4: Lower Extremity

    Figure 9

    A, Longitudinal tear with cavitation. B, The tendon after repair is shown.

    Achilles tendon lacerations are always surgically repaired. Ruptures may be treated surgically or nonsurgically. Achilles tendon repairs have approximately 10%
    complication rates (wound problems in 5% and rerupture in 5%). Without surgery, there are 10% reruptures. Posterior ankle incisions require great care with
    tissue handling. The presence of a palpable gap is a
    contraindication to nonsurgical treatment. The AAOS
    Clinical Practice Guideline on Achilles Tendon Ruptures (www.aaos.org/research/guidelines/atrsummary
    .pdf) recommends early postoperative protected weight
    bearing.

    Ligamentous Issues
    The anterior talofibular ligament is most frequently
    sprained. Continued lateral instability following nonsurgical management is an indication for lateral reconstruction of the ankle. The repairs fall into two main
    categories: anatomic and nonanatomic. Anatomic repair of the ligament ends is preferred. If the ligament is
    avulsed from bone, it is anchored appropriately into
    the fibular origin or talar insertion. Often this repair is
    augmented with fibular periosteum51 and extensor tendon retinaculum. The anterior talofibular repair is often done in conjunction with ankle arthroscopy, and
    appropriate placement of restricting tape during the arthroscopy enables the repair to be performed without
    significant fluid extravasation. When a primary repair
    cannot be performed, the use of a gracilis graft52 has
    been described. Using the native peroneal brevis tendon
    for ankle ligament reconstruction is rarely considered
    given the importance of the brevis tendon.

    Nerve Pain
    Patients with foot and ankle injuries often have persistent pain after nonsurgical or surgical treatment. Oc-

    2011 American Academy of Orthopaedic Surgeons

    Figure 10

    Photograph showing the accessory peroneal in a


    20-year-old woman who plays soccer and has
    lateral ankle pain. The aberrant tendon/muscle
    was reflected off the calcaneus.

    cult fractures or dislocations may be responsible for


    persistence of symptoms, which is common with nondisplaced tarsometatarsal dislocations and lateral process of the talus fractures. Additionally, tarsal tunnel
    syndrome should be anticipated and expected in patients with crush injuries (Figure 11). Studies of release
    of the tarsal tunnel per se show mixed results.53 The
    best surgical results are found when there is a spaceoccupying lesion within the tarsal tunnel. The inability
    to abduct the small toe is consistent with poor functioning of the lateral plantar nerve. Patients with complex regional pain syndrome should be referred to appropriate providers for medical management.
    Surgical neuromas are a common complication following foot and ankle surgery; the density of sensory
    nerves in the region may be a contributing factor. Surgery on the lateral aspect of the foot often requires traction of a branch of the sural nerve. Surgical incisions on
    the anteromedial aspect of the ankle often involve iat-

    Orthopaedic Knowledge Update 10

    529

    Section 4: Lower Extremity

    rogenic injury to the saphenous nerve. Diagnostic


    blocks with lidocaine can help differentiate the location
    of these neuromas. The neuromas or nerve irritation
    may occur proximal to the obvious orthopaedic injury,
    for example, the superficial peroneal nerve as it crosses
    from posteriorly to anteriorly in the lower leg.

    Diabetic Neuropathy

    4: Lower Extremity

    Diabetes has particular influence on foot and ankle reconstruction, beyond that of poor bone quality. The
    persistent microtrauma that develops in patients with
    diabetes results in deformities of the midfoot and hindfoot. Additionally, the insensate foot is susceptible to
    pressure ulcers.
    Forefoot ulcers occur as a result of skin breakdown
    secondary to increasing pressure. Because the patient

    530

    has lost protective sensation there is an absence of appropriate unloading of the offending areas, resulting in
    skin ulcerations. Forefoot pressure is exacerbated by a
    plantar-flexed ankle position secondary to either a tight
    Achilles tendon or a gastrocnemius tendon. Although
    ulcers may develop infections that necessitate amputation, the pressure ulcers can be successfully treated by
    unloading the affected area. Total contact casting is a
    useful tool in dispersing the overall forefoot pressure to
    a broad area. Additionally, correction of the plantar
    flexion contracture is successful in relieving forefoot
    pressure. Total contact casting is effective in treating
    Wagner grade 1 and 2 ulcers (absence of osteomyelitis)
    and after 4 weeks substantial healing should be apparent.54
    Ulcerations in the hindfoot tend to be vascular in nature and more difficult to heal. Ulcerations in the midfoot are caused by increased pressure secondary to architectural collapse. The offending bone (cuneiform or
    cuboid) needs to be resected, often by a separate incision from the area of ulceration to remove the bony
    prominence that is causing increasing pressure.
    Midfoot Charcot deformities in patients with diabetes require surgical intervention if there is an unbraceable deformity, a persistent or recurring ulceration, or
    an inability to provide support. Realignment fusions of
    the midfoot often require surgical implants that use
    locking plate technology or the addition of adjuvants to
    bone healing.
    Hindfoot involvement in diabetes is associated with
    severe bone loss and malalignment. Tibiotalar fusions
    in this setting often include the calcaneus55 (Figure 12).
    Implant fixation in patients with severe deformity and
    poor bone quality can be challenging.56 Nails for a calcaneotalar tibial fusion have a significant incidence of
    tibial stress fractures, if the nail is contained in the distal third of the tibia. Formal joint preparation of the
    subtalar joint may not be necessary.57

    Figure 11

    Photograph showing nerve release from scar.


    Note the constriction of the calcaneal branch.

    Figure 12

    Charcot deformity of the tibiotalar joint and hindfoot. A, CT reconstruction AP view. B, Postoperative lateral
    radiograph.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 40: Foot and Ankle Reconstruction

    treatment of ankle arthritis. Foot Ankle Int 2008;29(6):


    554-560.

    Chronic and Persistent Deforming Forces

    The authors studied 169 patients with crossover second


    toe. The predominant incidence occurs in women older
    than 50 years. There was no correlation between crossover toe and second metatarsal length or IMA. Level of
    evidence: IV.
    5.

    A focused discussion on ankle arthritis and its treatment


    including total ankle arthroplasty is presented. The authors are encouraged by the improvements of total ankle arthroplasty but highlight the need for long-term
    studies not performed by surgeons involved in the implants design. Level of evidence: V.
    6.

    7.

    Coetzee JC: Management of varus or valgus ankle deformity with ankle replacement. Foot Ankle Clin 2008;
    13(3):509-520.

    8.

    Kim BS, Choi WJ, Kim YS, Lee JW: Total ankle replacement in moderate to severe varus deformity of the ankle. J Bone Joint Surg Br 2009;91(9):1183-1190.
    Total ankle arthroplasty in 22 uninjured patients and 23
    patients with varus deformity were compared. No significant difference in outcomes at 27 months was noted.
    Numerous charts depict surgical planning/interventions.
    Level of evidence: IV.

    Annotated References
    Brown TD, Johnston RC, Saltzman CL, Marsh JL,
    Buckwalter JA: Posttraumatic osteoarthritis: A first estimate of incidence, prevalence, and burden of disease.
    J Orthop Trauma 2006;20(10):739-744.

    2.

    Weber BG, Simpson LA: Corrective lengthening osteotomy of the fibula. Clin Orthop Relat Res 1985;
    199(199):61-67.

    3.

    Lee HS, Wapner KL, Park SS, Kim JS, Lee DH, Sohn
    DW: Ligament reconstruction and calcaneal osteotomy
    for osteoarthritis of the ankle. Foot Ankle Int 2009;
    30(6):475-480.
    The authors studied clinical and radiologic results of
    calcaneal osteotomy, joint dbridement, and ligament
    reconstruction in the treatment of osteoarthritis of the
    ankle.
    Jeng CL, Kadakia A, White KL, Myerson MS: Fresh osteochondral total ankle allograft transplantation for the

    2011 American Academy of Orthopaedic Surgeons

    Wood PL, Prem H, Sutton C: Total ankle replacement:


    Medium-term results in 200 Scandinavian total ankle
    replacements. J Bone Joint Surg Br 2008;90(5):605-609.
    Two hundred STAR total ankle replacements were seen
    at a minimum of 5 years after surgery. Nineteen ankles
    were forward facing and 39 were backward facing;
    68% had good relief from pain. American Orthopaedic
    Foot and Ankle Society score did not change compared
    to that of the 2-year study. The authors anticipate that
    total ankle replacement will be as reliable as knee replacement.

    10.

    Conti SF, Dazen D, Stewart G, et al: Proprioception after total ankle arthroplasty. Foot Ankle Int 2008;
    29(11):1069-1073.
    Thirteen patients (mean age, 57 years) who received an
    ankle replacement were studied 2 years later for proprioceptive differences; none were noted. Level of evidence: III.

    11.
    4.

    DeOrio JK, Easley ME: Total ankle arthroplasty. Instr


    Course Lect 2008;57:383-413.
    A comprehensive description of total ankle arthroplasty
    is presented, including contraindications, specific manufactured implants, costs, and future developments. Level
    of evidence: V.

    9.

    1.

    Chou LB, Coughlin MT, Hansen S Jr, et al: Osteoarthritis of the ankle: The role of arthroplasty. J Am Acad Orthop Surg 2008;16(5):249-259.

    4: Lower Extremity

    Neuromuscular issues affect the ability of the foot to


    transfer force more proximally into the lower extremity. A persistent plantar-flexed deformity will result in a
    functionally lengthened limb and make gait difficult. If
    the deformity has been present for a short to moderate
    time, then lengthening the gastrocnemius tendon or the
    Achilles tendon may allow the foot to be placed into a
    neutral position. For a long-term deformity, release of
    the tibiotalar posterior capsule may be necessary. Additionally, shortened flexor tendons without excursion
    that are also contracted will need to be released.
    If there is no fixed plantar contracture but a loss of
    active dorsiflexion, then a transfer of the posterior tibial tendon from the posterior aspect of the ankle into
    the anterior midfoot can provide successful treatment
    of a foot drop. The surgical goal is to allow the ankle
    to dorsiflex such that the leg is able to swing unobstructed during the gait cycle and to provide eccentric
    contraction that will prevent foot slap. Additionally,
    acute ruptures or lacerations of the tibialis anterior are
    treated with repair or reattachment of the anterior tibial tendon into the navicular.
    Neuromuscular diseases such as Charcot-MarieTooth have predictable malalignments. With the weakened peroneus brevis, the foot develops a varus heel
    and posterior tibial tendon overpull. A weakened anterior tibial tendon results in plantar flexion of the first
    ray by the action of the peroneus longus. As previously
    discussed for the subtle cavus foot, a valgus heel slide
    and a dorsiflexion osteotomy of the first ray are required to place the foot into a position that can better
    facilitate the transfer of force from the ground to the
    lower extremity. The peroneus longus can be transferred to the brevis in conjunction with a heel slide to
    strengthen weak ankle evertors during stance phase.58

    Coetzee JC, Castro MD: Accurate measurement of ankle range of motion after total ankle arthroplasty. Clin
    Orthop Relat Res 2004;424:27-31.

    Orthopaedic Knowledge Update 10

    531

    Section 4: Lower Extremity

    12.

    4: Lower Extremity

    13.

    14.

    15.

    16.

    17.

    532

    Saltzman CL, Mann RA, Ahrens JE, et al: Prospective


    controlled trial of STAR total ankle replacement versus
    ankle fusion: Initial results. Foot Ankle Int 2009;30(7):
    579-596.
    This article discusses the initial STAR total ankle replacement compared with ankle fusion and results and
    an additional 448 total ankle arthroplasties 24 months
    after surgery. At 2 years, total ankle arthroplasty led to
    better function and pain relief. Patients weighing more
    than 250 lb were excluded. There is a significant learning curve. Level of evidence: II.
    Morgan SS, Brooke B, Harris NJ: Total ankle replacement by the Ankle Evolution System: Medium-term outcome. J Bone Joint Surg Br 2010;92(1):61-65.
    Thirty-eight consecutive patients received a three-part
    prosthesis with a mobile bearing component. Twentyeight patients were able to walk unaided; however,
    within the first year, nine patients underwent revision
    because of edge loading. Despite an American Orthopaedic Foot and Ankle Society score of 88.1, the device
    was removed from the market because of high rates of
    osteolysis. Level of evidence: III.
    Haddad SL, Coetzee JC, Estok R, Fahrbach K, Banel D,
    Nalysnyk L: Intermediate and long-term outcomes of
    total ankle arthroplasty and ankle arthrodesis: A systematic review of the literature. J Bone Joint Surg Am
    2007;89(9):1899-1905.
    Of 460 citations studied, there were 10 articles on pertinent total ankle arthroplasties and 39 on ankle fusion
    for comparison. The study showed both procedures
    yield satisfactory results. The authors postulate that the
    poor connotations associated with total ankle arthroplasty are caused by failures in first-generation implants.
    Level of evidence: IV.
    Sealey RJ, Myerson MS, Molloy A, Gamba C, Jeng C,
    Kalesan B: Sagittal plane motion of the hindfoot following ankle arthrodesis: A prospective analysis. Foot Ankle Int 2009;30(3):187-196.
    In 4 years, 48 patients were identified for a prospective
    study of sagittal plane motion following ankle fusion. A
    significant increase in hindfoot sagittal motion was noted
    as well as an uncoupling of the subtalar joint to the talonavicular joint. Patients with greater residual motion
    had better clinical outcomes. Level of evidence: II.
    Gentchos CE, Bohay DR, Anderson JG: Technique tip:
    A simple method for ankle arthrodesis using solid
    screws. Foot Ankle Int 2009;30(4):380-383.
    A simple and effective tip to using solid screws is provided for ankle fusion. Radiation exposure and implant
    cost are minimized. This technique is easily performed
    by orthopaedic residents.
    Eylon S, Porat S, Bor N, Leibner ED: Outcome of
    Ilizarov ankle arthrodesis. Foot Ankle Int 2007;28(8):
    873-879.
    Seventeen patients were treated with Ilizarov ankle arthrodesis. The American Orthopaedic Foot and Ankle Society score was 65 of 86 possible (14 points were for motion that is not attainable). Weight bearing began on the

    Orthopaedic Knowledge Update 10

    third day and the patients were fully weight bearing by 6


    weeks. Average follow-up was 6 years. No deterioration
    of results over time was noted. Level of evidence: IV.
    18.

    Tarkin IS, Mormino MA, Clare MP, Haider H, Walling


    AK, Sanders RW: Anterior plate supplementation increases ankle arthrodesis construct rigidity. Foot Ankle
    Int 2007;28(2):219-223.
    Six cadaver ankles (four matched pairs) were tested. Anterior plate supplementation increased the stiffness of
    the tibiotalar interface by minimizing micromotion to
    the prepared joints. There was substantial variability in
    the specimens. This result may support the use of anterior plating in clinically osteoporotic bone.

    19.

    Hintermann B, Barg A, Knupp M, Valderrabano V:


    Conversion of painful ankle arthrodesis to total ankle
    arthroplasty. J Bone Joint Surg Am 2009;91(4):850858.
    The authors discuss minimum 3-year follow-up on 30
    arthrodeses converted to total ankle arthroplasty using a
    three-component system. Indications were painful
    malunion or osteoarthritis of adjacent joints. Threecomponent systems are superior to the historically used
    two-component system. Level of evidence: IV.

    20.

    Culpan P, Le Strat V, Piriou P, Judet T: Arthrodesis after failed total ankle replacement. J Bone Joint Surg Br
    2007;89(9):1178-1183.
    Sixteen patients with failed total ankle arthroplasty underwent arthrodesis with screw fixation and an additional anterior bridging plate if necessary for stable fixation. Corticocancellous iliac crest graft was used to fill
    the void. This technique works best in patients with
    posttraumatic arthritis. One instance of nonunion occurred in a patient with juvenile rheumatoid arthritis.
    Level of evidence: IV.

    21.

    Radnay CS, Clare MP, Sanders RW: Subtalar fusion after displaced intra-articular calcaneal fractures: Does
    initial operative treatment matter? J Bone Joint Surg
    Am 2009;91(3):541-546.
    Seventy-five calcaneal fractures underwent subtalar fusion; 36 were treated initially with surgery and 39 were
    treated closed. The American Orthopaedic Foot and Ankle Society score was better for the initial surgery group
    (87 versus 74). Postoperative wound compliations were
    also lower. Level of evidence: III.

    22.

    Shawen SB, Anderson RB, Cohen BE, Hammit MD, Davis WH: Spherical ceramic interpositional arthroplasty
    for basal fourth and fifth metatarsal arthritis. Foot Ankle Int 2007;28(8):896-901.
    Thirteen patients with failed resection arthroplasty underwent ceramic ball interposition. The average American Orthopaedic Foot and Ankle Society score increased
    from 28.1 to 52.5. An extensive discussion of lateral
    midfoot arthrosis is presented. Level of evidence: IV.

    23.

    Lee K-B, Saltzman CL, Suh J-S, Wasserman L, Amendola A: A posterior 3-portal arthroscopic approach for
    isolated subtalar arthrodesis. Arthroscopy 2008;24(11):
    1306-1310.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 40: Foot and Ankle Reconstruction

    hallux valgus: A randomized controlled trial. Foot Ankle Int 2008;29(12):1209-1215.


    Chevron osteotomy was at least as effective as a scarf
    osteotomy in treating moderate and severe hallux valgus. Three of 70 patients receiving chevron osteotomy
    developed osteonecrosis, and 1 developed complex regional pain syndrome. Seven of 66 scarf osteotomy patients developed complex regional pain syndrome. Level
    of evidence: I.

    Ten feet with subtalar arthritis and no deformity were


    fused in the prone position using an extra (third) portal.
    Fusion was achieved in 10 weeks. There were no complications with the posteromedial portal with the patient
    prone. Level of evidence: IV.
    24.

    25.

    Sammarco VJ: Surgical correction of moderate and severe hallux valgus: Proximal metatarsal osteotomy with
    distal soft-tissue correction and arthrodesis of the metatarsophalangeal joint. Instr Course Lect 2008;57:415428.
    Various methods of proximal metatarsal osteotomy are
    discussed (chevron, scarf, Ludloff, Mau, and crescentic),
    including the authors preferred technique of fusion:
    cup-in-cone. Diagrams of intrinsically stable and unstable osteotomies are presented. Level of evidence: V.
    Trnka HJ, Hofstaetter SG, Easley ME: Intermediateterm results of the Ludloff osteotomy in one hundred
    and eleven feet: Surgical technique. J Bone Joint Surg
    Am 2009;91(Suppl 2 Pt 1):156-168.
    One hundred eleven feet underwent a Ludloff osteotomy for moderate to severe hallux valgus. American Orthopaedic Foot and Ankle Society scores increased from
    53 to 88. This is a poor procedure for osteoporotic
    bone. The first metatarsal shortened 2.2 mm. Excellent
    clinical photographs and diagrams of the technique are
    presented. Level of evidence: IV.

    27.

    Pinney S, Song K, Chou L: Surgical treatment of mild


    hallux valgus deformity: The state of practice among academic foot and ankle surgeons. Foot Ankle Int 2006;
    27(11):970-973.

    28.

    Pinney SJ, Song KR, Chou LB: Surgical treatment of severe hallux valgus: The state of practice among academic foot and ankle surgeons. Foot Ankle Int 2006;
    27(12):1024-1029.

    29.

    Murawski DE, Beskin JL: Increased displacement maximizes the utility of the distal chevron osteotomy for hallux valgus deformity correction. Foot Ankle Int 2008;
    29(2):155-163.
    Thirty-nine feet were followed for an average of 34
    months; American Orthopaedic Foot and Ankle Society
    score was 93. The lateral displacement of the chevron
    was 50% of the diaphysis. Postoperative American Orthopaedic Foot and Ankle Society hallux valgus score
    averaged 93, with a 7.9 improvement in intermetatarsal angle. Level of evidence: IV.

    30.

    Deenik A, van Mameren H, de Visser E, de Waal Malefijt M, Draijer F, de Bie R: Equivalent correction in
    scarf and chevron osteotomy in moderate and severe

    2011 American Academy of Orthopaedic Surgeons

    31.

    Coughlin MJ, Smith BW: Hallux valgus and first ray


    mobility: Surgical technique. J Bone Joint Surg Am
    2008;90(suppl 2, pt 2):153-170.
    One hundred twenty-two feet were reviewed 27 months
    after surgical repair consisting of a proximal crescentic
    osteotomy. Hypermobility of the first ray was not noted
    after surgery. Level of evidence: IV.

    32.

    Tai CC, Ridgeway S, Ramachandran M, Ng VA, Devic


    N, Singh D: Patient expectations for hallux valgus surgery. J Orthop Surg (Hong Kong) 2008;16(1):91-95.
    One hundred fifty-three patients were questioned concerning surgical expectations. The expectations differed
    in three age groups: younger than 40 years, 40 to 60
    years, and older than 60 years. A 10-minute questionnaire allows the surgeon to address specific expectations
    during preoperative counseling. Level of evidence: II.

    33.

    Coughlin MJ, Jones CP: Hallux valgus: Demographics,


    etiology, and radiographic assessment. Foot Ankle Int
    2007;28(7):759-777.
    One hundred twenty-two feet with moderate or severe
    hallux valgus were demographically studied. Constricting shoes were implicated in 34% of patients. Magnitude of deformity was not associated with Achilles tendon or gastrocnemius tightness or first ray mobility.
    Level of evidence: IV.

    34.

    Saro C, Jensen I, Lindgren U, Fellnder-Tsai L: Qualityof-life outcome after hallux valgus surgery. Qual Life
    Res 2007;16(5):731-738.
    Ninety-four Swedish women with hallux valgus were
    evaluated 1 year after surgery with the Medical Outcomes Study 36-Item Short Form. Quality of life was
    improved after surgery. The degree of radiologic correction does not correlate with quality of life. Level of evidence: IV.

    35.

    Coetzee JC, Resig SG, Kuskowski M, Saleh KJ: The


    Lapidus procedure as salvage after failed surgical treatment of hallux valgus: Surgical technique. J Bone Joint
    Surg Am 2004;86(suppl 1):30-36.

    36.

    Coetzee JC, Wickum D: The Lapidus procedure: A prospective cohort outcome study. Foot Ankle Int 2004;
    25(8):526-531.

    37.

    Malal JJ, Shaw-Dunn J, Kumar CS: Blood supply to the


    first metatarsal head and vessels at risk with a chevron
    osteotomy. J Bone Joint Surg Am 2007;89(9):20182022.
    Ten cadaver limbs were dissected to study the blood
    supply to the distal first metatarsal head. The dorsal as-

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    26.

    OLoughlin PF, Heyworth BE, Kennedy JG: Current


    concepts in the diagnosis and treatment of osteochondral lesions of the ankle. Am J Sports Med 2010;38(2):
    392-404.
    This review article discusses the authors preferred technique and thoroughly discusses the history and current
    treatment strategies for osteochondral lesions. Level of
    evidence: V.

    533

    Section 4: Lower Extremity

    pect of the neck had minor supply; the main supply to


    the capital fragment was the distal plantar-lateral corner. Therefore, a chevron osteotomy using a long plantar limb may decrease osteonecrosis.

    4: Lower Extremity

    38.

    39.

    Squires NA, Jeng CL: Posterior tibial tendon dysfunction. Operative Techniques in Orthopaedics 2006;
    16(1):44-52.

    40.

    Deland JT: Adult-acquired flatfoot deformity. J Am


    Acad Orthop Surg 2008;16(7):399-406.
    A review of the literature with the authors preferred
    treatments is presented. Level of evidence: V.

    41.

    Ellis SJ, Yu JC, Johnson AH, Elliott A, OMalley M, Deland J: Plantar pressures in patients with and without
    lateral foot pain after lateral column lengthening.
    J Bone Joint Surg Am 2010;92(1):81-91.
    Ten patients 2 years after lateral column lengthening
    and hardware removal were compared for the presence
    of lateral column pain. Those with pain had higher lateral midfoot pressure. These increased pressures were
    not as a result of excessive lengthening. Level of evidence: III.

    42.

    43.

    44.

    45.

    534

    Cronin JJ, Limbers JP, Kutty S, Stephens MM: Intermetatarsal angle after first metatarsophalangeal joint arthrodesis for hallux valgus. Foot Ankle Int 2006;27(2):
    104-109.

    Logel KJ, Parks BG, Schon LC: Calcaneocuboid distraction arthrodesis and first metatarsocuneiform arthrodesis for correction of acquired flatfoot deformity in a cadaver model. Foot Ankle Int 2007;28(4):435-440.
    Ten cadaver specimens were loaded in two-legged stance
    after lengthening the lateral column by 10 mm. Lateral
    pressure increased from 24.2 to 30.4 after lengthening
    and then decreased to 26.2 after the first tarsometatarsal joint fusion. No calcaneal slide was performed.
    Kaz AJ, Coughlin MJ: Crossover second toe: Demographics, etiology, and radiographic assessment. Foot
    Ankle Int 2007;28(12):1223-1237.
    One hundred sixty-nine patients with crossover second
    toe were studied. A prominent incidence in women
    older than 50 years was noted. There was no correlation
    between crossover toe and second metatarsal length or
    intermetatarsal angle. Level of evidence: IV.
    Summers H, Kramer PA, Benirschke SK: Percutaneous
    stabilization of traumatic peroneal tendon dislocation.
    Foot Ankle Int 2008;29(12):1229-1231.
    Nine patients were treated with an indirect, manual reduction of peroneal tendons and stabilization percutaneously. None had recurrence or tendon pathology. Level
    of evidence: IV.
    Heckman DS, Reddy
    Parekh SG: Operative
    disorders. J Bone Joint
    A review of peroneal
    Level of evidence: V.

    S, Pedowitz D, Wapner KL,


    treatment for peroneal tendon
    Surg Am 2008;90(2):404-418.
    tendon disorders is presented.

    Orthopaedic Knowledge Update 10

    46.

    Gentchos CE, Bohay DR, Anderson JG: Gastrocnemius


    recession as treatment for refractory achilles tendinopathy: A case report. Foot Ankle Int 2008;29(6):620-623.
    After 2 years of chronic, progressive pain with 5 cm of
    tendinopathy, a patient underwent a modified Vulpius
    gastrocnemius lengthening with complete resolution of
    pain. Level of evidence: V.

    47.

    Nicholson CW, Berlet GC, Lee TH: Prediction of the


    success of nonoperative treatment of insertional Achilles
    tendinosis based on MRI. Foot Ankle Int 2007;28(4):
    472-477.
    Four hundred eighty-eight patients over a 3-year period
    were refined to 157 patients with Achilles tendinitis. An
    MRI classification system based on short-tau inversion
    recovery images was developed. MRI type II and III
    tears required surgery (91% and 70%, respectively).
    Only 2 of 16 of type I tendons had unsuccessful nonsurgical treatment. Level of evidence: IV.

    48.

    Hammit MD, Hobgood ER, Tarquinio TA: Midline


    posterior approach to the ankle and hindfoot. Foot Ankle Int 2006;27(9):711-715.

    49.

    McGarvey WC, Palumbo RC, Baxter DE, Leibman BD:


    Insertional Achilles tendinosis: Surgical treatment
    through a central tendon splitting approach. Foot Ankle
    Int 2002;23(1):19-25.

    50.

    Wagner E, Gould JS, Kneidel M, Fleisig GS, Fowler R:


    Technique and results of Achilles tendon detachment
    and reconstruction for insertional Achilles tendinosis.
    Foot Ankle Int 2006;27(9):677-684.

    51.

    Kirk KL, Schon LC: Technique tip: periosteal flap augmentation of the Brostrom lateral ankle reconstruction.
    Foot Ankle Int 2008;29(2):254-255.
    The authors present a technique tip accompanied by
    clinical photographs.

    52.

    Boyer DS, Younger AS: Anatomic reconstruction of the


    lateral ligament complex of the ankle using a gracilis
    autograft. Foot Ankle Clin 2006;11(3):585-595.

    53.

    Sung KS, Park SJ: Short-term operative outcome of tarsal tunnel syndrome due to benign space-occupying lesions. Foot Ankle Int 2009;30(8):741-745.
    The authors discussed clinical results after surgical treatment for tarsal tunnel syndrome caused by benign
    space-occupying lesions and found significant improvement in average visual analog scale and American Orthopaedic Foot and Ankle Society scores, but subjective
    satisfaction was less favorable (54%) than expected.

    54.

    Coerper S, Beckert S, Kper MA, Jekov M, Knigsrainer A: Fifty percent area reduction after 4 weeks of
    treatment is a reliable indicator for healinganalysis of
    a single-center cohort of 704 diabetic patients. J Diabetes Complications 2009;23(1):49-53.
    A cohort of 704 diabetic patients were treated with initial sharp dbridement and adequate pressure offloading
    over a 10-year period. Wounds that do not reduce by
    half after 4 weeks require a modification of the patients
    treatment regimen. Level of evidence: IV.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 40: Foot and Ankle Reconstruction

    55.

    56.

    Chodos MD, Parks BG, Schon LC, Guyton GP, Campbell JT: Blade plate compared with locking plate for
    tibiotalocalcaneal arthrodesis: A cadaver study. Foot
    Ankle Int 2008;29(2):219-224.
    Nine matched pairs of cadavers were treated with either
    a locking proximal humerus plate or a blade plate. The
    locking plate was found to be mechanically superior in
    providing fixation under cyclical loads.
    Ahmad J, Pour AE, Raikin SM: The modified use of a
    proximal humeral locking plate for tibiotalocalcaneal
    arthrodesis. Foot Ankle Int 2007;28(9):977-983.
    Sixteen of 17 patients with significant medical comorbidities healed at 21 weeks; 15 had osteoporosis. The
    plate was placed laterally; American Orthopaedic Foot
    and Ankle Society scores increased from 15 to 77 (maximum, 86). Level of evidence: IV.

    57.

    Boer R, Mader K, Pennig D, Verheyen CC: Tibiotalocalcaneal arthrodesis using a reamed retrograde locking
    nail. Clin Orthop Relat Res 2007;463:151-156.
    The authors present a retrospective multicenter study
    with one implant and a technique that differed only on
    dbridement of the ankle joint (osteotome or drill bit).
    Both groups had a 100% tibiotalar union rate and
    American Orthopaedic Foot and Ankle Society scores of
    70 (out of 86) at a mean of 51 months. The subtalar
    joint was dbrided only by the reamer. Only 2 of 50
    subtalar joints developed symptomatic nonunions. Level
    of evidence: IV.

    58.

    Younger AS, Hansen ST Jr: Adult cavovarus foot. J Am


    Acad Orthop Surg 2005;13(5):302-315.
    4: Lower Extremity

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    535

    Chapter 41

    Lower Extremity Amputations


    Michael T. Mazurek, MD

    Scott Helmers, MD

    Background

    Dr. Mazurek is deceased. At the time of publication, Dr.


    Mazurek or an immediate family member had received
    research or institutional support from the Orthopaedic
    Trauma Extremity Research Program, a federally funded
    project. Neither Dr. Helmers nor any immediate family
    member has received anything of value from or owns
    stock in a commercial company or institution related directly or indirectly to the subject of this chapter.

    2011 American Academy of Orthopaedic Surgeons

    4: Lower Extremity

    Traditionally, the main indications for amputation have


    been to preserve life by removing a badly damaged limb
    or for the treatment of malignancy. Amputation surgery
    currently is known as a refined reconstructive procedure intended to prepare the residual limb for motor
    functions of locomotion as well as for sensory feedback
    and cosmesis.1 Common reasons for lower limb amputation are trauma, vascular pathology, neoplasm, infectious conditions, and congenital abnormalities.
    In developed countries, most lower extremity amputations are performed for peripheral vascular disease
    secondary to atherosclerosis and/or diabetes mellitus
    (DM). In developing countries, the main indications are
    for trauma and infection. Although the pathophysiology of traumatic amputation may be different than dysvascular amputation, rehabilitation strategies and prosthetic component prescriptions for both should
    maximize function and quality of life. One of the many
    challenges in managing individuals requiring a traumarelated amputation is addressing the wide variety of comorbid injuries common in the multiply injured patient. In war-related amputations, additional injuries to
    peripheral nerves, retained shrapnel, heterotopic ossification, contaminated wounds, burns, grafted skin, and
    fractures require modified rehabilitation strategies to
    maximize the performance of activities of daily living
    (ADL) and ambulation.
    The decision to amputate should be made by a surgeon comfortable with selection of level of amputation,
    muscle balancing, and wound closure2 and in conjunction with the patient and their needs. In the presence of
    trauma, careful consideration should be made with respect to the acute decision between limb salvage and
    amputation,3,4 especially in light of recent literature
    demonstrating that none of the currently used injury severity scores is predictive of outcome.5 When consider-

    ing amputation in the setting of neoplasm, an orthopaedic oncologist should be involved in the decisionmaking process.

    Preoperative Management
    The medical status of a patient undergoing an amputation should be optimized to facilitate the best surgical
    and rehabilitative outcomes. This includes managing
    any comorbidities present before proceeding with amputation; these will be reviewed later in the chapter.
    When possible, appropriate rehabilitation interventions
    should be initiated while the patient is awaiting amputation to maximize present function and prevent secondary complications.

    Amputation Level
    Level of amputation often dictates rehabilitation, functional outcome, and long-term quality of life. Several
    factors are important in determining level of amputation, including patient goals, the patients general medical condition, associated injuries, risks associated with
    additional surgeries, physiologic healing potential, surgeon experience, the soft-tissue zone of injury, and predicted functional outcome.
    Amputation should preserve as much of the limb as
    possible because a longer residual limb allows for better prosthetic control. If possible, the knee should be
    salvaged to decrease the energy consumption required
    for ambulating. In transtibial amputations, the energy
    expenditure in walking is 25% to 40% above normal,
    whereas in transfemoral amputations, it is 68% to
    100% above normal.6,7 This increased energy expenditure may result in a lower level of function in patients
    with cardiovascular or pulmonary comorbidities, rendering some patients nonambulatory.7 Level of amputation is more predictive of mobility than any other patient factor, including age, sex, diabetes, emergency
    admission, indication for amputation, and prior vascular surgery.8 The amount of residual limb needed varies
    with level of amputation.
    With transtibial amputation, an optimal residual
    limb allows adequate space for the prosthetic foot and
    sufficient muscle padding over the residual limb. The
    ideal location of amputation is the middle of the tibia.
    At a minimum, amputation should be performed at the

    Orthopaedic Knowledge Update 10

    537

    Section 4: Lower Extremity

    4: Lower Extremity

    skin.12-14 Values greater than 40 mg Hg indicate acceptable wound healing potential. Values less than 30 mm
    Hg indicate poor wound healing potential.12 The ischemic index, a ratio of Doppler pressure at the level being
    tested compared to the brachial systolic pressure, has
    been advocated as another noninvasive method to determine wound healing potential. An ischemic index of
    0.5 or greater at the surgical level has been shown to be
    necessary to support healing. These tests are useful adjuncts to the clinical decision-making process.
    The amputation level may ultimately be determined
    by the site of injury and damaged tissues. In addition to
    preserving length, it is important to ensure that the residual limb is adequately covered with muscle and sensate skin that is free of scar tissue.15 Although some authors have advocated the use of a through-knee
    amputation as an alternative, suggesting the benefits of
    a weight-bearing end, the Lower Extremity Assessment
    Project study suggested through-knee amputations have
    a worse Sickness Impact Profile (SIP) score than transfemoral amputations.16

    General Principles
    Figure 1

    Radiograph showing a bone bridge procedure.

    junction of the middle third and proximal third of the


    tibia, just below the flare of the tibial plateau, preserving the tibial tubercle (which allows sufficient tibia for
    weight bearing).
    With transfemoral amputation, an optimal residual
    limb allows space for an uncompromised knee system.
    The ideal location of amputation is typically just above
    the condylar flare at the level of the adductor tubercle.
    At a minimum, amputation should be performed at the
    junction of the middle third and proximal third of the
    femur (below the level about the lesser trochanter) to
    allow for a sufficient lever arm to operate the prosthesis. If there is uncertainty about the optimal length of
    the residual limb, preoperative consultation with an experienced physiatrist or prosthetist should be considered.
    The ultimate functional desires and expectations of
    the patient must be included in the decision-making
    process. A desire to return to high-level athletic activities may influence the ultimate level of ambulation in
    an attempt to preserve a longer limb with a lower
    chance of healing. Conversely, in the presence of severe
    medical conditions, amputation at a more proximal
    level with a greater chance of healing may be more reasonable.
    The potential for wound healing is another factor
    that must be included in surgical decision making.
    Healing potential may be determined by noninvasive
    tests to assess for vascular competency.9-11 The most reliable and sensitive test for wound healing is transcutaneous oxygen pressure measurement, which assesses
    the partial pressure of oxygen diffusing through the
    538

    Orthopaedic Knowledge Update 10

    The handling of the bone, muscles, and nerves during


    the surgical amputation can have a profound impact on
    the patients prosthetic fitting and rehabilitation. Bone
    cuts should be made transverse and beveled to avoid
    bony prominence. No periosteal stripping should be
    performed to avoid heterotopic bone formation. Bony
    prominences and heterotopic bone may complicate
    prosthetic fabrication and wear. Muscle should be divided distal to the bone resection to ensure adequate
    soft-tissue coverage. Myodeses may be performed in
    patients with good healing potential to facilitate muscle
    tone, balance, and strength in the residual limb. A balanced myoplasty can also be performed, approximating
    the antagonistic muscles together, centering the bone.
    Nerves should be individually identified, placed under
    gentle traction, sharply transected, and allowed to retract proximally. This will place the nerve in a scarless
    area in an attempt to reduce the risk of neuroma stimulation. When closing the wound, there should be no
    tension on the skin. The surgery flaps developed should
    be closed in a location that will not affect prosthetic fitting. It is a good idea to leave the sutures in longer than
    the usual 2-week period because when the patient lifts
    the stump, tension is placed on the wound. Sutures
    should be removed after adequate skin healing.
    Creating a bone bridge between the tibia and fibula
    can be considered in traumatic, nondysvascular transtibial amputations1 (Figure 1). Proponents of this technique argue that the creation of a bone bridge allows
    for weight bearing on the end of the residual limb. Others believe that although the technique does increase
    the surface area for distributing mechanical load and
    prevent pain from pathologic motion of the fibula, it
    should be reserved for young, active amputees whose
    potential to benefit from a better terminal weightbearing surface offsets the morbidity of additional sur-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 41: Lower Extremity Amputations

    Postoperative Dressing
    The appropriate postoperative dressing should be
    planned preoperatively. A proper dressing should protect the residual limb, decrease edema, and facilitate
    wound closure. There is inconclusive evidence for the
    use of any specific postoperative dressing, with or without an immediate postoperative prosthesis. Current
    protocols and decisions are based on local practice,
    skill, and intuition with the primary goal of maintaining the integrity of the residual limb.

    Pain Management
    Pain should be assessed at all phases of rehabilitation,
    preferably with a tool specifically designed for use in
    lower extremity amputees (Tables 1 and 2). Pain after
    amputation may occur in the phantom limb, the residual limb, the contralateral limb, or the lower back. The
    intensity of pain should be assessed separately at each
    significant site to achieve a thorough assessment of
    pain-related impairment. During the immediate postoperative phase, liberal narcotic analgesics should be considered. With progression through the rehabilitation
    process, a gradual transition to a nonnarcotic pharmacologic regimen combined with physical, psychological,
    and mechanical modalities should be used. Treatment
    should target pain related to the residual/phantom limb
    and address pain in other body parts. There is no consistent evidence to support any specific type of analgesia. Available modalities include pharmacologic agents
    such as antiseizure medications (gabapentin), tricyclic
    antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), nonsteroidal anti-inflammatory drugs
    (NSAIDs), N-methyl-D-aspartic acid (NMDA) receptor
    antagonists, and long-acting narcotics; epidural analgesia (patient-controlled analgesia [PCA] or regional
    analgesia); and nonpharmacologic agents such as transcutaneous electrical nerve stimulation (TENS), desensitization, scar mobilization, relaxation, acupuncture,
    biofeedback, and mirror therapy. Mirror therapy con-

    2011 American Academy of Orthopaedic Surgeons

    sisted of the patient placing their intact limb into a box


    with a mirror down the midline, so that when viewed
    from slightly off center, it would give the appearance of
    having two intact limbs. By using a series of limb movement exercises, some patients experienced a reduction
    in phantom limb pain. The exact mechanism behind
    mirror therapys effect is unknown, but it is thought to
    reverse this cortical remapping and alleviate pain.19
    Two recent studies have examined the development
    and treatment of pain following amputation. The first
    study examined the potential mechanisms for origin of
    phantom limb pain in a study of 96 upper limb amputees.20 A questionnaire was used to assess preamputation pain and the presence or absence of phantom pain, phantom sensation, stump pain, and stump
    sensation, with a median duration of follow-up of 3.2
    years (range, 0.9 to 3.8 years). The authors concluded
    that stump pain/sensation is the initial predominating
    source of patient discomfort and that phantom pain/
    sensation is a long-term consequence with some patients noting an onset almost a year after surgery.
    The second study examined modalities for the management of persistent pain following lower extremity
    amputation in a double-blind, randomized trial evaluating the effect of ketamine on pain and sensory processing in amputees.21 Fifty-three patients undergoing
    lower limb amputation participated. After receiving a
    combined intrathecal-epidural anesthetic for surgery,
    patients either received an epidural infusion of racemic
    ketamine and bupivacaine (group K) or saline solution
    and bupivacaine (group S). In the immediate postoperative period, group K patients had substantially lower
    pain scores than group S patients. After discontinuation
    of the epidural anesthetic until the time of the 1-year
    follow-up, the rates of stump and phantom pain did
    not differ between the two groups (21% and 50%, respectively, for group K compared with 33% and 40%,
    respectively, for group S). The levels of depression and
    anxiety were found to decrease significantly in group K
    patients during the course of the study, whereas a similar decrease was not seen in group S patients. This is
    believed to be due to the NMDA receptor antagonist
    effects of ketamine.

    4: Lower Extremity

    gery.17 One study examined a cohort of 20 consecutive


    patients who had a unilateral transtibial amputation
    with distal tibiofibular bone bridging following lower
    extremity trauma.17 These patients were compared to a
    historical control group of 15 highly functional patients
    with a traditional transtibial amputation. The groups
    were compared using the Prosthesis Evaluation Questionnaire, a validated outcomes measure that quantifies
    the effect of lower extremity amputation on quality of
    life. No significant difference was found between the
    groups,17 suggesting that distal tibiofibular bone bridging may not lead to improved outcomes, particularly
    when it requires an additional operation. The study
    also further highlights the need for prospective research
    to facilitate further understanding of the residual limb
    as an end-bearing surface in patients with transtibial
    amputation.18

    Medical Cormorbidity Management


    The cardiovascular demands of ambulation with a residual limb are significant, as are the risks that cardiovascular disease imparts on patients undergoing amputation. It has been estimated that the mean oxygen
    consumption is 9% to 40% higher in patients with unilateral transtibial amputations, 49% to 100% higher in
    unilateral transfemoral amputations, and 280% percent higher in bilateral transfemoral amputations.6,22
    Cardiac risk may impact the survival risk from the amputation surgery and thus may play a role in the decision regarding the level of amputation.23 Additionally,
    exercise tolerance testing may be warranted during the
    rehabilitation phase to help establish clear guidelines
    for cardiac precautions in therapy.

    Orthopaedic Knowledge Update 10

    539

    Section 4: Lower Extremity

    Table 1

    Pain Diagnosis and Treatment Options for Phantom and Sensational Limb Pain

    Etiology

    Key History or
    Examination
    Features

    Treatment
    Evaluation

    Nonpharmacologic

    Pharmacologic

    4: Lower Extremity

    Phantom Limb Pain (Pain distal to the end of the residual limb)
    Primary phantom limb
    pain

    Diagnosis of
    Onset usually later in
    exclusion once
    postamputation
    other causes of
    period.
    phantom limb
    Often nocturnal
    pain have been
    .Gradually reduced in
    ruled out.
    intensity and
    frequency over time.
    Can be excacerbated by
    residual limb pain.

    Desensitization
    Mirror therapy
    Residual limb compressive
    devices
    Prosthetic use
    TENS
    Acupuncture
    Alternative and
    complementary medicine
    Mental health evaluation and
    treatment (depression,
    PTSD)

    TCAs
    Anticonvulsants
    Antispasmodics
    SSRIs
    NMDA receptor
    antagonists

    Referred pain from


    proximal neurologic
    or musculoskeletal
    source

    Consider symptoms
    of typical musculoskeletal, radicular,
    causes.

    Imaging as
    appropriate.
    EMG/nerve
    conduction
    velocity studies.

    Treat underlying cause as


    appropriate

    Pharmacologic Rx as
    appropriate

    Referred pain from a


    neuroma

    Aggravated by
    prosthetic use.
    Local tinel or
    tenderness at the
    end of the nerve.

    Diagnostic injection
    Ultrasound or MRI.

    Prosthetic modification to
    reduce mechanical loads
    Corticosteroid injection
    Phenol ablation
    Surgical resection

    Consider
    pharmacologic Rx if
    nonresponsive to
    other treatments:
    TCAs
    Anticonvulsants
    Antispasmodics
    SSRIs
    NMDA receptor
    antagonists

    Phantom Limb Sensation (Nonpainful sensations distal to the residual limb; wide spectrum of sensory experiences that vary in
    intensity, frequency, and severity)
    If mild and not
    functionally limiting

    None

    Educate and reassure patient

    None

    If of adequate severity Onset in early


    postamputation
    that is perceived as
    uncomfortable or
    period.
    distressing
    Often nocturnal.
    Gradually reduced in
    intensity and
    frequency over time.

    No specific

    Desensitization
    Mirror therapy
    Residual limb compressive
    devices
    Prosthetic use
    TENS
    Acupuncture
    Alternative and
    complementary medicine

    Consider pharmacologic
    Rx if nonresponsive
    to other treatments:
    TCAs
    Anticonvulsants
    Antispasmodics
    SSRIs
    NMDA receptor
    antagonist

    Evidence indicates that individuals undergoing amputation have an incidence of deep venous thrombosis
    (DVT) ranging from 11% to 50%.24,25 Complications
    of venous thrombus formation may include thrombophlebitis, pulmonary embolism, or death. DVT prophylaxis is, therefore, warranted in all patients with amputation as per institutional and/or consensus guidelines.
    Considerable debate exists as to which prophylactic
    method is best. A recent study found equal efficacy of
    low-molecular-weight heparin (enoxaparin) with unfractionated heparin in this patient population.26 Care
    540

    Orthopaedic Knowledge Update 10

    should be taken when using anticlotting agents in


    multiple-trauma patients, especially those with suspected intracranial hemorrhage.
    Patients with conditions such as hyperlipidemia, hypertension, obesity, and diabetes should also be monitored carefully throughout the continuity of care. These
    health care concerns are the leading causes of morbidity and mortality. In the United States, 75% of amputations occur in people age 65 years or older, and 95%
    are performed because of peripheral vascular disease,
    with or without diabetes.27 Malnourished patients are

    2011 American Academy of Orthopaedic Surgeons

    Chapter 41: Lower Extremity Amputations

    Table 2

    Pain Diagnosis and Treatment Options for Residual Limb Pain

    Etiology

    Key History or
    Examination
    Features

    Treatment
    Evaluation

    Nonpharmacologic

    Pharmacologic

    Residual Limb Pain (Pain in the limb between the end of the residual limb and the next most proximal joint)
    Excacerbated by use of Evaluate prosthetic fit
    and alignment
    the prosthesis
    Associated with
    residual limb findings
    of redness, callous, or
    ulceration

    Refer to prosthetist

    Neuroma

    Pain with prothetic use


    Local tinel sign
    Possible palpable mass

    Diagnostic injection
    Ultrasound or MRI

    Prosthetic modification to Consider


    reduce mechanical loads
    pharmacologic Rx if
    Corticosteroid injection
    nonresponsive to
    Phenol ablation
    other treatments:
    Surgical resection
    TCAs
    Anticonvulsants
    Antispasmodics
    SSRIs
    NMDA receptor
    antagonist

    Ischemic

    Claudication with
    ambulation

    Vascular evaluation

    Treat as appropriate

    Infection
    Cellulitis
    Abcess
    Osteomyelitis

    Classical examination
    features
    Unexplained poor
    glucose control
    Pain unexplained by
    other causes

    Laboratory evaluation
    WBC
    CRP/ESR
    Glucose
    Imaging studies as
    appropriate

    Treat as appropriate

    Neuropathic
    Central (CRPS)
    Peripheral

    Hypersensitivity
    Autonomic features

    Consider triple phase


    bone scan

    Desensitization
    Residual limb compressive
    devices
    Prosthetic use
    TENS
    Acupuncture
    Alternative and
    complementary
    medicine
    Mental health evaluation
    and treatment
    (depression, PTSD)

    at greater risk for delayed wound healing, decubitus ulcer formation, infection, congestive heart failure, progressive weakness, apathy, and death. Evidence suggests that malnourishment is common in patients with
    amputations and that supplementary nutrition may improve healing.28

    Behavioral Health / Psychological Management

    Assessment
    Assessment of the amputee should focus on current
    psychiatric symptoms, with a particular focus on depressive and anxiety symptoms, including posttrau-

    2011 American Academy of Orthopaedic Surgeons

    Acetaminophen
    NSAIDs

    4: Lower Extremity

    Mechanical

    Consider
    pharmacologic Rx if
    nonresponsive to
    other treatments:
    TCAs
    Anticonvulsants
    Antispasmodics
    SSRIs
    NMDA receptor
    antagonists

    matic stress symptoms. Posttraumatic stress symptoms


    may include re-experiencing of the trauma (flashbacks),
    avoidance to the point of having a phobia of places,
    people, and experiences that remind the sufferer of the
    trauma, and chronic physical signs of hyperarousal
    (sleep problems, trouble concentrating, irritability, anger, poor concentration, blackouts, or difficulty remembering things). There is evidence that a relatively high
    percentage of patients experience such problems.29-32
    Posttraumatic stress disorder (PTSD) symptoms are
    more common and severe for individuals whose trauma
    involves combat-related injury.32 Levels of depression
    and anxiety appear to be relatively high for up to 2
    years after amputation and then decline to normal pop-

    Orthopaedic Knowledge Update 10

    541

    Section 4: Lower Extremity

    4: Lower Extremity

    Figure 2

    Drawing demonstrating an elastic bandaging technique. (Copyright Alvin L. Muilenburg and A. Bennett Wilson Jr,
    Houston, TX, 1996. http://www.oandp.com/resources/patientinfo/manuals/5.htm)

    ulation levels.30 There is good evidence that depression


    and posttraumatic stress can be effectively treated with
    both pharmacologic and psychotherapeutic interventions.
    Postoperative depression and anxiety can, therefore,
    resolve in a period of a few months, much more rapidly
    than was previously believed.33 During the immediate
    postoperative course, inpatient rehabilitation should be
    focused on teaching skills that can improve patient
    function by the time of discharge as such function is
    correlated with less depression even in patients who are
    in severe distress. Furthermore, patients at greater risk
    for postamputation depression (those with comorbidities or living alone) can be identified such that additional support be given both preoperatively and postoperatively.
    Assessment should also address major life stressors as
    well as a patients familial/social network, as these factors are likely to influence rehabilitation. Several studies
    indicate that social support enhances psychosocial adjustment, overall functioning, and pain management after amputation.30,31,34 Effective coping strategies may also
    enhance psychosocial adjustment and pain management,
    wheras ineffective strategies may diminish these characteristics.
    At later phases of rehabilitation (after the amputation), the provider should assess social and body image
    anxiety/discomfort, which is not uncommon, particularly among younger and female patients.30,35,36 The loss
    of a limb distorts the body image; lowers self-esteem;
    and increases social isolation, discomfort, and dependence on others, resulting in activity restriction (which
    may be a mediating factor for depression).30
    Advances in the cosmetic appearance of prostheses
    have led to the development of cosmetic covers that are
    remarkably similar in appearance to the contralateral
    limb. The appearance of the prosthesis affects the patients ability to disguise the disability and reduces the
    amputation-related body image concerns and perceived
    social stigma.37 Overall activity level, including the
    presence of excessive activity restriction, and satisfac542

    Orthopaedic Knowledge Update 10

    tion with the prosthesis should be assessed. Activity


    level is reciprocally related to depressive and anxiety
    symptoms, and excessive activity restriction compromises functional outcomes.

    Residual Limb Management

    Edema Control
    Edema control through compressive therapy is the
    foundation of limb shaping and will reduce pain and
    improve mobility. Edema can be controlled by rigid
    dressings with or without an attached pylon, residual
    limb shrinkers, or soft dressings such as an elastic
    wrap. Proper wrapping techniques are essential whenever soft dressings are used to reduce complications
    from poor application (Figure 2).

    Contracture Prevention
    Several passive strategies are available to prevent contractures at both the hip and the knee. Knee immobilizers and rigid dressings attempt to address the goal of
    knee flexion contracture prevention in the patient with
    a transtibial amputation. Active strategies to prevent
    contractures are well documented for the patient with a
    transtibial or transfemoral amputation and include bed
    positioning, prone activities, various stretching techniques, and knee and hip joint mobilization by therapists. A seemingly innocuous and caring gesture of placing a pillow under the residual limb actually encourages
    development of hip and knee flexion contractures. A
    pillow or rolled towel along the lateral aspect of the
    thigh, however, may help prevent a hip abduction contracture and should be considered as a preventive technique.

    Heterotopic Ossification in the Residual


    Limbs of Individuals With Traumatic and
    Combat-Related Amputations
    Reports on the occurrence and treatment of heterotopic
    ossification in patients with amputations are rare. Het-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 41: Lower Extremity Amputations

    4: Lower Extremity

    erotopic ossification in the residual limbs of patients with


    amputation may cause pain and skin breakdown and
    complicate or prevent optimal prosthetic fit (Figure 3).
    The recent experience of the military amputee centers
    with traumatic and combat-related amputations has
    demonstrated a surprisingly high prevalence of heterotopic ossification in residual limbs (up to 63%). Occurrence rates are related to amputations through the initial
    zone of injury and those that are caused by blast injuries.38 Primary prophylactic regimens, such as NSAIDs
    and local irradiation, which have proved to be effective
    in preventing or limiting heterotopic ossification in other
    patient populations, have not been studied in patients
    with amputations and generally are not feasible in the
    setting of acute traumatic amputation. Many patients are
    asymptomatic or can be successfully managed with modification of the prosthesis. For patients with refractory
    symptoms, surgical excision is associated with low recurrence rates and decreased medication requirements with
    acceptable complication rates.38

    Patient Education
    Patients who are active participants in their rehabilitation and maintain positive interactions with team members are more likely to have successful outcomes after
    amputation. Patients should be given appropriate advice and adequate information on rehabilitation programs, prosthetic options, and possible outcomes with
    realistic rehabilitation goals.39

    Prosthetic Management
    Amputees have wide-ranging personal, social, and professional demands. Their ability to meet these demands
    will be mediated by several factors, including residual
    limb characteristics, overall health, fitness, and other
    medical conditions. Based upon these factors, a best estimate of future activities needs to be made so that the
    patient may receive the most appropriate prosthetic
    prescription (Table 3).
    The Centers for Medicare and Medicaid Services,
    formerly known as the Health Care Financing Administration, requires a determination of functional level
    with certificates of medical necessity for a prosthesis.
    These are known as K levels.
    Prostheses are described at this phase as either preparatory (preliminary) or definitive. The preparatory
    prosthesis is fitted while the residual limb is still remodeling. This allows the patient to commence the rehabilitation program of donning and doffing, transfer training, building wear tolerance, improving balance, and
    ambulating with the prosthesis several weeks earlier. A
    preparatory prosthesis often allows a better fit in the final prosthesis as the preparatory socket can be used to
    decrease edema and shape the residual limb.40
    Technologic advances have led to vastly improved
    prostheses for amputees. With the changing nature of
    military combat, there have been an increasing number

    2011 American Academy of Orthopaedic Surgeons

    Figure 3

    Radiograph showing posttraumatic heterotopic


    bone formation.

    of young men and women who have sustained traumatic amputations, leading to to increased interest and
    research in the development of upper and lower extremity prostheses.41-45 Unfortunately, despite several
    well-designed gait analysis studies and many subjective
    observations by patients and clinicians, there are few
    objective data to guide the use of various hightechnology knee and foot systems.

    Rehabilitation
    The goal of rehabilitation is to achieve maximum independence and function. The individuals rehabilitation
    program takes into account preamputation lifestyle, expectations, and medical limitations. The following areas of interventions include a suggested step approach,
    indicating the key elements in each area during progression throughout the rehabilitation process.

    Range of Motion
    An amputation results in an inherent weakness of the
    residual limb due to the new attachments of the cut distal muscles to either bone or other muscle. The patient
    with a transfemoral amputation has a greater propensity for hip flexion and abduction contracture because
    of the relative weakness of the adductor magnus muscle, which normally is a strong hip adductor and exten-

    Orthopaedic Knowledge Update 10

    543

    Section 4: Lower Extremity

    Table 3

    4: Lower Extremity

    Prosthetic Prescription
    Functional Level

    Transtibial

    Transfemoral

    Unlimited household ambulatory (K1) The patient has the ability or potential
    to use the prosthesis for transfers or
    ambulation on level surfaces at a fixed
    cadence.

    Patella tendon bearing (PTB) or total


    surface bearing (TSB)
    Sleeve or pin/shuttle
    Soft foam or gel liner
    Flexible keel foot
    Endoskeletal or exoskeletal pylon

    Modified quadrilateral (quad) (improve


    sitting comfort)
    Silesian/pin/ shuttle/lanyard/total elastic
    suspension (TES)
    Gel liner or frame socket
    Knee systemsa
    Flexible keel or single-axis foot
    Endoskeletal pylon

    Limited community ambulatory (K2) The patient has the ability or potential
    for ambulation with the ability to
    traverse low-level environmental
    barriers such as curbs, stairs, or uneven
    surfaces.

    PTB or TSB
    Sleeve or pin/shuttle or suction
    Soft foam or gel liner or hard socket
    Flexible keel, multi-axial, or energy
    storage foot
    Endoskeletal or exoskeletal pylon

    Quad, modified quad, or ischial


    containment
    Pin/shuttle/lanyard/silesian/suction/TES
    Gel liner or frame socket
    Knee systemsa
    Flexible keel or single-axis foot
    Endoskeletal pylon

    Community ambulatory (K3) The patient has the ability or potential


    for ambulation with variable cadence,
    has the ability to traverse most
    environmental barriers, and may have
    vocational, therapeutic, or exercise
    activity that demands prosthetic
    utilization beyond simple locomotion.

    PTB or TSB
    Sleeve, pin/shuttle, suction, or vacuum
    Soft foam or gel liner or hard socket
    Flexible keel, multi-axial foot
    Torsion and/or vertical shock pylon
    Endoskeletal or exoskeletal pylon

    Quad, modified quad, or ischial


    containment
    Pin/shuttle, suction, silesian/suction/TES
    Gel liner or frame socket
    Knee systemsa
    Flexible keel, multi-axial, or energy
    storage foot
    Torsion and/or vertical shock pylon
    Endoskeletal pylon

    Exceeds basic ambulation (K4) Exhibiting high impact, stress, or energy


    levels typical of the prosthetic demands
    of the child, active adult, or athlete

    PTB or TSB
    Pin/shuttle/sleeve/suction
    Soft foam or gel liner
    Flexible, multiaxial, or energy storage
    foot
    Specialty foot (running)
    Torsion and/or vertical shock pylon
    Endoskeletal or exoskeletal pylon

    Ischial containment
    Suction/pin/shuttle/silesian/
    suction/combo
    Gel liner or frame socket
    Knee systemsa
    Quad, modified quad
    Flexible keel or specialty foot (running)
    Torsion and/or vertical shock pylon
    Endoskeletal pylon

    With variable specifications.

    sor. Some hip and knee flexion contractures can be accommodated by modifications in the prosthesis.
    However, normal range of motion of all joints should
    be pursued.
    Proper positioning will decrease the risk of developing joint contractures, particularly at the hip and knee
    of the involved limb. Contractures at these joints may
    adversely affect prosthetic fitting and subsequent mobility and function. The authors of one study used a
    clinically relevant regression model to demonstrate the
    effectiveness of early inpatient rehabilitation. Contractures were aggressively addressed and preventive strategies, such as prone lying, side lying, and aggressive
    pain control, were implemented to decrease the risk of
    contracture. The investigators found that these strategies, combined with the initiation of prosthetic gait
    training, led to a higher rate of successful prosthetic
    use.46 Another study found similar results when similar
    strategies were focused on the proximal joints.47
    544

    Orthopaedic Knowledge Update 10

    Strengthening
    It has been found that ambulating with a prosthesis results in an increase in energy expenditure.48 In addition,
    higher metabolic costs were found in patients with
    higher levels of amputation, advanced age, or a history
    of peripheral vascular disease.22 The amputee must,
    therefore, improve strength and cardiovascular endurance to maximize function.

    Mobility and Equipment


    The key to independence and reintegration after amputation is personal mobility, which comprises both ease
    and freedom of movement. Only walking provides freedom of movement and is indispensable for independence.49 Several studies describe a positive association
    between a patients mobility and his or her quality of
    life. Authors of one study used the Nottingham Health
    Profile in 1993 to determine that persons with amputations rated their overall quality of life as poor com-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 41: Lower Extremity Amputations

    pared to a control group. They found that mobility was


    the only significant factor that impacted this rating.50
    Another study emphasized that regaining ambulation is
    a key to returning patients to their previous lifestyles,
    roles, activities, and socialization.51 These studies suggest that the major focus of a rehabilitation program
    should be improving patient mobility.
    Long-term outcomes are assessed in relation to the
    ultimate rehabilitation goals. Successful long-term rehabilitation outcomes must take into account not only the
    success of prosthetic fitting but also an individuals
    overall level of function in a community setting.52

    Prosthetic Rehabilitation

    Community Reintegration
    Reintegration into a normal, preamputation level of
    work and physical activity is generally poor for the patient with an amputation in the areas of community
    mobility, work, and recreation. Return to work after
    severe lower extremity trauma remains a challenge.
    One study found that 75% of patients in the workingage group considered their integration into work unsuccessful, despite rating their perceptions of selfworth, home mobility, and psychosocial adjustment as
    satisfactory. Dependent factors were prior education,
    type of employment (sedentary compared with manual
    work), underlying medical condition, level of amputation, the availability of retraining assistance, the attitudes of employers and associates, and their own attitudes toward work. Emphasis should be placed on
    these aspects in rehabilitation.54

    Follow-up Care
    Follow-up care for all patients with amputations is
    needed to ensure continued optimal function in the home
    and community. Without scheduled follow-up care, patients may not recognize problems with the fit of their
    prosthesis, a change in their gait pattern, or changes in
    their contralateral or residual limb.55 As a result, major
    or minor secondary complications may arise. Given the

    2011 American Academy of Orthopaedic Surgeons

    4: Lower Extremity

    Prosthetic training follows the preprosthetic rehabilitation phase. Once a patient is deemed a candidate for a
    prosthesis, provisions are made for a prosthetic prescription, basic rehabilitation, prosthetic management,
    and gait training based on identified goals. If the patient is not a candidate for a prosthesis, the team will
    perform basic rehabilitation and provide durable medical equipment. At the conclusion of the prosthetic
    phase, the goal is to attain maximal functional independence and mobility with the artificial limb. Also desired
    are prosthetic fitting and intensive gait training interventions to reduce the occurrence of phantom pain and
    improve long-term outcomes, including returning to
    work. During this phase, patients are given advice on
    employment, recreational activity, driving, and vocational rehabilitation. The continuation of care at the
    community level should be promoted and arranged. A
    recent study has shown little benefit of early walking
    aids during this phase of rehabilitation.53

    importance of optimal socket fit, the patient must also


    be monitored for volumetric and anatomic changes,
    alignment adjustments, component replacement, and
    continuing education. A lifelong consultation with other
    health care providers regarding the interaction between
    other disease processes and the function of patients with
    an amputation may be required to prevent amputations
    of the contralateral limb or ipsilateral limb more proximally (with a rate reportedly as high as 21% within the
    first 18 months after amputation).56 For the patient with
    vascular disease or diabetes, long-term follow-up care
    should include appropriate foot care and patient education at every patient visit.
    In addition, the level of independent walking decreases with time. One third of persons who were
    young (average age of 24 years, with standard deviation of 10 years) at the time of amputation were successfully rehabilitated; however, in subsequent
    follow-up (average age of 54 years, with standard deviation of 15 years) were noted to have limitations in mobility. Reevaluations should be conducted as needed for
    modification of a prosthesis to accommodate changes
    in functional status.57 Reassessment of the available advancements in medical science and prosthetic technology will continue for the patients lifetime.
    There are no clinical trials that provide evidence of
    the need for lifelong care. Patients need to have access
    to primary care and amputation teams, but there is no
    evidence to indicate how often that follow-up should
    occur. However, follow-up visits to assess and modify
    the prosthesis become important because of changes
    that occur in amputees during the aging process.58
    The loss of a limb provides ongoing stress to other
    areas of the body. Musculoskeletal problems may arise
    in the residual and contralateral limbs, spine, and upper extremities.
    Approximately 65% of the amputations in people
    older than 50 years are due to vascular disease or the effects of diabetes. Of this population, 30% will lose a second limb to the same disease. Therefore, as much emphasis should be placed on preserving the contralateral
    limb as is placed on recovering from the amputation.59
    Changes associated with aging, changes in the residual limb, prosthetic wear, and new technologies are all
    reasons to order a new prosthesis. Better technology
    has provided more responsive components and lighter
    materials, allowing for increased mobility in older amputees.

    Annotated References
    1.

    Pinzur MS, Gottschalk F, Pinto MA, Smith DG: Controversies in lower extremity amputation. Instr Course
    Lect 2008;57:663-672.
    The authors discuss the history, decision making, and
    techniques in amputation surgery.

    2.

    Smith D; Clinical Standards of Practice Consensus Conference: Assessing outcomes and the future. J Prosthet-

    Orthopaedic Knowledge Update 10

    545

    Section 4: Lower Extremity

    13.

    Bosse MJ, MacKenzie EJ, Kellam JF, et al: A prospective evaluation of the clinical utility of the lowerextremity injury-severity scores. J Bone Joint Surg Am
    2001;83(1):3-14.

    Burgess EM, Matsen FA III, Wyss CR, Simmons CW:


    Segmental transcutaneous measurements of PO2 in patients requiring below-the-knee amputation for peripheral vascular insufficiency. J Bone Joint Surg Am 1982;
    64(3):378-382.

    14.

    Bosse MJ, McCarthy ML, Jones AL, et al; Lower Extremity Assessment Project (LEAP) Study Group: The
    insensate foot following severe lower extremity trauma:
    An indication for amputation? J Bone Joint Surg Am
    2005;87(12):2601-2608.

    Lalka SG, Malone JM, Anderson GG, Hagaman RM,


    McIntyre KE, Bernhard VM: Transcutaneous oxygen
    and carbon dioxide pressure monitoring to determine
    severity of limb ischemia and to predict surgical outcome. J Vasc Surg 1988;7(4):507-514.

    15.

    Kostuik J: Indications, levels and limiting factors in amputation surgery of the lower extremity, in Kostuik J,
    ed: Amputation Surgery and Rehabilitation: The Toronto Experience. New York, NY, Churchill Livingstone, 1981, pp 1725.

    16.

    Bosse MJ, MacKenzie EJ, Kellam JF, et al: An analysis


    of outcomes of reconstruction or amputation after legthreatening injuries. N Engl J Med 2002;12;347(24):
    1924-1931.

    17.

    Pinzur MS, Beck J, Himes R, Callaci J: Distal tibiofibular bone-bridging in transtibial amputation. J Bone
    Joint Surg Am 2008;90(12):2682-2687.
    This study examined 20 patients who underwent a unilateral traumatic transtibial amputation, with a distal
    tibiofibular bone-bridging technique performed by a single surgeon. Using a Prosthesis Evaluation Questionnaire (PEQ), a validated outcomes instrument designed
    to measure patient self-reported health-related quality of
    life after a lower-extremity amputation, the authors
    compared their responses to those of a previously reported control group of nondiabetic patients who had
    undergone transtibial amputation with the use of a traditional technique. No difference in scores between the
    bone-bridge group and those in the control group were
    noted.

    18.

    Hosalkar H, Pandya NK, Hsu J, Keenan MA: Whats


    new in orthopaedic rehabilitation. J Bone Joint Surg Am
    2009;91(9):2296-2310.

    19.

    Hanling SR, Wallace SC, Hollenbeck KJ, Belnap BD,


    Tulis MR: Preamputation mirror therapy may prevent
    development of phantom limb pain: A case series.
    Anesth Analg 2010;110(2):611-614.
    The authors found that preamputation mirror therapy
    may lead to improved postamputation compliance and
    decrease the incidence of phantom limb pain. Four patients were studied for 2 weeks before elective limb amputation.

    20.

    Schley MT, Wilms P, Toepfner S, et al: Painful and nonpainful phantom and stump sensations in acute traumatic amputees. J Trauma 2008;65(4):858-864.
    This study examined 96 patients with upper extremity
    amputations to look for factors in the formation, prevalence, intensity, course, and predisposing factors for
    phantom limb pain. The prevalence of phantom pain
    was 44.6%, phantom sensation 53.8%, stump pain
    61.5%, and stump sensation 78.5%. After its first appearance, phantom pain had a decreasing course in

    ics Orthotics 2004;16(3S). http://www.oandp.org/jpo/


    library/index/2004_03S.asp. Accessed February 2007.
    3.

    4.

    4: Lower Extremity

    5.

    Ly TV, Travison TG, Castillo RC, Bosse MJ, MacKenzie EJ; LEAP Study Group: Ability of lower-extremity
    injury severity scores to predict functional outcome after limb salvage. J Bone Joint Surg Am 2008;90(8):
    1738-1743.
    This study examined the clinical utility of the five commonly used lower-extremity injury severity scoring systems as predictors of final functional outcome in 407
    patients from the Lower Extremity Assessment Project
    (LEAP) study group: the Mangled Extremity Severity
    Score; the Limb Salvage Index; the Predictive Salvage Index; the Nerve Injury, Ischemia, Soft-Tissue Injury, Skeletal Injury, Shock, and Age of Patient Score; and the
    Hannover Fracture Scale-98. The analysis showed that
    none of the scoring systems were predictive of the SIP
    outcomes or patient recovery at 6 or 24 months.

    546

    6.

    Czerniecki JM: Rehabilitation in limb deficiency: 1.


    Gait and motion analysis. Arch Phys Med Rehabil
    1996;77(3, suppl )S3-S8.

    7.

    Volpicelli LJ, Chambers RB, Wagner FW Jr: Ambulation


    levels of bilateral lower-extremity amputees: Analysis of
    one hundred and three cases. J Bone Joint Surg Am
    1983;65(5):599-605.

    8.

    Turney BW, Kent SJ, Walker RT, Loftus IM: Amputations: No longer the end of the road. J R Coll Surg Edinb 2001;46(5):271-273.

    9.

    Apelqvist J, Castenfors J, Larsson J, Stenstrm A,


    Agardh CD: Prognostic value of systolic ankle and toe
    blood pressure levels in outcome of diabetic foot ulcer.
    Diabetes Care 1989;12(6):373-378.

    10.

    Wagner FW: Transcutaneous Doppler ultrasound in the


    prediction of healing and the selection of surgical level
    for dysvascular lesions of the toes and forefoot. Clin
    Orthop Relat Res 1979;142:110-114.

    11.

    Barnes RW, Shanik GD, Slaymaker EE: An index of


    healing in below-knee amputation: Leg blood pressure
    by Doppler ultrasound. Surgery 1976;79(1):13-20.

    12.

    Pinzur MS, Sage R, Stuck R, Ketner L, Osterman H:


    Transcutaneous oxygen as a predictor of wound healing
    in amputations of the foot and ankle. Foot Ankle 1992;
    13(5):271-272.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 41: Lower Extremity Amputations

    48%, was stable in 38%, and worsened in 7% of patient with amputations. Stump pain had a decreasing
    course in 48% but was stable in 30% of patients with
    amputations. Phantom pain occurred immediately after
    amputation in 28%, between 1 and 12 months in 10%,
    and after 12 months or more in 41% of patients with
    amputations.
    21.

    23.

    24.

    25.

    26.

    Huang CT, Jackson JR, Moore NB, et al: Amputation:


    Energy cost of ambulation. Arch Phys Med Rehabil
    1979;60(1):18-24.
    Fleisher LA, Beckman JA, Brown KA, et al; American
    College of Cardiology/American Heart Association Task
    Force on Practice Guidelines Writing Committee to Update the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery; American Society of Echocardiography; American Society of Nuclear
    Cardiology; Heart Rhythm Society; Society of Cardiovascular Anesthesiologists; Society for Cardiovascular
    Angiography and Interventions; Society for Vascular
    Medicine and Biology: ACC/AHA 2006 guideline update on perioperative cardiovascular evaluation for noncardiac surgery: Focused update on perioperative betablocker therapy. A report of the American College of
    Cardiology/American Heart Association Task Force on
    Practice Guidelines (Writing Committee to Update the
    2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery): Developed in collaboration with the American Society of Echocardiography,
    American Society of Nuclear Cardiology, Heart Rhythm
    Society, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society for Vascular Medicine and Biology.
    Circulation 2006;113(22):2662-2674.
    Burke B, Kumar R, Vickers V, Grant E, Scremin E:
    Deep vein thrombosis after lower limb amputation. Am
    J Phys Med Rehabil 2000;79(2):145-149.
    Yeager RA, Moneta GL, Edwards JM, Taylor LM Jr,
    McConnell DB, Porter JM: Deep vein thrombosis associated with lower extremity amputation. J Vasc Surg
    1995;22(5):612-615.
    Lastria S, Rollo HA, Yoshida WB, Giannini M, Moura
    R, Maffei FH: Prophylaxis of deep-vein thrombosis af-

    2011 American Academy of Orthopaedic Surgeons

    27.

    Leonard JA: The elderly amputee, in Felsenthal G, Garrison SJ, Stienberg FU, eds: Rehabilitation of the Aging
    and Elderly Patient. Baltimore, MD, Williams &
    Wilkins, 1994, pp 397406.

    28.

    Eneroth M, Apelqvist J, Larsson J, Persson BM: Improved wound healing in transtibial amputees receiving
    supplementary nutrition. Int Orthop 1997;21(2):104108.

    29.

    Cansever A, Uzun O, Yildiz C, Ates A, Atesalp AS: Depression in men with traumatic lower part amputation:
    A comparison to men with surgical lower part amputation. Mil Med 2003;168(2):106-109.

    30.

    Horgan O, MacLachlan M: Psychosocial adjustment to


    lower-limb amputation: A review. Disabil Rehabil 2004;
    26(14-15):837-850.

    31.

    Jensen MP, Ehde DM, Hoffman AJ, Patterson DR, Czerniecki JM, Robinson LR: Cognitions, coping and social environment predict adjustment to phantom limb
    pain. Pain 2002;95(1-2):133-142.

    32.

    Koren D, Norman D, Cohen A, Berman J, Klein EM:


    Increased PTSD risk with combat-related injury: A
    matched comparison study of injured and uninjured soldiers experiencing the same combat events. Am J Psychiatry 2005;162(2):276-282.

    33.

    Singh R, Hunter J, Philip A: The rapid resolution of depression and anxiety symptoms after lower limb amputation. Clin Rehabil 2007;21(8):754-759.

    34.

    Williams RM, Ehde DM, Smith DG, Czerniecki JM,


    Hoffman AJ, Robinson LR: A two-year longitudinal
    study of social support following amputation. Disabil
    Rehabil 2004;26(14-15):862-874.

    35.

    Fukunishi I: Relationship of cosmetic disfigurement to


    the severity of posttraumatic stress disorder in burn injury or digital amputation. Psychother Psychosom
    1999;68(2):82-86.

    36.

    Rybarczyk BD, Nyenhuis DL, Nicholas JJ, Schulz R,


    Alioto RJ, Blair C: Social discomfort and depression in
    a sample of adults with leg amputations. Arch Phys
    Med Rehabil 1992;73(12):1169-1173.

    37.

    Donovan-Hall MK, Yardley L, Watts RJ: Engagement in


    activities revealing the body and psychosocial adjustment in adults with a trans-tibial prosthesis. Prosthet
    Orthot Int 2002;26(1):15-22.

    38.

    Potter BK, Burns TC, Lacap AP, Granville RR, Gajewski DA: Heterotopic ossification following traumatic
    and combat-related amputations. Prevalence, risk factors, and preliminary results of excision. J Bone Joint
    Surg Am 2007;89(3):476-486.

    Orthopaedic Knowledge Update 10

    4: Lower Extremity

    22.

    Wilson JA, Nimmo AF, Fleetwood-Walker SM, Colvin


    LA: A randomised double blind trial of the effect of preEmptive epidural ketamine on persistent pain after
    lower limb amputation. Pain 2008;135(1-2):108-118.
    This study examined the effect of preemptively modulating sensory input with epidural ketamine (an NMDA
    antagonist) on postamputation pain and sensory processing on 53 patients undergoing lower limb amputation. Patients were randomized to receive epidural infusion (group K received racemic ketamine and
    bupivacaine; group S received saline and bupivacaine).
    At 1 year, there was no significant difference between
    groups (group K=21% and 50%; and group S=33% and
    40% for stump and phantom pain, respectively). Postoperative analgesia was significantly better in group K,
    with reduced stump sensitivity which may reflect acute
    effects of ketamine on central sensitization.

    ter lower extremity amputation: comparison of low molecular weight heparin with unfractionated heparin.
    Acta Cir Bras 2006;21(3):184-186.

    547

    Section 4: Lower Extremity

    4: Lower Extremity

    This study examined the prevalence of and risk factors


    for heterotopic ossification following trauma-related
    amputation as well as the preliminary results of surgical
    excision in 187 patients with a total of 213 traumatic
    and combat-related amputations. Heterotopic ossification was present in 63% of residual limbs. A final amputation level within the zone of injury and blast mechanism were risk factors for the development of
    heterotopic ossification. For 25 patients with refractory
    symptoms (12%), surgical excision is associated with
    low recurrence rates (8%) and decreased medication requirements, with acceptable complication rates (32%).
    There was a significant decrease in the use of pain medication following surgery.
    39.

    Pandian G, Kowalske K: Daily functioning of patients


    with an amputated lower extremity. Clin Orthop Relat
    Res 1999;361(361):91-97.

    40.

    Bodeau VS: Lower limb prosthetics. http://www.


    emedicine.com/pmr/topic175.htm. Accessed February
    12, 2007.

    41.

    Adderson JA, Parker KE, Macleod DA, Kirby RL,


    McPhail C: Effect of a shock-absorbing pylon on transmission of heel strike forces during the gait of people
    with unilateral trans-tibial amputations: A pilot study.
    Prosthet Orthot Int 2007;31(4):384-393.
    This study examined the effects on walking with a
    shock-absorbing pylon (SAP) in seven patients with unilateral transtibial amputations. The SAP provided no
    significant shock absorption as indicated by either the
    mean peak proximal accelerations of 3.19 g and 2.82 g
    without and with the SAP, respectively, or the mean difference between the peak proximal and distal accelerometers, 0.16 g and 0.19 g. Unfortunately, variances
    were high and the study was likely underpowered to determine the efficacy of SAPs.

    42.

    43.

    548

    Raichle KA, Hanley MA, Molton I, et al: Prosthesis use


    in persons with lower- and upper-limb amputation.
    J Rehabil Res Dev 2008;45(7):961-972.
    This study examined factors related to prosthesis use in
    107 patients with upper limb amputation (ULA) and
    752 patients with lower limb amputation (LLA) and the
    effect of phantom limb pain (PLP) and residual limb
    pain (RLP) on prosthesis use. Factors related to greater
    use (hours per day) for persons with LLA included
    younger age, full- or part-time employment, marriage, a
    distal amputation, an amputation of traumatic etiology,
    and an absence of PLP. Less use was associated with reports that prosthesis use worsened RLP, and greater
    prosthesis use was associated with reports that prosthesis use did not affect PLP. Having a proximal amputation and reporting lower average PLP were related to
    greater use in hours per day for persons with a ULA,
    while having a distal amputation and being married
    were associated with greater use in days per month. Participants with LLA were significantly more likely to
    wear a prosthesis than those with ULA.
    Sansam K, Neumann V, OConnor R, Bhakta B: Predicting walking ability following lower limb amputation: A systematic review of the literature. J Rehabil
    Med 2009;41(8):593-603.
    This systematic literature review examined factors that
    predict walking with a prosthesis after lower limb am-

    Orthopaedic Knowledge Update 10

    putation in 57 studies. Predictors of good walking ability following lower limb amputation include cognition,
    fitness, ability to stand on one leg, independence in activities of daily living and preoperative mobility. Longer
    time from surgery to rehabilitation and stump problems
    are predictors of poor outcome. In general, unilateral
    and distal amputation levels, and younger age were predictive of better walking ability.
    44.

    Tang PC, Ravji K, Key JJ, Mahler DB, Blume PA, Sumpio B: Let them walk! Current prosthesis options for leg
    and foot amputees. J Am Coll Surg 2008;206(3):548560.

    45.

    Versluys R, Beyl P, Van Damme M, Desomer A, Van


    Ham R, Lefeber D: Prosthetic feet: State-of-the-art review and the importance of mimicking human anklefoot biomechanics. Disabil Rehabil Assist Technol
    2009;4(2):65-75.
    This review discussed the numerous prosthetic feet currently on the market for individuals with a transtibial
    amputation, each device aimed at raising the 3C-level
    (control, comfort and cosmetics) with emphasis on
    energy-storing-and-returning feet and the recent socalled bionic feet.

    46.

    Munin MC, Espejo-De Guzman MC, Boninger ML,


    Fitzgerald SG, Penrod LE, Singh J: Predictive factors for
    successful early prosthetic ambulation among lowerlimb amputees. J Rehabil Res Dev 2001;38(4):379-384.

    47.

    Davidson JH, Jones LE, Cornet J, Cittarelli T: Management of the multiple limb amputee. Disabil Rehabil
    2002;24(13):688-699.

    48.

    Waters RL, Perry J, Antonelli D, Hislop H: Energy cost


    of walking of amputees: The influence of level of amputation. J Bone Joint Surg Am 1976;58(1):42-46.

    49.

    Collin C, Collin J: Mobility after lower-limb amputation. Br J Surg 1995;82(8):1010-1011.

    50.

    Pell JP, Donnan PT, Fowkes FG, Ruckley CV: Quality


    of life following lower limb amputation for peripheral
    arterial disease. Eur J Vasc Surg 1993;7(4):448-451.

    51.

    Esquenazi A, DiGiacomo R: Rehabilitation after amputation. J Am Podiatr Med Assoc 2001;91(1):13-22.

    52.

    Purry NA, Hannon MA: How successful is below-knee


    amputation for injury? Injury 1989;20(1):32-36.

    53.

    Barnett C, Vanicek N, Polman R, et al: Kinematic gait


    adaptations in unilateral transtibial amputees during rehabilitation. Prosthet Orthot Int 2009;33(2):135-147.
    This randomized study examined the use of two different early walking aids (EWAs) in individuals who have
    recently undergone unilateral transtibial amputation on
    kinematic gait patterns during early rehabilitation. Patients were randomly assigned to use the Amputee Mobility Aid or the Pneumatic Postamputation Aid prior to
    receiving their functional prosthesis. A threedimensional motion capture system recorded kinematic
    data from their first steps up to discharge from rehabil-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 41: Lower Extremity Amputations

    This study examined the rates and risk factors for ipsilateral reamputation in 121 patients with diabetic foot
    and prior amputation. The authors found that 21.5% of
    patients required reamputation during a mean follow-up
    of 18 months. Most reamputations were performed
    within the first 6 months of the initial amputation. Patients older than 70 years and those with heel lesions are
    at greatest risk for reamputation.

    itation. The results from this study would suggest that


    neither EWA was more beneficial for gait retraining during rehabilitation.
    Nissen SJ, Newman WP: Factors influencing reintegration to normal living after amputation. Arch Phys Med
    Rehabil 1992;73(6):548-551.

    55.

    Gailey R, Allen K, Castles J, Kucharik J, Roeder M: Review of secondary physical conditions associated with
    lower-limb amputation and long-term prosthesis use.
    J Rehabil Res Dev 2008;45(1):15-29.
    The authors discussed the musculoskeletal imbalances
    or pathologies that often develop into secondary physical conditions or complications that may affect the mobility and quality of life of people with lower limb amputation. They reviewed the literature on secondary
    complications among people with lower limb loss who
    are long-term prosthesis wearers.

    56.

    57.

    Burger H, Marincek C, Isakov E: Mobility of persons


    after traumatic lower limb amputation. Disabil Rehabil
    1997;19(7):272-277.

    58.

    Frieden RA: The geriatric amputee. Phys Med Rehabil


    Clin N Am 2005;16(1):179-195.

    59.

    Jeffries GE: Aging americans and amputation. In Motion


    1996
    Apr-May;6(2).
    http://www.amputeecoalition.org/inmotion/apr_may_96/aging_amputees.
    pdf. Accessed October 28, 2010.

    4: Lower Extremity

    54.

    Skoutas D, Papanas N, Georgiadis GS, et al: Risk factors for ipsilateral reamputation in patients with diabetic foot lesions. Int J Low Extrem Wounds 2009;8(2):
    69-74.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    549

    Chapter 42

    Spinal Tumors
    Scott D. Daffner, MD

    Introduction
    Primary spinal tumors are relatively rare, typically representing less than 5% of all spinal tumors;1 however,
    the spine is the most common site for skeletal metastases. Initial symptoms may be subtle, leading to a delay
    in diagnosis. As treatment algorithms continue to
    evolve, survival rates for patients with many types of
    cancer have improved, underlying the importance of
    early detection and treatment. However, patients with
    spinal tumors are challenging to treat; questions remain
    about which patients should have surgery, the timing of
    surgery, and the optimal surgical procedure.

    Epidemiology

    Table 1

    Common Spinal Tumors


    Metastatic

    Breast
    Gastrointestinal
    Lung
    Kidney
    Prostate
    Thyroid

    Primary benign

    Aneurysmal bone cyst


    Eosinophilic granuloma
    Giant cell tumor
    Hemangioma
    Neurofibroma
    Osteoid osteoma
    Osteoblastoma
    Osteochondroma

    Primary malignant

    Chondrosarcoma
    Chordoma
    Ewing sarcoma
    Multiple myeloma
    Osteosarcoma

    Evaluation
    A thorough history and physical examination are of utmost importance in evaluating a patient with a suspected spinal tumor. Pain is the most common presenting complaint, occurring in approximately 85% of
    patients with spinal tumors. This pain is typically axial
    in nature and of insidious onset. Night pain is common
    and may be unrelated to activity, but may be caused by
    the normal variation of endogenous steroid secretion,
    which decreases at night but helps mitigate inflamma-

    Dr. Daffner or an immediate family member has stock or


    stock options held in Amgen and Pfizer.

    2011 American Academy of Orthopaedic Surgeons

    5: Spine

    Lesions of the spine may affect patients of any age. Benign lesions are more commonly seen in children and
    tend to localize to the posterior elements, whereas malignant tumors are more common in adults and more
    frequently affect the vertebral body.1 The spine is the
    most common site for skeletal metastases, which have a
    predilection for the thoracic region. Autopsy studies
    suggest that between 30% and 80% of patients with
    cancer have evidence of bony metastases.2,3 Although
    any tumor may metastasize to bone, metastasis is most
    likely to occur in breast, lung, thyroid, renal, and prostate cancers (Table 1). Although the different prevalence of cancer types in men and women leads to variable rates of skeletal metastases, the distribution of
    primary bony tumors of the spine is almost equal between men and women. Malignant primary tumors are
    more common in males and benign tumors are more
    common in females.1

    tory mediators released by tumors when present. Mechanical pain, pain with activity, or pain with changing
    positions suggests spinal instability. Acute onset or
    worsening of axial pain is suggestive of a fracture. Although axial pain is more common, patients may also
    present with symptoms of neurologic impingement. In
    this population, approximately 61% present with
    radicular pain, 37% present with a motor deficit, and
    2% have an isolated sphincter dysfunction.4 Neurologic
    impairment may have an acute onset in 28% of patients.4
    Patients should be questioned to determine history
    of cancer, no matter how remote. The presence of constitutional symptoms such as weight changes, fatigue,
    and changes in appetite should be noted. Adult patients
    should be asked whether their primary care provider
    has performed age-appropriate screening studies (such
    as colonoscopy or mammography). In addition, the social history should include documentation of any tobacco usage or possible occupational exposure to carcinogens; a family history of cancer also should be
    probed. A thorough physical examination should be
    performed with particular attention to details such as
    focal spinal tenderness, limited range of motion, or
    subtle neurologic deficits.

    Orthopaedic Knowledge Update 10

    553

    Section 5: Spine

    5: Spine

    Plain radiographs are the initial study of choice and


    allow an assessment of overall spinal alignment, general bone quality, and localization of the lesion. Because lesions typically cannot be seen on plain radiographs until 30% to 50% of the bone has been
    destroyed, a negative plain radiograph cannot exclude
    the presence of a tumor. CT provides excellent bony detail, and MRI provides soft-tissue detail and is of great
    benefit in demonstrating neurologic impingement. MRI
    should be performed with intravenous gadolinium contrast when a tumor is suspected because more vascular
    regions will be highlighted. Metastatic tumors typically
    have decreased signal on T1-weighted MRI, with surrounding hyperintense fatty marrow. Whole-body
    technetium-99 bone scans performed with or without
    single photon emission CT (SPECT) can identify remote lesions and assist in staging the disease as well as
    potentially locating a lesion that may be more easily biopsied.
    Laboratory evaluation is helpful in establishing a
    differential diagnosis, particularly in patients with no
    known primary tumor. A complete blood count with
    differential, serum and urine electrolytes, erythrocyte
    sedimentation rate, and C-reactive protein can be a useful starting point. Other tests may be ordered depending on the suspected primary cancer; for example,
    thyroid-stimulating hormone and thyroxine (free T4) if
    thyroid cancer is suspected, prostate-specific antigen in
    patients who may have prostate cancer, or liver function tests and carcinoembryonic antigen for gastrointestinal cancers. Serum and urine protein electrophoresis
    typically demonstrate a monoclonal gammopathy in
    multiple myeloma.

    Diagnosis, Staging, and Surgical Planning


    When taken together, the patient history, physical examination, laboratory studies, and imaging should provide most of the needed information for a diagnosis.
    Definitive diagnosis, however, is provided by biopsy.
    The workup may demonstrate remote sites of tumor
    that may be more amenable to biopsy than the spine.
    When necessary, CT- or MRI-guided transpedicular
    fine-needle aspiration or core biopsies are the study of
    choice.5-7 The accuracy of CT-guided biopsy has been
    reported at approximately 89%, with better yield from
    lytic lesions (93%) than sclerotic lesions (76%).8 The
    tract of the needle biopsy should be tattooed to allow
    resection at the time of definitive surgery. On occasion,
    open excisional biopsy may be required. If this is the
    case, meticulous surgical technique to reduce the risk of
    contamination should be followed. Open biopsy can be
    performed at the time of definitive surgical treatment
    (resection, decompression, and/or stabilization); however, new drapes and instruments should be used after
    the biopsy is obtained to minimize potential seeding of
    unaffected tissue. Image-guided biopsies should be performed by the interventional neuroradiologist or musculoskeletal radiologist in consultation with the treating surgeon. Open biopsy, when necessary, should be
    554

    Orthopaedic Knowledge Update 10

    performed by the surgeon performing definitive treatment.


    Staging of spinal tumors can aid in surgical planning. The Enneking classification of musculoskeletal tumors is useful in oncologic staging; however, because
    its applicability to the surgical staging of spinal lesions
    is limited, it will not be discussed. This is because performing a true en bloc resection of a spinal tumor
    would frequently require excision of the spinal cord.
    The most widely accepted staging system for spinal tumors is the Weinstein, Boriani, and Biagini (WBB) system9 (Figure 1). This system divides the axial plane of
    the involved vertebral body into 12 zones resembling a
    clock face. Additionally, the spine is divided into five
    layers (A to E) moving from peripherally centrally,
    from the paraspinal extraosseous soft tissues to the intradural space. Based on this system, a vertebrectomy
    can be performed when the tumor is isolated to the vertebral body and at least one pedicle is free of tumor. A
    sagittal resection can be performed for tumors involving one side of the vertebral body, a pedicle, and transverse process, and resection of the posterior arch alone
    can be performed for lesions isolated to the posterior
    elements with tumor-free pedicles.9

    Primary Benign Lesions

    Aneurysmal Bone Cyst


    Aneurysmal bone cysts (ABCs) most frequently arise in
    the second decade of life. Approximately 20% of ABCs
    occur within the spine, predominantly in the posterior
    elements. Radiographs typically demonstrate an expansile, lytic lesion with a rim of reactive bone. The fluidfluid levels seen on MRI are virtually pathognomonic.
    Treatment options include radiation therapy, selective
    arterial embolization, curettage, and en bloc resection.
    Recently, selective arterial embolization has become the
    first-line treatment of choice.10 Larger lesions can cause
    compression of the neural elements or instability of the
    spine resulting from bony destruction. In such cases, en
    bloc resection (if limited to posterior elements) or intralesional extracapsular excision followed by reconstruction and fusion is appropriate. Similarly, surgical
    treatment is recommended for local recurrence or failure of embolization. Preoperative embolization to reduce blood loss is recommended.

    Eosinophilic Granuloma
    Eosinophilic granuloma (also known as Langerhans cell
    histiocytosis) affects the vertebral body during the first
    and second decades of life. Vertebra plana is commonly
    seen on plain radiographs. Because multiple other benign and malignant tumors may also cause this deformity, a histologic diagnosis is critical. Intralesional injection of corticosteroid at the time of biopsy (once
    histologically confirmed) can be helpful.11 Most lesions
    will spontaneously resolve, with near-complete restoration of vertebral body height.12

    2011 American Academy of Orthopaedic Surgeons

    Chapter 42: Spinal Tumors

    Figure 1

    The WBB surgical staging system for spinal tumors. The extent of the vertebral tumor in the axial plane is described
    with reference to 12 radiating zones (numbered 1 to 12, clockwise) and to five concentric layers (A to E, from peripheral to central). The longitudinal extent of the tumor is recorded according to the levels involved. (Reproduced
    with permission from Boriani S, Weinstein JN, Biagini R: Primary bone tumors of the spine. Spine
    1997;22:1036-1044.)

    Giant Cell Tumor

    Neurofibroma
    Intraspinal neurofibromas are associated with neurofibromatosis and should be suspected in any patients
    with typical skin lesions of this condition (caf-au-lait
    spots, cutaneous neurofibromas). They typically occur
    within the dura, although they may occur within the
    neuroforamen and have a classic dumbbell shape. Radiographic findings may include penciling of the rib
    heads, enlarged neuroforamina, or scalloping of the
    vertebra. Symptomatic lesions should be treated with a
    marginal excision. Neurofibromas can be associated
    with rapidly progressive scoliosis, which should be
    treated aggressively with spinal fusion.

    Hemangioma

    Osteoid Osteoma

    Asymptomatic hemangiomas are frequent incidental


    findings seen on MRI scans. Larger lesions may cause
    instability, pathologic fractures, or compression of neural elements. On radiographs, larger lesions typically
    demonstrate vertical striations within the vertebral
    body; these lesions have a speckled appearance on CT.
    On MRI, hemangiomas have increased signal intensity
    on both T1- and T2-weighted images. In the setting of
    impending pathologic fracture, percutaneous cement

    Typically occurring in the second decade of life, osteoid


    osteoma frequently presents with pain unrelated to activity that is worse at night and resolves with the use of
    nonsteroidal anti-inflammatory drugs (NSAIDs). It may
    also cause painful scoliosis. CT demonstrates a nidus of
    bone surrounded by a sclerotic rim and bone scan
    shows a very hot lesion, most in the posterior elements of the lumbar spine. First-line treatment is longterm use of NSAIDs. Resolution of symptoms is good,

    2011 American Academy of Orthopaedic Surgeons

    5: Spine

    Although histologically benign, giant cell tumors can be


    locally aggressive. They typically occur in adults (third
    decade of life) and occur most commonly in the vertebral body. The sacrum is most frequently affected. Radiographically, a giant cell tumor appears as an expansile, lytic lesion, frequently with an associated softtissue mass. In the mobile spine, en bloc excision is
    curative.13 Certain lesions may not be amenable to this
    because of adjacent neurologic or vascular structures;
    therefore, intralesional, extracapsular excision is the
    next choice of management. Preoperative embolization
    reduces intraoperative blood loss. Adjuvant radiation
    therapy may increase the success rate, but with a 5% to
    15% risk of developing a high-grade sarcoma. Recurrence rates can be high (83%), but are significantly
    lower (18%) if patients are treated at a tertiary tumor
    referral center.13

    augmentation of the vertebral body is recommended.14


    Lesions causing neurologic compromise should be
    treated with surgical decompression and stabilization,
    which may also include the use of cement augmentation.

    Orthopaedic Knowledge Update 10

    555

    Section 5: Spine

    but takes an average of 36 months.15 Radiofrequency


    ablation has been used to treat osteoid osteoma elsewhere in the body but is not routinely used in the spine
    because of the proximity of neural elements. For lesions
    that are safely away from neurologic structures, radiofrequency ablation can provide excellent relief, whereas
    lesions close to neurologic structures are best treated
    with percutaneous or open excision.16 Associated scoliosis will spontaneously resolve following en bloc resection if performed within 15 months of onset of the
    curvature.

    Osteoblastoma
    Approximately 40% of osteoblastomas occur in the
    spine, most frequently affecting the posterior elements
    of the cervical or lumbar regions. It generally affects the
    same patient population as osteoid osteoma and has
    similar presenting symptoms, although pain is not as
    reliably controlled with NSAIDs and neurologic symptoms may also be present. Painful scoliosis also may be
    present. Although histologically indistinguishable from
    osteoid osteoma, osteoblastoma is larger (diameter
    > 2 cm) and may include expansion into the soft tissue.
    Radiographs show an expansile, lytic lesion. Welldefined lesions confined to the bone can be treated with
    intralesional curettage; en bloc resection (when feasible) can be curative.17

    Osteochondroma

    5: Spine

    Most frequently affecting the posterior elements of the


    cervical and upper thoracic spine, osteochondromas are
    frequently asymptomatic. Plain radiographs may demonstrate a pedunculated mass, although CT or MRI
    will better show the cartilaginous cap. Asymptomatic
    lesions require no treatment other than observation. En
    bloc excision is recommended for persistently painful
    lesions or those that cause neurologic compromise. A
    single lesion has an approximately 1% risk of malignant transformation into a chondrosarcoma, although
    that risk is up to 25% in patients with multiple hereditary exostoses.18

    Chordoma
    Although rare, chordomas are the most common primary malignant spinal tumor in adults and are typically
    diagnosed in the fifth or sixth decade. They are most
    commonly found in the sacrum but may occur elsewhere in the spine, with the upper cervical spine being
    the second most common location. Because they evolve
    from remnants of the notochord, they have a midline
    location. Plain radiographs show a lytic or mixed lyticblastic lesion. CT or MRI will demonstrate the large
    degree of soft-tissue extension. Because they are slow
    growing, onset of symptoms may be subtle (constipation, tenesmus, low back pain). A mass is usually palpable on digital rectal examination in sacral lesions.
    En bloc resection is the treatment of choice, and survival is directly related to the quality of margins obtained.21,22 Surgical treatment of sacral lesions places
    patients at extremely high risk for bowel and bladder
    incontinence and sexual dysfunction after total or partial sacrectomy. Whenever possible, efforts to save either the bilateral S2 nerve roots or the unilateral S2, S3,
    and S4 roots should be made to possibly allow retention of near-normal bowel and bladder function. Functional outcome, however, should be carefully weighed
    against the need for negative surgical margins, and
    nerve roots may have to be sacrificed to help ensure a
    more favorable long-term outcome. Frequently, extensive bony and soft-tissue reconstruction follows resection of the tumor.
    Long-term outcomes vary depending on the surgical
    margins, the time of diagnosis, and the location of the
    tumor. Survival in patients with sacral lesions may average 8 to 10 years, whereas those with lesions at other
    sites have a 5-year average survival. Although once believed to be highly resistant to both chemotherapy and
    radiation therapy, recent evidence suggests a possible
    role for proton-photon beam radiation, particularly in
    cases of recurrence.23 In addition, chordomas have been
    found to respond favorably to chemotherapeutic agents
    targeted against molecular tyrosine kinase and angiogenesis pathways.24

    Ewing Sarcoma
    Primary Malignant Lesions

    Chondrosarcoma
    Chondrosarcomas typically present in the fifth decade
    of life. When occurring in the posterior elements of the
    spine, they may represent malignant transformation of
    a preexisting osteochondroma. When they occur in the
    vertebral body, they are more likely a primary lesion. A
    lytic lesion with poor margins and stippled calcifications is seen radiographically, although plain radiographs typically underestimate the size because of the
    cartilaginous cap and associated soft-tissue mass. En
    bloc excision is the treatment of choice as curettage is
    associated with higher recurrence and mortality.19 Proton and photon beam radiation therapy may prove useful in treating lesions that are not amenable to complete resection with clean margins.20
    556

    Orthopaedic Knowledge Update 10

    Ewing sarcoma presents in the second decade of life,


    typically with pain, swelling, and constitutional symptoms. Within the spine, Ewing sarcoma most often affects the sacrum. Neurologic symptoms are common.
    The radiographic appearance is of moth-eaten permeative destruction with poor margins. MRI may demonstrate significant soft-tissue extension. A multimodal
    treatment approach is essential. Current treatment recommendations are neoadjuvant chemotherapy followed by radiation therapy or en bloc excision.25 Neoadjuvant chemotherapy can substantially reduce the
    size of the tumor. The use of radiation for definitive
    treatment, however, is associated with progressive kyphosis and radiation-induced myelopathy; therefore, en
    bloc excision may offer a better long-term solution. Radiation should be used when en bloc resection is not
    feasible or if surgical margins are positive.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 42: Spinal Tumors

    Multiple Myeloma

    Osteosarcoma
    Osteosarcoma affects younger individuals, typically in
    the second decade of life. It rarely affects the spine;
    however, neurologic symptoms are fairly common
    when it does. Lesions are usually in the vertebral body,
    but frequently extend to cause compression of the spinal cord. The radiographic appearance can be lytic,
    blastic, or mixed. A biopsy should be performed (preferably by the treating surgeon) to establish the diagnosis. Once established, staging studies including a wholebody bone scan, chest CT, and CT and MRI of the
    lesion should be performed.
    Neoadjuvant chemotherapy with subsequent en bloc
    excision and postoperative chemotherapy is the treatment of choice. Local recurrence is significantly more
    common if clean margins are not obtained at the time
    of resection.31 Radiation therapy is not recommended
    postoperatively unless there is concern for tumor con-

    2011 American Academy of Orthopaedic Surgeons

    tamination at the time of resection. Survival rates correlate with the percentage of tumor death accomplished
    with preoperative chemotherapy; if tumor kill is greater
    than 90%, the 5-year survival is 85%, whereas it is
    only 25% if tumor kill is less than 90%. In general, spinal osteosarcoma portends a worse prognosis than an
    isolated extremity lesion.

    Metastatic Disease
    Most spinal column tumors are metastatic, and the
    spine is the most common site of bony metastases. Between 30% and 80% of patients who die of cancer
    have evidence of spinal metastases on autopsy.2,3 Frequently, metastatic tumors include those of the lung,
    prostate, breast, kidney, and gastrointestinal system.32
    The vertebral body is the most affected site, and the intervertebral disk spaces are usually spared. In patients
    with a known history of cancer, new onset of back pain
    should be assumed to be caused by spinal metastases
    until proven otherwise. Radiographic evidence of bony
    destruction only becomes visible when 30% to 50% of
    the vertebra has been affected. Any patient with a
    known history of cancer, or those with persistent back
    pain despite 4 to 6 weeks of appropriate nonsurgical
    management should undergo spinal imaging. A simplified algorithm for evaluating patients for spinal tumors
    is shown in Figure 2. As discussed earlier, plain radiographs offer a starting point, with CT and MRI providing added information as to the degree of bony destruction and soft-tissue involvement or neural compression.
    Imaging studies should also evaluate for systemic metastases (Table 2).
    Treatment of spinal metastases depends on the individual patients overall health, ambulatory status, tumor type, tumor load, spinal level involved, presence of
    neurologic compromise, and spinal stability. The modified Tokuhashi scoring system for patients with metastatic spinal tumors can guide treatment based on the
    prognosis.33 This system allows a total of 15 points for
    various degrees of severity of six main patient characteristics: general medical condition, number of extraspinal bone metastases, number of spinal metastases, metastases to internal organs, primary site of cancer, and
    neurologic impairment (Table 3). Patients scoring 8
    points or less have a prognosis of less than 6 months
    and are offered conservative or palliative treatments.
    Those with scores of 9 to 11 points have a predicted
    prognosis of greater than 6 months and are offered palliative surgery, although a single lesion without visceral
    metastases may be treated with excisional surgery. Patients scoring 12 or more points have a predicted survival greater than 1 year and are treated with excisional
    surgery. This system showed consistency of 82% to
    86% comparing the predicted to actual survival.33 It
    has recently been shown to correlate well with neurologic outcome in cases of metastatic spinal cord compression.34 Age is also an important predictor of neurologic outcome and survival in patients with spinal
    metastases. Authors of a 2009 study found that as age

    Orthopaedic Knowledge Update 10

    5: Spine

    Multiple myeloma is the most common primary malignancy of bone and is the result of malignant transformation of plasma cells causing destruction of bone locally and abnormal immunoglobulin production. It
    typically affects older individuals in the sixth or seventh
    decade of life. Initial presentation may be a painful vertebral compression fracture. On occasion, patients may
    present with a neurologic deficit. Radiographs demonstrate punched-out discrete lytic lesions, although the
    spine may also simply appear as diffusely osteopenic.
    Lesions are cold on bone scans. MRI may show diffuse involvement at multiple levels not readily seen on
    plain radiographs. Laboratory testing shows a monoclonal gammopathy on serum and/or urine electrophoresis.
    Chemotherapy and radiation therapy are the standard treatments.26 Bracing is indicated for pain control
    in patients with compression fractures. In the setting of
    epidural compression and neurologic deficit, administration of corticosteroids may help decrease symptoms.
    Bisphosphonates can help allay the effects of bony destruction.27 Combined therapy with thalidomide and
    dexamethasone has had better response and longer
    time to progression than dexamethasone alone and has
    become the regimen of choice in patients with newly diagnosed multiple myeloma.28 Patients with continued
    back pain caused by bony destruction or compression
    fractures may benefit from percutaneous cement augmentation (vertebroplasty or kyphoplasty).29,30
    Multiple myeloma may represent the progression of
    a solitary plasmacytoma. These lesions occur as single,
    isolated plasma cell neoplasms. Up to 50% of these lesions will progress to multiple myeloma. Although radiographically they may appear to be a single lesion,
    MRI should be performed to evaluate for occult lesions
    elsewhere. They are highly radiosensitive. Surgery is indicated in cases of spinal instability or severe neurologic compromise. The median survival of patients with
    plasmacytoma is more than 60 months, whereas that of
    patients with multiple myeloma is 28 months.

    557

    Section 5: Spine

    5: Spine

    Figure 2

    Algorithm for evaluating patients with suspected metastatic disease to the spine. (Reprinted from White AP, Kwon
    BK, Lindskog DM, Friedlaender GE, Grauer JN: Metastatic disease of the spine. J Am Acad Orthop Surg
    2006;14:589.)

    Table 2

    Metastatic Imaging Evaluation


    Whole-body bone scan
    Chest radiograph
    CT of the chest, abdomen, or pelvis
    CT of the head
    CT of the spine (cervical, thoracic, lumbar)
    Long-bone series

    increased, the benefits of surgery over radiation alone


    narrowed; while the ability to ambulate was preserved
    for a longer duration following surgery in patients
    younger than 65 years, for older patients there was no
    difference in outcome regardless of treatment type.35
    The presence of a neurologic deficit represents a
    challenge in treatment. Deficits of rapid onset or complete paraplegia have a less favorable prognosis than
    deficits with insidious onset. Up to one third of deficits
    may be caused by multifocal spinal lesions; therefore,
    558

    Orthopaedic Knowledge Update 10

    MRI of the entire spine is recommended in patients


    with any neurologic symptoms. Radiation therapy is
    appropriate for patients with neurologic deficit who are
    not surgical candidates or for patients with radiosensitive tumors such as lymphoma or myeloma. Administration of systemic corticosteroids may slow the progression of neurologic deficits.
    One useful decision-making tool for the treatment of
    patients with spinal metastases is the NOMS (neurologic, oncologic, mechanical instability, systemic disease) system36 (Figure 3). Evaluation of neurologic impairment includes assessment of function (myelopathy
    or radiculopathy) as well as radiographic spinal cord
    compression. Oncologic evaluation refers primarily to
    the radiosensitivity of the tumor. Mechanical instability
    focuses on motion-related pain, which is to be differentiated from baseline biologic tumor pain (for example,
    night pain). Mechanical pain is reflective of bony destruction and potentially heralds structural failure. Systemic disease includes an assessment of the patients
    overall medical condition, including not only the extent
    of tumor burden but also other medical comorbidities.
    In general, patients with significant spinal cord compression from radioresistant tumors or those who demonstrate mechanical instability should be offered sur-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 42: Spinal Tumors

    2011 American Academy of Orthopaedic Surgeons

    Table 3

    Modified Tokuhashi Scoring Systema


    Characteristic

    Score

    General Condition
    Poor

    Moderate

    Good

    Number of extraspinal bone metastases


    3

    1-2

    Number of vertebral body metastases


    3

    Metastases to major internal organs


    Unresectable

    Resectable

    No metastases

    Primary site of cancer


    Lung, osteosarcoma, stomach, bladder,
    esophagus, pancreas

    Liver, gallbladder, unidentified

    Other

    Kidney, uterus

    Rectum

    Thyroid, breast, prostate, carcinoid

    5: Spine

    gery (assuming their systemic disease will allow it).


    Those with radiosensitive tumors should be offered radiation therapy. Patients with radioresistant tumors
    without significant spinal cord compression may benefit from treatment with newer, more focused radiation
    treatment such as image-guided intensity modulated radiation therapy (IGIMRT).36
    IGIMRT offers potential advantages over traditional
    external beam radiation, particularly in its potential for
    treating what have been believed to be radioresistant
    tumors (Table 4). Traditional therapy, while focused
    around the general region of a tumor, also exposed a
    substantial three-dimensional radius of normal tissue to
    radiation. Advanced imaging techniques now allow
    more sophisticated, geographic treatment planning. Image guidance techniques and procedures to focus or
    adapt radiation therapy have evolved to allow more
    precise delivery of radiation to tumors (Figure 4). It
    was recently reported that use of IGIMRT for palliative
    care in patients not responding to other treatments can
    be performed efficiently.37 Although potentially effective, a 39% rate of vertebral fracture progression was
    noted after just a single fraction of IGIMRT, particularly for lytic lesions involving greater than 40% of the
    vertebral body and located caudal to T10.38 Patients
    with low-grade spinal cord compression caused by radioresistant tumors probably benefit from IGIMRT
    treatment, whereas those with high-grade compression
    should be offered surgical decompression followed by
    IGIMRT.36
    As previously mentioned, the role of surgical excision depends on many factors. Data suggest that
    among patients with epidural compression caused by
    metastatic disease (of nonradiosensitive tumors), decompressive surgery combined with radiation therapy
    proved superior to radiotherapy alone.39 In a randomized, prospective study, more patients in the surgical
    group maintained (84%) or regained (62%) the ability
    to ambulate after treatment than patients in the radiotherapy group (57% and 19%, respectively).39 Another
    recent study showed that en bloc resection of metastatic lesions results in lower local recurrence rates than
    debulking procedures. The median survival time was
    41 months for en bloc resection compared with 25
    months for debulking, a substantial, but not statistically significant, difference.40
    Patients with painful vertebral body compression
    fractures caused by metastases may also be treated with
    percutaneous cement augmentation. Pain relief can be
    dramatic and sustained over the long term, with the additional benefit of spinal stability.41 Because the procedure is performed in a percutaneous, minimally invasive fashion and does not rely on the need for bone
    fusion or wound healing, chemotherapy or radiation
    therapy may be instituted without the necessary delay
    recommended for open procedures.
    Surgical treatment of spinal metastases can lead to
    improved quality of life with low complication rates.42
    One recent study found that surgery, whether en bloc
    excision, debulking, or palliative, led to improvement
    in pain in 71% of patients, return or maintenance of in-

    Palsy
    Complete (Frankel A, B)

    Incomplete (Frankel C, D)

    None (Frankel E)

    Patients are assigned points based on general condition, number of extraspinal


    bony metastases, number of spinal metastases, metastases to major visceral
    organs, type of primary tumor, and neurologic status. A total of 15 points is
    possible. Point totals are prognostic: 12 points predicts survival >12 months, 9 to
    11 points predicts survival > 6 months, and 8 points predicts survival < 6 months.

    dependent mobility in 53% of patients, and return of


    urinary control in 39% of patients.43 Functional improvement and survival was highest among those patients undergoing en bloc excision and lowest among
    those who received palliative surgery. Although surgical
    treatment offers potentially improved quality of life, it
    is not without complications. Among those admitted
    for surgical management of spinal metastases, inhospital mortality is 5.6%, and the overall complication rate is nearly 22% with pulmonary complications
    and bleeding or hematoma the most common.44 Complications are more likely in older patients and those
    with two or more comorbidities.

    Orthopaedic Knowledge Update 10

    559

    Section 5: Spine

    5: Spine

    Figure 3

    The NOMS system. ESCC = epidural spinal cord compression, MM = multiple myeloma, RCC = renal cell carcinoma,
    NSCL = non-small cell lung carcinoma, ROI = region of interest. (Reprinted with permission from Bilsky M, Smith M:
    Surgical approach to epidural spinal cord compression. Hematol Oncol Clin North Am 2006;20:1313.)

    Table 4

    Surgical Technique

    Radiosensitivity of Common Metastatic


    Spinal Tumors
    Radiosensitive

    Myeloma
    Lymphoma

    Moderately radiosensitive

    Breast
    Prostate

    Radioresistant

    Lung
    Colon
    Renal cell
    Sarcoma
    Melanoma

    Following treatment, whether radiation or surgery,


    the patient must be followed closely for potential recurrence. One of the earliest presentations of tumor recurrence is pain. Serum tumor markers (when appropriate)
    should be monitored intermittently as a potential sign
    of recurrence. Routine MRI may show recurrent
    masses. Reoperation may be considered based on the
    patients potential for meaningful recovery.
    560

    Orthopaedic Knowledge Update 10

    Tumor type and location are the prime determinants of


    the type of surgical treatment performed. En bloc excision with negative margins is ideal, but not always
    practical. This can be performed on lesions contained
    entirely within the anterior vertebral body, the posterior elements, or the distal sacrum. Tumors that lie adjacent to or involve critical neurovascular structures
    (for example, tumors extending into the bilateral vertebral artery foramina) and tumors that extend from vertebral body through the pedicle into the lamina are best
    managed with intralesional extracapsular excision.
    When possible, functionally important nerve roots
    should be spared. This makes true en bloc resection in
    the cervical spine virtually impossible; typically a combined anteroposterior approach is required. However,
    tumors located from T2 to T12 are amenable to en bloc
    resection because sacrifice of nerve roots has minimal
    functional impact. This can be done from a posterior
    only approach. In the lumbar spine, the nerve roots can
    usually be spared during en bloc resection, although
    this may require a combined posteroanterior approach.
    Proximal sacral lesions also typically require a com-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 42: Spinal Tumors

    In a retrospective review of a tumor registry, the authors


    identified 2,750 cases of primary osseous tumors, of
    which only 126 (4.6%) occurred in the spine. Multiple
    myeloma and plasmacytoma were most common, followed by osteosarcoma. Pain was the most common
    presenting symptom.

    Figure 4

    IGIMRT allows radiation to be focused on the


    specific target organ, significantly reducing the
    exposure of surrounding tissues to high-dose
    radiation. A, IGIMRT (left) and traditional field
    radiation therapy (right) of a sacral lesion.
    B, Treatment of two adjacent sites of vertebral
    metastases with IGIMRT (left) versus traditional
    field radiation (right). Numbers and colors on
    the center bar represent radiation dosage (Gy);
    colors on the images correlate with dosage and
    radiation field. (Reproduced with permission
    from Samant R, Gerig L, Montgomery L, et al:
    The emerging role of IG-IMRT for palliative
    radiotherapy: A single-institution experience.
    Curr Oncol 2009;16:43.)

    Ortiz Gmez JA: The incidence of vertebral body metastases. Int Orthop 1995;19(5):309-311.

    3.

    Wong DA, Fornasier VL, MacNab I: Spinal metastases:


    The obvious, the occult, and the impostors. Spine (Phila
    Pa 1976) 1990;15(1):1-4.

    4.

    Constans JP, de Divitiis E, Donzelli R, Spaziante R,


    Meder JF, Haye C: Spinal metastases with neurological
    manifestations: Review of 600 cases. J Neurosurg 1983;
    59(1):111-118.

    5.

    Carrino JA, Khurana B, Ready JE, Silverman SG, Winalski CS: Magnetic resonance imaging-guided percutaneous biopsy of musculoskeletal lesions. J Bone Joint
    Surg Am 2007;89(10):2179-2187.
    In this retrospective case series, the authors review the
    results of MRI-guided biopsies for musculoskeletal lesions in 45 consecutive patients. They report that overall, 91% of samples taken contained sufficient material
    for diagnostic purposes. For bone lesions, this number
    was 95%, with a sensitivity of 0.92, specificity of 1.00,
    positive predictive value of 1.00, and negative predictive
    value of 0.86.

    6.

    Nourbakhsh A, Grady JJ, Garges KJ: Percutaneous


    spine biopsy: A meta-analysis. J Bone Joint Surg Am
    2008;90(8):1722-1725.
    The authors report a meta-analysis of adequacy and accuracy of percutaneously obtained spinal biopsies, noting that adequacy, accuracy, and complications increased as needle inner diameter increased and that CT
    guidance was associated with a lower complication rate
    (3.3%) than fluoroscopically assisted biopsy (5.3%).

    7.

    Ogilvie CM, Torbert JT, Finstein JL, Fox EJ, Lackman RD: Clinical utility of percutaneous biopsies of
    musculoskeletal tumors. Clin Orthop Relat Res 2006;
    450:95-100.

    8.

    Lis E, Bilsky MH, Pisinski L, et al: Percutaneous CTguided biopsy of osseous lesion of the spine in patients
    with known or suspected malignancy. AJNR Am J Neuroradiol 2004;25(9):1583-1588.

    9.

    Boriani S, Weinstein JN, Biagini R: Primary bone tumors of the spine: Terminology and surgical staging.
    Spine (Phila Pa 1976) 1997;22(9):1036-1044.

    10.

    Boriani S, De Iure F, Campanacci L, et al: Aneurysmal


    bone cyst of the mobile spine: Report on 41 cases. Spine
    (Phila Pa 1976) 2001;26(1):27-35.

    11.

    Yasko AW, Fanning CV, Ayala AG, Carrasco CH, Murray JA: Percutaneous techniques for the diagnosis and
    treatment of localized Langerhans-cell histiocytosis (eo-

    Summary
    Obtaining a comprehensive history, detailed physical
    examination, and relevant radiographic studies will
    help the surgeon determine the optimal treatment of patients with primary or metastatic tumors of the spine.
    The suspected diagnosis should be confirmed by biopsy.
    The treating surgeon should be competent and comfortable with both conservative and aggressive surgical
    management of tumors. Patients should be presented
    with a realistic assessment of their prognosis, welldefined goals of treatment, potential outcomes, and different treatment options. Both surgical and nonsurgical
    management can lead to improved quality of life in
    terms of pain control and functional independence.

    Annotated References
    1.

    Kelley SP, Ashford RU, Rao AS, Dickson RA: Primary


    bone tumours of the spine: A 42-year survey from the
    Leeds Regional Bone Tumour Registry. Eur Spine J
    2007;16(3):405-409.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    5: Spine

    bined approach, whereas those below S2 can be excised


    through a posterior approach. As mentioned earlier, accurate surgical staging can help direct treatment.9 The
    use of titanium implants is favored as they have less ferromagnetic artifact if postoperative MRI is required to
    assess for recurrence.

    2.

    561

    Section 5: Spine

    survival rate was 65%, disease-free survival was 53.8%,


    and the local control rate was 72% with this regimen.
    This effect was most pronounced with treatment of primary disease rather than recurrence.

    sinophilic granuloma of bone). J Bone Joint Surg Am


    1998;80(2):219-228.
    12.

    13.

    14.

    Hart RA, Boriani S, Biagini R, Currier B, Weinstein JN:


    A system for surgical staging and management of spine
    tumors: A clinical outcome study of giant cell tumors of
    the spine. Spine (Phila Pa 1976) 1997;22(15):17731782, discussion 1783.
    Jones JO, Bruel BM, Vattam SR: Management of painful vertebral hemangiomas with kyphoplasty: A report
    of two cases and a literature review. Pain Physician
    2009;12(4):E297-E303.
    The authors report on two patients with painful vertebral hemangiomas unresponsive to conservative care
    who were successfully treated with cement augmentation (kyphoplasty).

    15.

    Kneisl JS, Simon MA: Medical management compared


    with operative treatment for osteoid-osteoma. J Bone
    Joint Surg Am 1992;74(2):179-185.

    16.

    Hadjipavlou AG, Tzermiadianos MN, Kakavelakis KN,


    Lander P: Percutaneous core excision and radiofrequency thermo-coagulation for the ablation of osteoid
    osteoma of the spine. Eur Spine J 2009;18(3):345-351.
    The authors report a case series of four patients who underwent percutaneous radiofrequency ablation and
    three patients who underwent percutaneous core excision of osteoid osteoma. The overall success rate was
    85.7%, with improved pain scores for both groups. The
    authors concluded that the former treatment is safe and
    effective when intact cortex separated the nidus from
    the neural elements, but that the latter technique reduces the risk of thermal damage when lesions are in
    close proximity to neurologic structures.

    5: Spine

    562

    Garg S, Mehta S, Dormans JP: Langerhans cell histiocytosis of the spine in children: Long-term follow-up.
    J Bone Joint Surg Am 2004;86(8):1740-1750.

    17.

    Boriani S, Capanna R, Donati D, Levine A, Picci P,


    Savini R: Osteoblastoma of the spine. Clin Orthop
    Relat Res 1992;278:37-45.

    18.

    Sharma MC, Arora R, Deol PS, Mahapatra AK, Mehta


    VS, Sarkar C: Osteochondroma of the spine: An enigmatic tumor of the spinal cord. A series of 10 cases.
    J Neurosurg Sci 2002;46(2):66-70, discussion 70.

    19.

    Boriani S, De Iure F, Bandiera S, et al: Chondrosarcoma


    of the mobile spine: Report on 22 cases. Spine (Phila Pa
    1976) 2000;25(7):804-812.

    20.

    Wagner TD, Kobayashi W, Dean S, et al: Combination


    short-course preoperative irradiation, surgical resection,
    and reduced-field high-dose postoperative irradiation in
    the treatment of tumors involving the bone. Int J Radiat
    Oncol Biol Phys 2009;73(1):259-266.
    The authors evaluated a regimen of preoperative radiation, surgical resection, and reduced-field high-dose
    postoperative radiation in 48 patients with tumors of
    the spine and pelvis. They found that the 5-year overall

    Orthopaedic Knowledge Update 10

    21.

    Fourney DR, Rhines LD, Hentschel SJ, et al: En bloc resection of primary sacral tumors: Classification of surgical approaches and outcome. J Neurosurg Spine 2005;
    3(2):111-122.

    22.

    Fuchs B, Dickey ID, Yaszemski MJ, Inwards CY, Sim


    FH: Operative management of sacral chordoma. J Bone
    Joint Surg Am 2005;87(10):2211-2216.

    23.

    Park L, Delaney TF, Liebsch NJ, et al: Sacral chordomas: Impact of high-dose proton/photon-beam radiation therapy combined with or without surgery for primary versus recurrent tumor. Int J Radiat Oncol Biol
    Phys 2006;65(5):1514-1521.

    24.

    Tamborini E, Miselli F, Negri T, et al: Molecular and


    biochemical analyses of platelet-derived growth factor
    receptor (PDGFR) B, PDGFRA, and KIT receptors in
    chordomas. Clin Cancer Res 2006;12(23):6920-6928.

    25.

    Marco RA, Gentry JB, Rhines LD, et al: Ewings sarcoma of the mobile spine. Spine (Phila Pa 1976) 2005;
    30(7):769-773.

    26.

    Rao G, Ha CS, Chakrabarti I, Feiz-Erfan I, Mendel E,


    Rhines LD: Multiple myeloma of the cervical spine:
    Treatment strategies for pain and spinal instability.
    J Neurosurg Spine 2006;5(2):140-145.

    27.

    Berenson JR, Hillner BE, Kyle RA, et al; American Society of Clinical Oncology Bisphosphonates Expert Panel: American Society of Clinical Oncology clinical practice guidelines: The role of bisphosphonates in multiple
    myeloma. J Clin Oncol 2002;20(17):3719-3736.

    28.

    Rajkumar SV, Rosiol L, Hussein M, et al: Multicenter,


    randomized, double-blind, placebo-controlled study of
    thalidomide plus dexamethasone compared with dexamethasone as initial therapy for newly diagnosed multiple myeloma. J Clin Oncol 2008;26(13):2171-2177.
    The authors conducted a randomized, double-blind,
    placebo-controlled study comparing the use of thalidomide and dexamethasone versus dexamethasone alone
    for treatment of multiple myeloma. A total of 235 patients were randomized to each group. The authors reported a better overall response rate (63% versus 46%),
    longer time to progression (22.6 versus 6.5 months), but
    higher rates of adverse events (30.3% versus 22.8%)
    with the thalidomide-dexamethasone group.

    29.

    Masala S, Anselmetti GC, Marcia S, Massari F, Manca


    A, Simonetti G: Percutaneous vertebroplasty in multiple
    myeloma vertebral involvement. J Spinal Disord Tech
    2008;21(5):344-348.
    The authors describe treatment of 64 patients with painful spinal lesions associated with multiple myeloma who
    underwent percutaneous vertebroplasty, reporting excellent early and sustained pain relief.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 42: Spinal Tumors

    30.

    31.

    32.

    McDonald RJ, Trout AT, Gray LA, Dispenzieri A,


    Thielen KR, Kallmes DF: Vertebroplasty in multiple myeloma: Outcomes in a large patient series. AJNR Am J
    Neuroradiol 2008;29(4):642-648.
    The authors conducted a retrospective review of 64 patients with multiple myeloma who had undergone percutaneous vertebroplasty. Activity-related pain, pain
    during rest, and functional outcomes demonstrated
    early and sustained improvement.
    Rao G, Suki D, Chakrabarti I, et al: Surgical management of primary and metastatic sarcoma of the mobile
    spine. J Neurosurg Spine 2008;9(2):120-128.
    In this retrospective review of 80 patients who underwent 110 intralesional or en bloc resections of spinal
    sarcomas, the authors report a mean survival time of
    20.6 months (40.2 for primary lesions and 17.3 for
    metastatic lesions). There was no significant difference
    in survival rate or local recurrence rate between intralesional or en bloc resections, although there were fewer
    resections (12) in the latter group.
    Destombe C, Botton E, Le Gal G, et al: Investigations
    for bone metastasis from an unknown primary.
    Joint Bone Spine 2007;74(1):85-89.
    The authors retrospectively reviewed 152 patients who
    presented with metastatic lesions to the spine from an
    unknown primary tumor. The most common primary
    tumor site was the lung (37 patients), followed by prostate (26), breast/female genital tract (24), urologic system (11), gastrointestinal tract (11), head and neck (6),
    and other sites (4).
    Tokuhashi Y, Matsuzaki H, Oda H, Oshima M, Ryu J:
    A revised scoring system for preoperative evaluation of
    metastatic spine tumor prognosis. Spine (Phila Pa 1976)
    2005;30(19):2186-2191.

    34.

    Putz C, Wiedenhfer B, Gerner HJ, Frstenberg CH:


    Tokuhashi prognosis score: An important tool in prediction of the neurological outcome in metastatic spinal
    cord compression. A retrospective clinical study. Spine
    (Phila Pa 1976) 2008;33(24):2669-2674.
    In a retrospective review of 35 patients who underwent
    surgical treatment of vertebral metastases with associated incomplete spinal cord injury, the authors reported
    that patients with a Tokuhashi score of 9 showed improved motor scores, those with a score of 8 showed no
    change, and those with a score of 7 deteriorated.

    35.

    Chi JH, Gokaslan Z, McCormick P, Tibbs PA, Kryscio


    RJ, Patchell RA: Selecting treatment for patients with
    malignant epidural spinal cord compression: Does age
    matter? Results from a randomized clinical trial. Spine
    (Phila Pa 1976) 2009;34(5):431-435.
    The authors analyzed data from a randomized clinical
    trial of surgical treatment versus radiation therapy for
    malignant epidural spinal cord compression and reported that as age increases, the likelihood of outcomes
    from surgery being equal to those of radiation alone
    also increases. There was no difference in outcomes
    between treatments in patients older than 65 years,
    whereas the ability to preserve ambulation was significantly improved in those younger than 65 years.

    2011 American Academy of Orthopaedic Surgeons

    Bilsky M, Smith M: Surgical approach to epidural spinal cord compression. Hematol Oncol Clin North Am
    2006;20(6):1307-1317.

    37.

    Samant R, Gerig L, Montgomery L, et al: The emerging


    role of IG-IMRT for palliative radiotherapy: A singleinstitution experience. Curr Oncol 2009;16(3):40-45.
    The authors report a single-institution experience over
    2 years in the use of IGIMRT for short-course palliative
    therapy, describing its use in four general scenarios. It
    was concluded that for patients not responding to other
    therapies, palliative IGIMRT is feasible and efficient.

    38.

    Rose PS, Laufer I, Boland PJ, et al: Risk of fracture after


    single fraction image-guided intensity-modulated radiation therapy to spinal metastases. J Clin Oncol 2009;
    27(30):5075-5079.
    The authors followed 62 patients who underwent single
    fraction IGIMRT and noted a 39% rate of fracture progression following treatment. Lytic lesions were 6.8
    times more likely to fracture than sclerotic or mixed lesions; lesions caudal to T10 were 4.6 times more likely
    to fracture.

    39.

    Patchell RA, Tibbs PA, Regine WF, et al: Direct decompressive surgical resection in the treatment of spinal
    cord compression caused by metastatic cancer: A randomised trial. Lancet 2005;366(9486):643-648.

    40.

    Li H, Gasbarrini A, Cappuccio M, et al: Outcome of excisional surgeries for the patients with spinal metastases.
    Eur Spine J 2009;18(10):1423-1430.
    The authors report on 131 patients who underwent either en bloc resection or debulking procedures. The local recurrence rate was significantly less in en bloc resection. En bloc resection resulted in a mean survival time
    of 41 months compared to 25 months for debulking
    (not statistically significant).

    41.

    Lim BS, Chang UK, Youn SM: Clinical outcomes after


    percutaneous vertebroplasty for pathologic compression
    fractures in osteolytic metastatic spinal disease. J Korean Neurosurg Soc 2009;45(6):369-374.
    The authors performed vertebroplasty procedures at
    185 levels (102 patients) with painful spinal lesions
    caused by metastases (81%) and multiple myeloma
    (19%). They report nearly immediate pain relief from a
    visual analog scale score of 8.24 preoperatively to 3.59
    at 1 day postoperatively. The relief was sustained with a
    mean visual analog scale score of 5.22 at 1 year.

    42.

    Falicov A, Fisher CG, Sparkes J, Boyd MC, Wing PC,


    Dvorak MF: Impact of surgical intervention on quality
    of life in patients with spinal metastases. Spine (Phila Pa
    1976) 2006;31(24):2849-2856.

    43.

    Ibrahim A, Crockard A, Antonietti P, et al: Does spinal


    surgery improve the quality of life for those with extradural (spinal) osseous metastases? An international multicenter prospective observational study of 223 patients.
    Invited submission from the Joint Section Meeting on
    Disorders of the Spine and Peripheral Nerves, March
    2007. J Neurosurg Spine 2008;8(3):271-278.

    Orthopaedic Knowledge Update 10

    5: Spine

    33.

    36.

    563

    Section 5: Spine

    44.

    Patil CG, Lad SP, Santarelli J, Boakye M: National inpatient complications and outcomes after surgery for
    spinal metastasis from 1993-2002. Cancer 2007;110(3):
    625-630.
    The authors used the National Inpatient Sample to identify 26,233 patients who underwent surgical treatment of
    spinal metastases and found that the overall in-hospital
    mortality rate was 5.6% with an overall complication
    rate of 22%. Pulmonary and bleeding complications were
    most common. Postoperative complications substantially
    increased both length of stay and mortality; risk of complications was highest in patients with medical comorbidities.

    5: Spine

    The authors report on outcomes of 223 patients undergoing surgical treatment (en bloc resection, debulking,
    or palliative decompression) for spinal lesions, noting
    that pain was improved in 71% of patients, mobility
    was improved in 53%, and urinary sphincter control
    was regained in 39%. Patients undergoing excisional
    procedures demonstrated significantly increased survival
    rates and functional improvement than those undergoing palliative surgery.

    564

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 43

    Spinal Infections
    Thomas E. Mroz, MD

    Michael P. Steinmetz, MD

    Introduction
    There are various types of infections that can involve
    the spine, and each is unique with regard to epidemiology, natural history, and treatment. Biomechanical variations in different regions of the spinal column should
    be taken into account when designing a rational treatment.
    Most infections occurring in developed countries are
    caused by pyogenic bacteria, whereas nonpyogenic
    pathogens such as Mycobacteriae, Brucella species, and
    fungi are important pathogens in underdeveloped regions of the world and in immunocompromised patients.

    Pyogenic Vertebral Osteomyelitis

    Pathophysiology

    Dr. Mroz or an immediate family member has stock or


    stock options held in PearlDiver and is a member of a
    speakers bureau or has made paid presentations on behalf of Stryker and AO Spine. Dr. Steinmetz or an immediate family member serves as a board member, owner,
    officer, or committee member of the Congress of Neurological Surgeons AANS/CNS Section on Disorders of the
    Spine and Peripheral Nerves Council of State Neurosurgical Societies; is a member of a speakers bureau or has
    made paid presentations on behalf of Stryker; and has
    received research or institutional support from DePuy, a
    Johnson & Johnson Company, Stryker, and Synthes.

    2011 American Academy of Orthopaedic Surgeons

    5: Spine

    Two vascular theories have been proposed to explain


    the evolution of vertebral osteomyelitis (VO). An arteriole theory was proposed, in which bacteria become
    entrapped in the end arteriole system near the vertebral
    end plate.1 In Batsons2 venous theory, bacteria gain entry into the perivertebral venous system via retrograde
    flow from the pelvic venous plexus.
    Whichever vascular theory is responsible, bacteria
    become entrapped in the rich vascularity of the vertebral bodies near the end plates, which have a relatively
    poor vascular supply. The total action of the pyogenic
    enzymes and the host immune response result in progressive loss of osseous integrity of the body and destruction of the intervertebral disk. The destruction of

    the intervertebral disk can result in involvement of the


    adjacent body. As a focal consideration, the loss of
    structural integrity can result in pathologic fracture,
    which has serious implications for overall spinal alignment and for the neural elements. Abscess formation
    can occur focally within the disk space, the vertebral
    body, and/or the spinal canal. In rare instances, bacterial meningitis can result. Spread of the infection can occur via the prevertebral fascia in the cervical spine to
    spread to other levels of the prevertebral space, including the mediastinum inferiorly. Infection in the lumbar
    spine can spread via the anterior longitudinal ligament
    and psoas muscle fascia to result in abscess formation in
    the piriformis fossa, perianal region, and psoas muscle.
    Biomechanical characteristics and neural anatomy of
    the spinal region must be considered when treating spinal infections. The cervical and thoracic columns have
    narrower canal diameters, and this has serious implications in the case of epidural abscess and/or VO management. The cervical, thoracic, and lumbar columns
    are anatomically and biomechanically unique, and this
    must be taken into account during both nonsurgical
    and surgical treatment.

    Epidemiology
    Hematogenous VO is a serious infection that is associated with a mortality rate of up to 15%.3-5 In developed
    countries, Staphylococcus aureus accounts for approximately 50% of cases of VO; however, gram-negative
    (for example, Escherichia coli, Enterococcus) and other
    gram-positive (for example, Proteus species) bacteria,
    mycobacteria, and fungi also should be considered. Patients with diabetes and penetrating injuries are prone
    to developing anaerobic infections. Pseudomonas infections have a higher incidence among intravenous drug
    abusers. VO is more common in males and in the fifth
    and sixth decades of life.2,5 The lumbar spine is affected
    in about 50% of cases of VO; thoracic involvement is
    second, followed by the cervical spine (approximately
    5%). Although patients with VO often will have an
    identifiable source of infection (for example, complicated urinary tract infection, infected central line, cutaneous infection) or an immunocompromised state (for
    example, history of organ transplant, dialysis, HIV, intravenous drug use, recent dental procedure, diabetes
    mellitus, or chemotherapy), healthy patients without
    any risk factor may also present with spontaneous VO.

    Orthopaedic Knowledge Update 10

    565

    Section 5: Spine

    Figure 1

    Sagittal (A) and coronal (B) CT reconstruction of a


    patient with T6-7 pyogenic osteomyelitis. Note
    the extent of vertebral body destruction.

    Clinical Presentation

    5: Spine

    Pain in the affected region, which occurs in 90% of patients with VO, is the most common complaint and is
    associated with paraspinal muscle spasm. The pain may
    be described as dull or sharp, constant or intermittent.
    As the process progresses with loss of structural integrity, the pain worsens and becomes more mechanical in
    nature. Constitutional signs and symptoms including
    fever and malaise occur in about half of affected patients. Range of motion may become limited by pain,
    and focal tenderness can be present. The physician
    must be alert to meningeal symptoms and signs. In patients with psoas involvement, resisted hip flexion or
    passive hip extension may exacerbate pain. Upper cervical involvement may result in torticollis.
    Neurologic impairment occurs in approximately
    17% of cases of VO, and it is more common with cervical and thoracic involvement because of a smaller
    space available for the spinal cord in these areas. Neurologic involvement can result from pathologic fracture
    with retropulsion of material into the canal or from
    epidural abscess/phlegmon formation in the canal.
    Neurologic involvement is a surgical emergency and requires prompt surgical treatment. The neurologic picture will depend on the region of the spine affected.
    Lumbar spine VO can present with radiculopathy or
    cauda equine syndrome (rarely), whereas involvement
    of the cervical or thoracic spine result in myelopathy or
    myeloradiculopathy.

    Imaging
    Plain radiography is helpful in the evaluation of infection and if possible should be performed with the patient standing to detect structural changes under physiologic loading. The typical changes of disk space
    narrowing, end plate irregularity, and end plate sclerosis take several weeks to appear on radiographs. Stand566

    Orthopaedic Knowledge Update 10

    ing radiographs may demonstrate angular and/or translational instability in cases of diskitis or osteomyelitis.
    A thorough assessment must be made of the prevertebral soft-tissue shadows in the cervical spine and mediastinal width, and soft-tissue gas must be ruled out in
    cases of anaerobic infection. CT with coronal and sagittal reconstructions is very useful in delineating psoas
    abscess and the pattern and extent of structural degradation, and should be a part of any workup in patients
    with advanced VO (Figure 1).
    MRI with gadolinium is a standard imaging technique and has a sensitivity of 96% and a specificity of
    93% in diagnosing VO. T1-weighted images demonstrate hypointense signal intensity in the disk space and
    adjacent vertebral bodies. Conversely, the same regions
    appear hyperintense on T2-weighted images. Contrasted images are helpful in identifying abscess formation and in delineating neoplasm (Figure 2). Serial
    MRIs obtained during the course must be carefully interpreted because the scans will often look worse despite clinical improvement. Thus, serial scanning is not
    typically necessary. Figure 3 demonstrates an illustrative case of T12-L1 osteomyelitis treated nonsurgically.
    Radionuclide scans can be a useful tool in patients
    with infection. Technetium Tc-99m scintigraphy has a
    sensitivity of approximately 90% but lacks specificity.
    It is dependent on blood flow, and cases of enhanced
    perfusion (degeneration) or diminished flow (extremes
    of patient age) decrease the utility of the test. Gallium
    Ga-67 citrate scan, when performed with bone scan,
    has a sensitivity of 92%, specificity of 100%, and accuracy of 94% in detecting VO.6 Gallium scans normalize
    with resolution of the infection and can be useful for
    following the response to treatment.

    Laboratory Assessment
    All patients should have a complete white blood cell
    (WBC) count with differential, Westergren erythrocyte
    sedimentation rate (ESR), and C-reactive protein (CRP)
    level. It is important to note that WBC count is often
    normal in patients with VO, particularly with indolent
    organisms. CRP level and ESR are elevated in more
    than 90% of patients with pyogenic VO. CRP level will
    rise and fall more quickly than ESR and should be used
    serially to judge the effectiveness of treatment. The nutritional status should also be assessed by checking the
    total lymphocyte count and prealbumin and transferrin
    levels.
    Blood cultures should be obtained in all patients
    with suspected VO and will yield a positive culture in
    85% of patients.7 If blood cultures do not identify an
    organism, then a CT-guided biopsy is indicated and will
    be successful in organism identification in 50% to 75%
    of patients.7 The avoidance of antibiotic treatment before cultures is extremely important because the likelihood of a positive culture is substantially diminished;
    this detail should be made known to all involved in the
    care of the patient.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 43: Spinal Infections

    Figure 2

    Imaging studies of a 45-year-old man with incomplete quadriplegia due to a large epidural abscess from a C6-7
    osteomyelitis. A, Midsagittal T1-weighted cervical spine image with gadolinium enhancement. B, Axial T1-weighted
    image with gadolinium demonstrating a well-circumscribed enhancing epidural abscess.

    Epidemiology
    Multiple organisms including Mycobacterium species
    (M tuberculosis, M avium-intracellulare), Nocardia,
    Brucella, Actinomyces and fungi (Candida, Aspergillus,
    Coccidioides, Petrillidium, and Spirochaetes) induce a
    granulomatous immune response and can result in nonpyogenic VO. Tuberculosis, caused by M tuberculosis,
    is the most common cause of granulomatous spinal VO
    (Potts disease).8 There has been a resurgence of the disease worldwide because of the increase in immunocompromising states (such as AIDS, chemotherapy regimens, and immunosuppressive therapy [for example,
    for organ transplants]). Systemic tuberculosis results in
    spine involvement in approximately 50% of patients,
    and it is thought that hematogenous seeding from the
    lungs or genitourinary tract is the primary route. Peak
    ages are the fourth and fifth decades. Neurologic involvement varies widely from 10% to 47%, and in
    large part is due to the time to diagnosis and treatment
    and the degree of kyphotic deformity. In contrast to
    pyogenic VO, tuberculosis occurs more commonly in
    the thoracic spine, followed by the lumbar spine, and
    rarely occurs in the cervical spine.

    2011 American Academy of Orthopaedic Surgeons

    5: Spine

    Nonpyogenic Osteomyelitis

    Pathogenesis
    M tuberculosis is an acid-fast bacteria that causes a
    unique pattern of infection. The disk space is resistant
    to infection, and thus is typically spared. Hence the radiographic hallmark is osseous destruction with preservation of the disk space. Tuberculosis of the spine is an
    indolent infection that is often diagnosed late, and this
    underscores why many patients present with large kyphotic deformities. Three types of body involvement
    have been defined: anterior, peridiskal, and central. Anterior involvement refers to progression of the infection
    along the dorsal side of the anterior longitudinal ligament resulting in scalloping of the ventral vertebral
    bodies. Peridiskal involvement involves the metaphyseal portion of the vertebral bodies and can result in
    substantial collapse and deformity. The infection may
    be confined to the central body (central pattern) and is
    often confused with malignancy.

    Clinical Presentation and


    Laboratory Diagnosis
    The clinical presentations of pyogenic and nonpyogenic
    VO share similarities. Both result in pain due to loss of
    structural integrity, which occurs later in nonpyogenic
    VO and is a result of the indolent pathogenesis. Fever

    Orthopaedic Knowledge Update 10

    567

    5: Spine

    Section 5: Spine

    Figure 3

    568

    Imaging studies of a 59-year-old woman with a 3-week history of progressive thoracolumbar pain. A, Lateral radiograph demonstrating spondylotic changes at L2-3. Nine weeks after symptom onset, the patient was treated nonsurgically for 6 weeks, but pain worsened, prompting another radiograph (B) that showed loss of veterbral height
    of L1 and T12, irregularity of the end plates, and a focal kyphosis. C,MRI showing diskitis and osteomyelitis at T12L1. A CT-guided biopsy yielded Staphylococcus aureus. The patient was started on antibiotics and placed in a thoracolumbosacral orthosis. Seventeen weeks after onset of symptoms, the patients pain was improved after 7 weeks
    on parenteral antibiotics and brace management. D, T1-weighted midsagittal MRI at 17 weeks after symptom onset. The image demonstrates vertebral end plate and body erosion typical of diskitis and osteomyelitis. E, Midsagittal CT demonstrates findings typical of osteomyelitis: loss of structural integrity, sclerosis of the adjacent bone, and
    focal kyphosis. The patient was treated with 6 weeks of parenteral antbiotics, 6 weeks of oral antiobiotics, and 3
    months in the brace. F, Eight months after symptom onset, the patient was pain free. Full-length radiograph shows
    a focal thoracolumbar kyphosis but overall acceptable sagittal balance.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 43: Spinal Infections

    may or may not be present. Patients with nonpyogenic


    VO often have a history and appearance of chronic illness and malnourishment (characterized by weight loss,
    fatigue, night sweats, temporal wasting, and depletion
    of nutritional markers). Tuberculosis should be suspected in patients with this presentation and coexisting
    risk factors (for example, immunocompromised state,
    travel to or residence in underdeveloped countries or
    the southwest United States [prevalence of coccidioidomycosis], history of tuberculosis). In patients with
    advanced stages of tuberculosis, a kyphotic or gibbus
    deformity is often present.
    Like pyogenic disease, ESR and CRP levels in nonpyogenic VO will be elevated, and the WBC count is
    often normal. A tuberculin skin test should be performed, but a false-negative test can occur in anergic
    patients who have advanced immunoincompetency. In
    patients with tuberculosis, a biopsy specimen positive
    for acid-fast bacillus is ideal; however, this identification method has a sensitivity of only about 50%. For
    this reason, polymerase chain reaction can be used to
    identify mycobacterium with a sensitivity and accuracy
    of 94.7% and 92%, respectively.

    Imaging
    Plain radiographs, CT, and MRI with contrast should
    be obtained in all patients. The MRI characteristics of
    nonpyogenic VO are similar to those of pyogenic VO,
    but there are features such as tuberculosis that are
    unique to nonpyogenic VO. Tuberculosis is often accompanied by abscess formation, a heterogenous signal, preservation of disk spaces, multiple affected vertebral bodies, and a predisposition for the thoracic spine.
    Radionuclide studies can be helpful.

    Medical Management
    It is advantageous to include an infectious disease consultation for patients with any spinal infection. Once a
    culture has been obtained, empiric antibiotics should be
    started in the patient with sepsis or who is immunocompromised. Parenteral antibiotics tailored to the
    identified organism are administered for 2 to 6 weeks,
    and then oral therapy is administered. The length of
    each treatment arm will be predicated, in part, on the
    type of organism, host factors such as immune and nutritional status, and risk factors (for example, intravenous drug abuse, diabetes mellitus), and whether the
    patient has retained instrumentation. The nutritional
    status must be optimized. As mentioned, CRP level and
    ESR can be used to monitor response to medical therapy. Serial clinical examinations are also an important
    measure, as the resolution of pain correlates with a
    positive response to treatment. In the improving patient, it is not necessary to obtain serial radiographs.
    Infective endocarditis must be considered in patients
    who have spinal infections, particularly those with persistent bacteremia or fever who are not responding appropriately to medical management. An echocardiogram should be obtained to rule out endocarditis. With

    2011 American Academy of Orthopaedic Surgeons

    Surgical Management
    There are four main indications for surgery: failure of a
    CT-guided biopsy or blood culture to yield an organism, thus necessitating open or percutaneous retrieval
    of more tissue; failure of medical therapy (persistent
    pain or fever); development of neurologic demise; and
    structural decompensation.
    Whether the indication for surgery is neurologic or
    structural demise, the most appropriate surgical procedure is determined after a meticulous assessment of the
    structural integrity. For example, lumbar epidural abscess with neurologic impairment that occurred from
    direct extension of a spondylodiskitis without loss of
    vertebral body integrity (confirmed by CT) should be
    treated much differently than epidural abscess with
    neurologic impairment with a 50 kyphosis caused by
    pathologic fracture. In this example, the lumbar epidural abscess associated with spondylodiskitis can be
    treated with posterior decompression, evacuation of the
    abscess, and disk dbridement. The other condition requires a more extensive dbridement and reconstruction.
    The algorithm for surgical treatment is actually quite
    simple when considering the four goals of surgical
    management and the pathogenesis of VO: thoroughly
    dbriding infectious foci and necrotic material, relieving all pressure on the neural elements, restoring normal sagittal and coronal alignment, and providing rigid
    fixation in the presence of instability. Rigid fixation is
    particularly important considering the pathogenesis. As
    an infection progresses, thrombosis of the microvasculature limits the clearance of the infection as well as the
    formation of new bone. In addition, angiogenesis in the
    affected region is impaired with continued motion and
    persistent infection. Thus, rigid fixation will promote
    healing of the infection and ankylosis in the case of fusion.
    Vertebral osteomyelitis affects the ventral columns of
    the spine, and with loss of vertebral body integrity kyphosis often will result. It is important to thoroughly
    dbride the disk space and body, reconstruct the cavity
    created, and provide adequate fixation. This can be
    done via a ventral approach, a combined ventral and
    posterior approach, or a posterior approach (costotransversectomy). The type of surgery performed will
    be predicated on many factors, including surgeon expertise, availability of an access surgeon, bone quality
    (whether osteoporosis is present), sagittal and coronal
    alignment, physiologic reserve of the patient, and degree of structural loss. A laminectomy is contraindi-

    Orthopaedic Knowledge Update 10

    5: Spine

    Treatment

    tuberculosis, therapy is highly dependent on the susceptibility and immune status of the host, but is typically a
    prolonged multidrug regimen. With fungal infection,
    the appropriate regimen is delivered over a course of
    months.
    Rigid bracing or immobilization is recommended in
    patients with VO, regardless of the affected region.
    Bracing often will help with pain relief and is effective
    in minimizing the development of kyphosis.

    569

    Section 5: Spine

    cated in patients with VO because of the kyphosis that


    it causes. If the appropriate surgical procedure cannot
    be done for whatever reason, the patient should be referred to a tertiary care center for definitive treatment.
    It is technically more challenging to salvage a failed
    first attempt at surgical management.
    Although there is agreement that rigid fixation is
    necessary in cases of infection with loss of structural integrity (kyphosis), the optimal type of implant is controversial. Structural autograft and allograft bone and
    titanium and poly-ethyl-ether-ketone (PEEK) reconstruction cages are all viable options for ventral reconstruction after partial or complete corpectomy. Ventral
    plates and posterior pedicle fixation are added to augment the fixation when necessary. The decision to use
    ventral plates alone or with posterior fixation is predicated on several factors, including the degree of instability, region of the spine (thoracolumbar junction versus midthoracic spine), and surgeon experience.

    ent in about 50% of patients. The reported range of


    symptom onset varies widely from days to months, and
    the period of neurologic demise ranges from hours
    to days.

    Laboratory and Diagnostic Imaging


    Although ESR, CRP level, and WBC count are typically
    elevated in patients with epidural abscesses, this is not
    a specific indication for the disease. Both MRI with
    gadolinium and CT myelography have a sensitivity
    greater than 90% for detection of an abscess, but the
    former is less invasive and the modality of choice to
    make the diagnosis. MRI with gadolinium will demonstrate the size and degree of neurologic compression. A
    ring-enhancing lesion is pathognomonic for abscess and
    distinguishes it from neoplasm. In patients who have
    associated diskitis or VO, then plain radiography and
    CT are essential to define the extent of osseous destruction.

    Treatment
    Epidural Abscess

    Epidemiology

    5: Spine

    Epidural abscess is a rare but serious disease that is associated with the risk of neurologic demise and even fatality. Hematogenous spread is responsible for about
    half of cases, direct extension from diskitis for about a
    third, and a source is not identified in the remaining
    cases. S aureus is the number one pathogen; however,
    methicillin-resistant S aureus is an important cause,
    particularly in patients with retained vascular or spinal
    implants. Less common etiologies include Staphylococcus epidermidis and gram-negative bacteria such as
    E coli (for example, urinary tract infections) and
    Pseudomanas aeruginosa (for example, intravenous
    drug abuse).9 Anaerobic bacteria, fungi, and parasites
    are rare causes. Epidural abscesses are more common
    dorsally, and are more common in the thoracolumbar
    spine. Most abscesses are secondary to diskitis and osteomyelitis, and this underscores the need to treat these
    infections quickly. It is often difficult to obtain a thorough history and to interpret neurologic deficits (real
    versus secondary to cognitive deficits) in the elderly
    population. It is important to maintain a high index of
    suspicion in elderly patients to avoid a missed diagnosis
    of epidural abscess.

    570

    No randomized controlled trials have been performed


    to generate level I evidence on the treatment of epidural
    abscess. Most retrospective studies have demonstrated
    that the mainstay of treatment is direct surgical decompression followed by antibiotic administration tailored
    to the organism isolated during surgery. The type of
    surgery performed is predicated on the site of the abscess and degree of bony involvement. Indirect decompression (laminectomy for a ventral cervical or thoracic
    abscess) is typically not the procedure of choice. Antibiotic therapy alone is controversial, and results are
    limited to few retrospective series. It should only be attempted in patients with small abscesses and no neurologic deficits, and in patients who will have very close
    serial clinical follow-up. The 4% to 22% incidence of
    permanent paralysis in patients with epidural abscess
    underscores the need to promptly treat these patients
    and provides a strong argument for surgical management. The addition of spinal instrumentation is dependent on the type of surgery performed (such as cervical
    laminectomy) and the degree of bony destruction, if
    present. The main indicator of clinical outcome is degree of neurologic impairment preoperatively.

    Postoperative Infections

    Clinical Presentation

    Epidemiology

    The pathogenesis of neurologic demise may stem from


    direct compression and/or septic thrombophlebitis with
    resultant venous spinal cord infarction. The precise
    mechanism is not known. The clinical presentation
    varies and will be predicated on the degree and type
    of neurologic compression and region of the spine
    involved. Common findings include pain (three fourths
    of patients) in the affected region, radicular pain from
    root compression, or neurologic deficit (one third of
    patients) correlative to the compressed level of the
    spinal cord, cauda equina, or nerve root. Fever is pres-

    Infections are a relatively common acute postoperative


    complication.10 The likelihood of infection varies with
    several factors: predisposing factors of the patient,
    complexity of the case, and prophylactic antibiotics.
    The infection rate for lumbar microdiskectomy is
    0.7%, but it doubles when a microscope is used during
    the case. Instrumentation increases the infection rate, as
    does a posterior procedure. Anterior procedures are not
    associated with higher rates. Infection rates of 2.8% to
    6.0% have been reported for elective fusion with instrumentation. Spine trauma treated surgically is asso-

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 43: Spinal Infections

    ciated with infection rates up to 10%, and higher rates


    are correlated with delay in surgery beyond 16 hours
    and multilevel surgery.
    Risk factors include obesity (body mass index
    greater than 35), smoking, diabetes mellitus, alcohol
    abuse, malnutrition, chronic steroid use, prior infection, revision surgery, surgery longer than 3 hours, and
    blood loss greater than 1.0 L. Age has inconsistently
    been associated with an increased risk of infection. The
    most common pathogen is S aureus; however, S epidermidis and methicillin-resistant S aureus are other relatively frequent etiologies. Gram-negative and anaerobic
    pathogens occur less frequently, but can cause serious
    disease. Prevention has been extensively studied, and
    preoperative intravenous antibiotics are efficacious in
    decreasing infection rates. Cefazolin is effective against
    S aureus and S epidermidis, and should be given 1 hour
    before incision and readministered if the surgery exceeds 4 hours. Clindamycin or vancomycin should be
    given for patients allergic to cephalosporins.

    Clinical Presentation

    Laboratory and Diagnostic Imaging


    Laboratory studies should include ESR, CRP level, and
    complete blood cell count with differential. ESR will
    often remain elevated for up to 6 weeks after surgery,
    and this makes ESR a less useful study in the immediate
    postoperative period. CRP level remains elevated for up
    to 2 weeks postoperatively. Cultures or swabs of incision drainage often will confound the diagnosis because
    of skin colonization. The most reliable cultures are obtained at surgery.
    Plain radiographs typically contribute much information, as the time frame between surgery and early infection is narrow. CT may show fluid collections. MRI
    with gadolinium should be obtained, but the results
    must be interpreted carefully. The normal postoperative
    changes can look very similar to the infection. Enhancing fluid collections are pathognomonic for infection.

    2011 American Academy of Orthopaedic Surgeons

    The treatment of postoperative infections is dependent


    on type of infection and the patients immune, neurologic, and clinical status. Postdiskectomy diskitis is often an indolent infection that results in a delayed diagnosis. Patients often will present with progressive
    mechanical back pain and elevation of serologic markers. In the absence of a disk space abscess, a needle biopsy to obtain a pathogen can be followed by a course
    of appropriate antibiotics. If the infection progresses
    into a disk space or epidural abscess, the patient has intractable pain or develops instability or deformity, then
    surgery is indicated.
    Postoperative wound infections generally respond
    poorly to antibiotic therapy alone, and surgical irrigation and dbridement is indicated in most patients. Attempts to clinically treat a draining wound rarely will
    result in spontaneous resolution, and waiting will result
    in increased soft-tissue necrosis and possible progression to osteomyelitis. Hence, prompt surgical management is advantageous. The goals of surgery include
    evacuation of all fluid collections and a thorough mechanical dbridement of all necrotic soft tissue. Instrumentation should be left in place if it remains intact, as
    this will aid in eradication of the infection for reasons
    noted earlier.11,12 Similarly, bone graft should be left in
    place unless it appears grossly contaminated.
    Vacuum-assisted closure has been shown to be a safe
    treatment of complex postoperative infections;13 however, absolute indications have not been defined in the
    literature. The use of vacuum-assisted closure dressings
    is a reasonable approach for grossly contaminated
    wounds, ones with large areas of dead space, immuneincompetent patients, and patients in whom previous
    irrigation and dbridement with attempted primary closure has failed. The VAC dressing can be used as a transition to a primary closure, or in recalcitrant cases, it
    can be used serially to secondary closure.

    5: Spine

    Postoperative infections may be classified as superficial,


    most commonly suprafascial, and deep. Most postoperative infections occur early within the first few weeks
    after the index procedure, but others occur late or latent (years after surgery). The most common presentation of an early postoperative infection is pain at the incision site. This pain usually will begin several days
    after the surgery and typically is progressive. Constitutional symptoms and signs such as fever, fatigue, and
    malaise are also common. Examination findings include drainage, which can range from serosanguinous
    to frankly purulent, and peri-incisional erythema, induration, warmth, and tenderness. Benign-appearing serosanguinous or serosanguinous drainage that does not
    cease within the first week postoperatively is worrisome for infection. In severe cases, mental status
    changes, high fever, and sepsis can occur, and this scenario warrants emergent surgical treatment.

    Management

    Annotated References
    1.

    Wiley AM, Trueta J: The vascular anatomy of the spine


    and its relationship to pyogenic vertebral osteomyelitis.
    J Bone Joint Surg Br 1959;41:796-809.

    2.

    Batson OV: The vertebral system of veins as a means for


    cancer dissemination. Prog Clin Cancer 1967;3:1-18.

    3.

    Garcia A Jr, Grantham SA: Hematogenous pyogenic


    vertebral osteomyelitis. J Bone Joint Surg Am 1960;
    42A:429-436.

    4.

    Eismont FJ, Bohlman HH, Soni PL, Goldberg VM,


    Freehafer AA: Pyogenic and fungal vertebral osteomyelitis with paralysis. J Bone Joint Surg Am 1983;65(1):
    19-29.

    5.

    Krogsgaard MR, Wagn P, Bengtsson J: Epidemiology of


    acute vertebral osteomyelitis in Denmark: 137 cases in
    Denmark 1978-1982, compared to cases reported to the

    Orthopaedic Knowledge Update 10

    571

    Section 5: Spine

    after surgery, along with risk factors and preventive


    measures.

    National Patient Register 1991-1993. Acta Orthop


    Scand 1998;69(5):513-517.
    6.

    Modic MT, Feiglin DH, Piraino DW, et al: Vertebral osteomyelitis: assessment using MR. Radiology 1985;
    157(1):157-166.

    7.

    Brodke DS, Fassett DR: Infections of the spine, in Spivak JM, Connolly PJ, eds: Orthopaedic Knowledge Update: Spine, ed 3. Rosemont, IL, American Academy of
    Orthopaedic Surgeons, 2006, pp 367-375.

    8.

    Jain AK: Tuberculosis of the spine. A fresh look at an


    old disease. J Bone Joint Surg Br 2010;92:905-913.
    The use of antitubercular drugs, modern diagnostic aids,
    and advancements in surgical treatment of tuberculosis
    of the spine are discussed.

    9.

    Darouiche RO: Spinal epidural abscess. N Engl J Med


    2006;355(19):2012-2020.
    Sasso RC, Garrido BJ: Postoperative spinal wound infections. J Am Acad Orthop Surg 2008;16(6):330-337.
    This article discusses spinal wound infections that occur

    Mok JM, Guillaume TJ, Talu U, et al: Clinical outcome


    of deep wound infection after instrumented posterior
    spinal fusion: A matched cohort analysis. Spine 2009;
    34(6):578-583.
    The authors determined that deep wound infection
    should be treated aggressively with early irrigation and
    dbridement to allow preservation of instrumentation
    and successful fusion.

    12.

    Rayes M, Colen CB, Bahgat DA, et al: Safety of instrumentation in patients with spinal infection. J Neurosurg
    Spine 2010;12(6):647-659.
    The authors concluded that instrumentation after radical dbridement will not lead to an increased risk of recurrent infection. Spinal stabilization may be more beneficial and promote accelerated healing.

    13.

    Mehbod AA, Ogilvie JW, Pinto MR, et al: Postoperative


    deep wound infections in adults after spinal fusion:
    Management with vacuum-assisted wound closure.
    J Spinal Disord Tech 2005;18(1):14-17.

    5: Spine

    10.

    11.

    572

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 44

    Spinal Cord Injury


    Brian K. Kwon, MD, PhD, FRCSC

    Introduction

    Early Management of Acute SCI

    Emergency Assessment
    Acute SCI occurs in the context of trauma, and so the
    initial treatment of patients with neurologic impairment is still guided by the Advanced Trauma Life Support (ATLS) protocols. The first priorities are the assessment and management of the airway, breathing,

    Dr. Kwon or an immediate family member serves as a paid


    consultant to Medtronic Sofamor Danek and has received
    research or institutional support from Medtronic Sofamor
    Danek.

    2011 American Academy of Orthopaedic Surgeons

    5: Spine

    Each year in the United States, approximately 12,000


    individuals sustain an acute spinal cord injury (SCI).1
    These individuals join a growing population of chronically paralyzed SCI patients, which recently was estimated by the Christopher Reeve Foundation to exceed
    1.25 million. This figure is almost four times higher
    than previous estimates.2 With the aging population, a
    greater number of persons older than 60 years suffer
    SCI. As a result, the average age at injury has risen
    from 29 years in the mid-1970s to almost 40 years
    since 2005. Irrespective of the age at which an individual has an SCI, the personal loss and societal costs are
    astronomical. Although personal loss cannot be quantified, recent estimates of societal costs place the lifetime
    medical costs of caring for a complete quadriplegic or
    paraplegic between $1 and $3 million.
    It is hoped that the considerable research efforts currently under way will soon produce an effective treatment of SCI that will bring about a measurable and
    meaningful improvement in neurologic function. A
    greater understanding of the neurobiologic challenges
    imposed by SCI is emerging, and clinicians currently
    are witnessing a growing number of experimental treatments that are entering or have already initiated human
    evaluation.3,4 The initiation of such human trials fuels
    the hope that an effective treatment may be imminent.
    It is important that clinicians be aware of the basic
    principles of early management of acute SCI, and the
    therapies that are about to or have already begun evaluation in human clinical trials.

    and circulation (ABCs). Although the ATLS protocols


    are familiar to most, there are important considerations
    in patients with acute SCI. First, the airway should be
    maintained and the cervical spine protected to minimize further displacement of cervical column injuries
    and additional insult to the spinal cord. Upper cervical
    spine injuries may impair diaphragmatic function and
    lead to rapid hypoxic respiratory failure (often at the
    injury scene). More commonly, lower cervical spine injuries and the resultant paralysis of intercostal muscles
    lead to poor chest wall expansion and a slower hypercarbic ventilatory failure within the first 24 to 48 hours
    of injury. Poor chest wall expansion and slower hypercarbic ventilator failure may require intubation and
    mechanical ventilation, which needs to be done with
    cervical spine protection. Disruption of sympathetic
    outflow with cervical SCI can lead to bradycardia,
    whereas the loss of vasomotor tone can result in profound hypotension. This combination of hypotension
    and bradycardia is often referred to as neurogenic
    shock, and requires vasopressor support with pharmacologic agents. Such interventions should be instituted
    only after hemorrhagic shock from other injuries is addressed with volume expansion and/or blood products.
    The term neurogenic shock is often confused with spinal shock, which refers to the absence of spinal reflexes
    that occurs after a severe SCI and is operationally defined as ending when the bulbocavernosus reflex returns.

    Neurologic Assessment
    The screening examination for neurologic impairment
    (the D stands for disability in the ABCs of the ATLS
    protocol) constitutes a quick assessment of whether the
    patient can voluntarily move the four extremities. The
    clinical characterization of the SCI, however, requires a
    formal neurologic assessment according to the American Spinal Injury Association (ASIA) guidelines, which
    have been adopted as the international standard for
    evaluating patients with SCI (Figure 1). The current
    ASIA examination entails a motor and sensory examination, although work is also being done to incorporate a clinical assessment of autonomic instability. The
    motor examination is conducted by measuring the
    strength of five key upper extremity myotomes (C5, elbow flexion; C6, wrist extension; C7, elbow extension,
    C8, long finger flexion; and T1, small finger abductors)
    and five lower extremity myotomes (L2, hip flexion;
    L3, knee extension; L4, ankle dorsiflexion; L5, great

    Orthopaedic Knowledge Update 10

    573

    Section 5: Spine

    5: Spine

    Figure 1

    The American Spinal Injury Association (ASIA) Impairment Scale and Assessment Form. Acute SCI patients should be
    evaluated according to the ASIA standards of assessment. This involves both motor and sensory testing, and most
    importantly, an evaluation of function in the lowest sacral segments (S4-S5). The motor score is derived from 10
    key myotomes in the upper and lower extremities. Patients are graded on the ASIA Impairment Scale based on
    whether or not they demonstrate function at S4-S5 (complete versus incomplete) and how much residual motor
    and sensory function they have maintained (to determine the extent of incompleteness).

    toe extension; and S1, ankle plantar flexion). Motor


    strength is documented according to the Medical Research Council (MRC) grading scheme from 0 to 5.
    Grade 0 represents complete paralysis, grade 1 is a palpable or visible contraction, grade 2 is full active range
    of motion with gravity eliminated, grade 3 is full active
    range of motion against gravity, grade 4 is full active
    range of motion against resistance, and grade 5 is normal strength. It is important during this examination
    not to confuse spastic or reflexive movements with voluntary motor function. For example, it is not uncommon when testing ankle plantar flexion to see reflexive
    extension of the great toe or ankle in response to touching the sole of the foot (akin to a Babinski reflex response). If this is witnessed by the patient or family,
    who are obviously desperately hopeful for some motor
    recovery, it can be easily misinterpreted as preserved
    motor function.
    The sensory examination is performed by assessing
    light touch and pinprick sensation along 28 dermatomes (S4-S5 is one). The sensation is documented
    as absent, impaired, or normal and is scored 0, 1, or 2,
    respectively. The most common mistake in the sensory
    testing of individuals with SCI is misinterpreting the
    574

    Orthopaedic Knowledge Update 10

    dermatomal distribution in the upper thorax. It is important to remember that the C4 dermatome extends
    down in a capelike distribution along the upper chest
    and shoulders, and ends just rostral to the nipple line.
    Because most physicians associate the nipple line with a
    T4 sensory distribution, it is not uncommon for the inexperienced examiner to test pinprick sensation along
    the upper chest, and document that there is a T4 sensory level because the sensation remains intact near
    the nipple line. This finding means that the C4 dermatome is intact.
    Arguably, the most important aspect of the ASIA examination is the rectal examination. In the patient with
    an acute SCI, it should be determined whether he or she
    has pinprick and/or light touch sensation around the
    perianal region and voluntary anal contraction. The
    presence or absence of function at this S4/S5 level defines whether the patient has a complete or incomplete
    SCI; this distinction currently has the most significant
    prognostic implications for the patient. With the motor
    and sensory examination completed and the rectal examination completed, the severity of paralysis can be
    classified. The ASIA Impairment Scale is the universally
    accepted system for broadly categorizing the neurologic

    2011 American Academy of Orthopaedic Surgeons

    Chapter 44: Spinal Cord Injury

    Investigation
    There is little argument that MRI is the most valuable
    imaging study for the assessment of SCI. It should be
    remembered that the acute SCI is an evolving biologic
    process, and so, the MRI appearance of the spinal cord
    is likely to be influenced by the timing of the imaging
    study. Edema and hemorrhage can be seen within the
    cord parenchyma, and the presence and rostrocaudal
    extent of these factors may be useful in predicting the
    eventual neurologic outcome.5 (Figure 2) MRI can also
    help in the surgical planning to guide the decompression.

    Treatment
    Most acute SCIs occur with some spinal column instability, and hence, are typically treated with surgical stabilization with or without decompression. The most
    controversial aspect of this treatment is the timing of
    surgical decompression. Despite fairly convincing data

    2011 American Academy of Orthopaedic Surgeons

    Figure 2

    A and B, MRIs of acute cervical SCI. MRI is the


    most important imaging modality for evaluating
    SCIs. Acute cord injury is characterized by
    edema and hemorrhage (arrows) within the
    cord. Acutely, the hemorrhage appears dark,
    and its presence has traditionally been viewed
    as a poor prognostic sign.

    from animal models that early surgical decompression


    promotes a better neurologic outcome than late decompression, it has been difficult to reproduce these results
    in human patients with SCI. The Surgical Treatment of
    Acute Spinal Cord Injury Study is a prospective observational study that is attempting to address this issue in
    hundreds of patients who have been enrolled at multiple North American sites. At the time of this writing,
    the preliminary data from this study have suggested a
    small benefit to early decompression. Whatever the final results of this trial, basic trauma care principles
    would indicate that the overall medical care of SCI patients is facilitated by expedient surgical stabilization to
    allow for mobilization and rehabilitation. The historical practice, therefore, of consciously delaying the surgical management of patients with spinal column injuries and spinal cord impairment with the intention of
    letting their spinal cords cool down should probably
    be abandoned. The one exception to this tenet is in the
    patient with a central cord syndrome incomplete SCI
    but without any spinal column instability; substantial
    unresolved controversy remains about whether such
    patients would benefit from early decompression, or a
    later decompression after reaching a neurologic plateau.

    5: Spine

    function of patients with an SCI (Figure 1). Patients in


    whom no motor or sensory function is preserved in the
    lowest sacral segments (S4-S5) are deemed to be ASIA
    A complete. Those with sensory sparing in the lowest
    sacral segments with no motor function are ASIA B incomplete. Those with preserved motor function below
    the neurologic level with the majority of myotomes
    having a muscle grade of two or less are ASIA C incomplete, whereas those with a muscle grade of three or
    more are ASIA D incomplete. Patients with normal motor and sensory function are considered to be ASIA E.
    The ASIA Impairment Scale highlights the importance
    of the rectal and perianal examination to confirm the
    presence or absence of sacral sparing and to determine
    if the SCI is complete or incomplete. A variety of syndromes of incomplete paralysis have been described
    and include central cord syndrome, Brown-Squard
    syndrome, anterior or posterior cord syndrome, and
    cruciate paralysis. Because they all are forms of incomplete paralysis, varying degrees of neurologic improvement can be expected. The most common syndrome of
    incomplete paralysis is that of central cord syndrome,
    which is characterized by disproportionately greater
    deficits in the upper extremity than the lower extremity.
    This is most commonly observed in elderly patients
    with preexisting cervical spondylosis and stenosis who
    kink their spinal cord with sudden hyperextension of
    the neck, often during low-energy falls. Although the
    greater upper extremity involvement in central cord
    syndrome has been attributed to the arm and hand fibers of the corticospinal tract running more medially/
    centrally within the cord than the lower extremity fibers, this somatotopic organization of the corticospinal
    tract has never been anatomically demonstrated. More
    contemporary studies reveal that the upper extremity
    involvement in central cord syndrome is better explained by the dominant role that the corticospinal
    tract has in upper extremity function in humans (and
    hence, injuries to this tract are prominently manifest in
    the upper extremities).

    Biologic Challenges to Recovery


    A comprehensive description of the pathophysiology
    and pathology of SCI is beyond the scope of this chapter. The primary injury to the spinal cord is caused by
    the acute traumatic forces imparted upon it by the mechanically failing spinal canal. Following the primary
    injury, an interrelated series of pathophysiologic processes including ischemia, excitotoxicity, inflammation,
    and oxidative stress contribute to further secondary
    damage.6 The aim of neuroprotection strategies is to attenuate these processes and thus limit secondary dam-

    Orthopaedic Knowledge Update 10

    575

    Section 5: Spine

    5: Spine

    age. The recognition that ongoing ischemia may


    worsen secondary damage has led to the practice of aggressively avoiding hypotension and the promotion of
    spinal cord perfusion through an elevated mean arterial
    pressure (MAP).7 Clinical practice guidelines published
    in 2008 by the Paralyzed Veterans of America advocate
    for judicious hemodynamic management, but acknowledge that the optimal MAP to maintain and for what
    duration remains unknown.7 A 2009 study in which
    lumbar subarachnoid drains were inserted in patients
    with acute SCI reported that an increase in intrathecal
    pressure during the acute postinjury phase, and thus,
    the management of MAP alone may overestimate the
    extent to which spinal cord perfusion pressure is actually being supported.8
    As for other relevant acute pathophysiologic mechanisms, the local and systemic inflammatory and immunologic response to SCI has garnered increasing interest
    in recent years. It has become evident that these are potentially important contributors not only to further
    neural damage and axonal retraction at the cord injury
    site,9 but also for mediating the development of neuropathic pain,10 and for increasing the vulnerability to infection.11
    Beyond targeting the acute pathophysiologic processes that induce secondary damage during the acute
    stages of injury, strategies to encourage axonal sprouting and regeneration are needed to restore connectivity
    across the injury site. It is well recognized that such regeneration is inhibited by the nonpermissive environment of the injured central nervous system (CNS). CNS
    myelin contains several inhibitory molecules that block
    axonal growth, including Nogo, myelin-associated glycoprotein (MAG), and oligodendrocyte myelin glycoprotein (OMgp).12 Additionally, the astrocytic response
    to injury elicits a glial scar, which also contains molecules that inhibit axonal growth, including chondroitin
    sulfate proteoglycans.13 Overcoming these molecular
    inhibitors of axonal growth is the subject of intense research investigation and represents the underlying rationale for several emerging therapeutic strategies, including the anti-NOGO antibodies Cethrin, and
    chondroitinase ABC (ChABC).14
    The pathology of SCI often includes some degree of
    cystic cavitation at the injury site,15 and at the periphery, the demyelination of axons that have otherwise escaped disruption across the injury site.16 The transplantation of cellular substrates into this cystic cavity has
    historically been done to provide a more permissive environment for axonal growth. More recently, such cell
    transplantation strategies have focused on the cells myelinating demyelinated axons, and thus improving signal transduction across the injury site.17

    Experimental Therapies Currently


    in Human Clinical Trials
    Several experimental therapies are either in the midst of
    human evaluation or are about to begin clinical trials.
    For each therapy, some of the historical and scientific
    576

    Orthopaedic Knowledge Update 10

    background is provided to explain the biologic rationale for their evaluation in human SCI (Table 1).

    Methylprednisolone
    Although methylprednisolone is no longer in investigational human trials, its use in treating acute SCI in humans continues to be debated both in the clinical and
    scientific literature. Reports from the earlier half of this
    decade focused on the conduct and interpretation of
    the National Acute SCI Studies (NASCIS) 2 and 3,18,19
    which established the administration of methylprednisolone for acute SCI as a standard practice. A recent
    systematic review of animal studies that evaluated
    methylprednisolone in models of SCI revealed that beneficial effects were only reported in 34%, whereas 58%
    of studies reported no benefit, and 8% observed mixed
    results.20 In the clinical literature, a growing number of
    reports have been published that describe the lack of efficacy and the increasing risk of complications such as
    pneumonia and sepsis with the use of methylprednisolone in humans.21,22 A Canadian survey published in
    2008 revealed that most spine surgeons (67%) no longer administer methylprednisolone for acute SCI, which
    is a dramatic shift in practice from 5 to 6 years prior.23
    However, in the United States, the fear of litigation will
    compel many surgeons to continue administering methylprednisolone despite their perspectives on its efficacy.21,24

    Anti-Nogo Antibodies
    Pioneering work in the late 1980s revealed that oligodendrocytes and their myelin membranes were inhibitory to axonal regeneration within the CNS.25 These
    studies confirmed the principle that the injured spinal
    cord represented a nonpermissive environment to axonal growth, in contrast to the injured peripheral
    nerve, which was known to regenerate relatively successfully. From CNS myelin, two inhibitory fractions of
    35 and 250 kDa were isolated (named NI-35 and NI250), and then a monoclonal IgM antibody called IN-1
    was developed that could block their inhibitory properties in vitro.26 This antibody was reported to promote
    axonal regeneration and improve function in animal
    models of SCI.27,28 The actual protein antigen that was
    targeted and inhibited by IN-1 was eventually characterized in 2000 and given the name Nogo, and an
    IgG anti-Nogo antibody for intrathecal application after SCI was developed. The anti-Nogo antibody was
    subsequently shown in rat and primate models of SCI
    to promote axonal sprouting and functional improvements.29,30
    This anti-Nogo IgG intrathecal approach has been
    commercialized by Novartis (Basel, Switzerland), which
    in 2006 initiated an open-label, nonrandomized human
    clinical trial currently being conducted as a multicenter
    study across Europe and in Canada (ClinicalTrials.gov
    Identifier: NCT00406016). Eligible patients were to be
    ASIA A complete thoracic paraplegics or cervical quadriplegics, with the treatment to begin between 4 and 14
    days after injury. The antibody is infused intrathecally,

    2011 American Academy of Orthopaedic Surgeons

    Chapter 44: Spinal Cord Injury

    Table 1

    Therapeutic Approaches Currently in or About to Begin Human Evaluation


    Therapy

    Commercial
    Sponsor

    Anti-Nogo antibodies

    Novartis (Basel,
    Switzerland)

    Cethrin

    Alseres
    Inhibit rho, an intracellular GTPase Multicenter study of ASIA A thoracic and cerviPharmaceuticals within the axonal growth cone
    cal SCI began in 2005 and completed in 2007.
    (Hopkinton,
    that mediates the effects of inhibTreatment applied directly to dura during surMA)
    itory proteins (such as Nogo-A).
    gery within 7 days of injury. Subsequent randomized trial planned.

    Minocycline

    None

    Reduce posttraumatic inflammation Single-center study of compete and incomplete


    and apoptotic cell death.
    SCI began in 2004 and is now analyzing data.
    Treatment administered intravenously within
    12 h of injury.

    Systemic hypothermia

    None

    Slow metabolic rate, reduce inflammation and oxidative stress.

    Riluzole

    None

    A sodium channel blocker approved Multicenter study of ASIA A, B, and C thoracic


    by the US Food and Drug Adminand cervical SCI expected to begin in 2010.
    istration (FDA) for the treatment
    Treatment to be given orally and initiated
    of amyotrophic lateral sclerosis.
    within 12 h of injury.

    Magnesium
    (NeuroShield)

    Medtronic (Mem- A physiologic antagonist to


    phis, TN)
    N-methyl-D-aspartate receptors.

    Multicenter study of ASIA A cervical SCI expected to begin in 2010. Treatment to be


    given intravenously within 12 h of injury.
    Phase I safety study in humans complete.

    Human embryonic
    stem cell-derived
    oligodendrocyte
    progenitors

    Geron (Menlo
    Park, CA)

    Multicenter study of ASIA A thoracic SCI to begin when FDA approval is granted. Transplantation of cells to occur 7 to 14 days postinjury.

    Therapeutic Rationale

    Study Design

    Inhibit activity of Nogo-A, a protein


    in CNS myelin that inhibits axonal
    growth.

    Multicenter study of ASIA A thoracic and cervical


    SCI began in 2006. Treatment initiated 7 to 14
    days postinjury and administered intrathecally.

    Remyelinate demyelinated axons


    and restore conduction.

    Cethrin
    The recognition that CNS myelin prompted the cessation of axonal regeneration led researchers to question
    what was occurring within the tip of the axon (the axonal growth cone) that caused this response. From a
    therapeutic standpoint, if multiple inhibitory molecules
    within CNS myelin all ultimately converge upon the
    same intracellular signaling pathway within the axonal
    growth cone to halt its growth, then a single intervention targeting this pathway might counteract the effects
    of many inhibitors (unlike the anti-Nogo antibody,
    which is specific to the Nogo inhibitory protein).
    Rho, a small guanosine triphosphatase, is an important intracellular signaling molecule that regulates axonal growth when exposed to inhibitory CNS myelin,
    and thus represents such a point of convergence for
    therapeutic intervention.31 The strategy of antagonizing
    Rho with C3 transferase (a rho antagonist) applied directly to the cord was shown to promote recovery in an

    2011 American Academy of Orthopaedic Surgeons

    5: Spine

    initially via an indwelling catheter and more recently by


    repeated lumbar punctures. The clinical trial of approximately 50 patients was expected to conclude recruitment during 2010.

    Single-center study of ASIA A complete SCI began in 2006. Systemic hypothermia initiated
    within 12 h of injury in most patients.

    animal model of SCI.32 Based on these preclinical findings, a cell-permeable version of C3 transferase (Cethrin) was commercialized by BioAxone Therapeutic
    Inc, Montreal, QC) a Canadian biotechnology firm,
    and a multicenter clinical trial was launched in 2005
    across North America. This study included patients
    with cervical and thoracic SCI who were deemed to be
    ASIA A complete, and the treatment was administered
    within 7 days of injury. Cethrin was mixed within Tisseal and applied to the dura overlying the injured spinal
    cord at the time of spinal cord decompression. This
    phase IIA study was concluded in the summer of 2007
    after 37 patients were enrolled. The results of this study
    have yet to be published. A subsequent prospective randomized clinical trial is in the planning stages.

    Minocycline
    Minocycline is a tetracycline antibiotic that has significant anti-inflammatory and antiapoptotic properties.
    Because the inflammatory response is considered to be
    an important contributor to secondary damage after
    SCI, the ability of minocycline to inhibit microglial activation and the release or activity of proinflammatory
    mediators (cytokines, reactive oxygen species, and ma-

    Orthopaedic Knowledge Update 10

    577

    Section 5: Spine

    trix metalloproteinases) has made it an attractive agent


    to study in SCI models.33 Numerous independent laboratories have reported on the efficacy of minocycline in
    various animal models of SCI.34-36 These positive results, however, have more recently been countered by
    studies reporting that no functional benefit was conferred to animals treated with minocycline.37,38
    However, the early positive data on minocycline in
    animal models of SCI from independent laboratories
    stimulated the initiation of a human clinical trial in
    Calgary, AB, Canada. This was a randomized controlled trial in which approximately 50 patients with
    acute SCI (cervical and thoracic) of both complete and
    incomplete injury severities were randomized to either
    intravenous minocycline or placebo within 12 hours of
    injury. At the time of this writing, the results of this
    study have not been published.

    Systemic Hypothermia

    5: Spine

    Hypothermia has interested scientists and clinicians because it may have a neuroprotective role in traumatic
    and ischemic brain injury and SCI.39 In animal models
    of SCI, both local and systemic hypothermia have been
    investigated for decades.40 In such in vivo experiments,
    moderate systemic hypothermia (around 30 to 32C)
    has been shown to have a wide range of histologic and
    biochemical effects, such as the attenuation of neutrophil invasion, reduced oxidative stress, and reduced
    secondary damage.
    Interest in systemic hypothermia exploded in the fall
    of 2007 after the highly publicized case of Kevin Everett, a professional football player who suffered a cervical SCI while tackling an opposing player and was
    treated with systemic hypothermia (in addition to
    methylprednisolone and an urgent surgical decompression). Significant neurologic recovery was achieved.41
    No peer-reviewed publication describing systemic hypothermia in human SCI had been published at the
    time, making it difficult for scientists and clinicians to
    interpret the efficacy of hypothermia in general. Investigators at the Miami Project to Cure Paralysis have
    had a long-standing interest in hypothermia, and have
    conducted a pilot study on the safety and feasibility of
    systemic hypothermia for acute SCI. A retrospective review of 14 ASIA A acute SCI patients treated with
    modest systemic hypothermia (33C) for 48 hours was
    performed.42 The incidence of complications (such as
    atelectasis, pneumonia, acute respiratory distress syndrome) was very similar to that commonly observed in
    such patients.

    Riluzole
    Riluzole is an orally administered sodium channel
    blocker that is currently approved by the FDA for use
    in treating ALS, and hence many questions around its
    safety, tolerability, and pharmacokinetics in humans
    have been answered. Sodium channels have long been
    implicated in white matter damage after SCI, as the influx of sodium through voltage-gated sodium channels
    can ultimately lead to the loss of calcium homeostasis.43
    578

    Orthopaedic Knowledge Update 10

    Systemically administered riluzole has been evaluated


    by numerous investigators in acute SCI models.44,45
    These studies report a significant reduction in secondary damage around the injury site, and improved functional recovery in riluzole-treated animals.
    Encouraged by these preclinical results and the established safety to human patients, a prospective multicenter clinical trial of riluzole for human patients with
    acute SCI is soon to be initiated through the North
    American Clinical Trials Network, sponsored by the
    Christopher and Dana Reeve Foundation. The daily
    dose will be that which has been previously approved
    by the FDA for the treatment of ALS, although it is recognized that this human oral dose is substantially less
    than that which has been administered via intraperitoneal injection to rats in experimental SCI studies. The
    investigators are currently targeting a total of 36 patients to be enrolled into this study.

    Magnesium
    Magnesium is a physiologic N-methyl-D-aspartate
    (NMDA) receptor antagonist. Glutamate levels rise
    rapidly after CNS injury, and glutamates overstimulation of NMDA receptors can lead to a massive influx of
    calcium, leading to cell death, a process broadly referred to as excitotoxicity.46 The widespread distribution of NMDA receptors has prompted extensive study
    into NMDA-receptor antagonists (including magnesium) as a neuroprotective strategy for SCI, brain injury, and other neurologic conditions.47 The role of
    magnesium therapy in acute SCI models has been investigated by multiple independent laboratories. These
    studies have described improved biochemical, physiologic, and histologic outcomes with magnesium administration, as well as improved locomotor recovery.48,49
    However, it is important to point out that most of these
    studies use a magnesium dosage (approximately 300 to
    600 mg/kg) that far exceeds human safety limits.
    More recently, a formulation that consists of magnesium within polyethylene glycol (PEG) has been investigated as a potential neuroprotective agent for brain
    injury and SCI. A recent study has revealed that PEG
    allows for a much lower dose of magnesium to be applied effectively in SCI models.50 This magnesium dosage is similar to that which was safely administered to
    patients in previous trials who had experienced stroke,
    cardiac arrest, and preeclampsia. This formulation of
    magnesium chloride within PEG (NeuroShield,
    Medtronic, Memphis, TN) has received FDA approval
    to begin human studies. A phase I study of healthy human volunteers was completed in the spring of 2009,
    and revealed no significant adverse events. A phase II
    multicenter study of human SCI patients was expected
    to be initiated in 2010.

    Human Embryonic Stem CellDerived


    Oligodendrocyte Progenitors
    As described earlier, one of the prime targets of interest
    for the cell transplantation field is demyelinated axons
    that still traverse the injury site, as the remyelination of

    2011 American Academy of Orthopaedic Surgeons

    Chapter 44: Spinal Cord Injury

    such axons may facilitate improved signal conduction.


    Many different cell substrates may promote remyelination, including Schwann cells and various stem cells.
    Oligodendrocyte progenitor cells derived from a human
    embryonic stem cell (hESC) line are one such cell. As
    undifferentiated embryonic stem cells have the predilection to generate teratomas, the more rational approach
    is to control the in vitro differentiation of these multipotent cells down to an oligodendrocyte progenitor cell
    population, and then transplant these more committed cells whose fate is more certain. This strategy was
    demonstrated in a study that showed the implantation
    of hESC-derived oligodendrocyte progenitors 7 days after injury promoted remyelination and functional recovery.51 Unfortunately, animals that received the cell
    transplants many months after injury (representing a
    chronic injury) did not experience functional recovery.
    The hESC-derived oligodendrocyte progenitor technology received widespread international publicity in
    January 2009 when the FDA granted approval to conduct a human SCI trial with these cells, the first-ever
    human clinical trial using embryonic stem cell derivatives. The primary end point of this small study will be
    safety, as the concern for teratoma formation is of paramount importance. The trials were placed on clinical
    hold by the FDA in August 2009 after concerns were
    raised about findings from dose-escalation safety studies conducted in animal models.52

    Emerging Concepts

    2011 American Academy of Orthopaedic Surgeons

    Annotated References
    1.

    National Spinal Cord Injury Statistical Center: Spinal


    cord injury facts and figures at a glance. J Spinal Cord
    Med 2008;31(3):357-358.
    The National Spinal Cord Injury Database has been in
    existence since 1973 and captures data from an estimated 13% of new SCI cases in the US Since its inception, 26 federally funded Model SCI Care Systems have
    contributed data to the National SCI Database. As of
    October 2007 the database contained information on
    25,415 persons who sustained traumatic SCIs.

    2. One Degree of Separation; Paralysis and Spinal Cord


    Injury in the United States. Short Hills, NJ, Christopher
    and Dana Reeve Foundation, 2009.
    This is an extensive survey of more than 33,000 households across the United States that was conducted to
    capture the prevalance of SCI and paralysis across the
    nation. It represents one of the largest population-based
    samples of any disability ever conducted, and importantly, documented a far greater prevalance of paralysis
    than was previously estimated.
    3.

    Hawryluk GW, Rowland J, Kwon BK, Fehlings MG:


    Protection and repair of the injured spinal cord: A review of completed, ongoing, and planned clinical trials
    for acute spinal cord injury. Neurosurg Focus 2008;
    25(5):E14.
    This is a review of past, present, and future clinical trials
    of therapies in acute SCI. It describes the biological rationale for a number of experimental treatments that are
    either in human trials currently or are about to enter
    clinical investigation.

    4.

    Baptiste DC, Fehlings MG: Emerging drugs for spinal


    cord injury. Expert Opin Emerg Drugs 2008;13(1):6380.
    This is a review of novel pharmacologic treatments that
    are emerging from the laboratory for the treatment of
    acute SCI.

    5.

    Miyanji F, Furlan JC, Aarabi B, Arnold PM, Fehlings


    MG: Acute cervical traumatic spinal cord injury: MR
    imaging findings correlated with neurologic outcome:
    Prospective study with 100 consecutive patients. Radiology 2007;243(3):820-827.
    This study evaluated maximum spinal cord compression, maximum canal compromise, and lesion length in
    100 patients with traumatic cervical SCIs. It reported

    Orthopaedic Knowledge Update 10

    5: Spine

    There is cautious optimism that therapies for SCI will


    soon be emerging. The scientific community has realized that none of these therapies will represent a cure
    for SCI, and that these experimental treatments will
    lead to relatively small improvements in neurologic
    function. Such small improvements should not be dismissed, however. History will show that the widespread
    adoption of methylprednisolone was similarly based on
    very small changes in neurologic function in the NASCIS trials. Additionally, for an injury condition of such
    catastrophic implications, any meaningful improvement would be welcomed.
    It is important to recognize that the initiation of a
    clinical trial is far from evidence that the therapy actually works. Although several treatments have been undergoing evaluation in human subjects, much larger,
    time-consuming, and expensive clinical trials to actually prove their efficacy are still necessary and will not
    yield an answer about the actual clinical effectiveness
    of these therapies for many years. The last major acute
    SCI intervention to be tested in a prospective randomized fashion (Sygen) took over 20 major neurotrauma
    institutions across North America the better part of a
    decade to complete.53 There is a greater awareness of
    the difficulties in conducting clinical trials, with discussion in the literature.54-57 In particular, the high rate of
    spontaneous neurologic recovery is highlighted, which
    makes it necessary to enroll large numbers of patients
    to have sufficient statistical power to assess neurologic

    efficacy. This is particularly an issue in patients with


    acute/subacute SCI, where the extent of their injuries
    may not be so obvious, and neurologic assessment is
    often impaired by other factors (such as head injury or
    multiple trauma). All of the clinical trial initiatives discussed will enroll patients in this acute/subacute stage
    and all will be subject to the challenges related to high
    spontaneous recovery rates. Therefore, more information is needed before conclusions can be made about
    the efficacy of these technologies.

    579

    Section 5: Spine

    Current status of acute spinal cord injury pathophysiology and emerging therapies: Promise on the horizon.
    Neurosurg Focus 2008;25(5):E2.
    This is a review of the pathophysiology of acute SCI and
    how our understanding of this has enabled the development of a number of emerging therapies.

    that maximum spinal cord compression, and the presence of hemorrhage and cord swelling were predictive of
    neurologic outcome.
    6.

    7.

    8.

    5: Spine

    9.

    10.

    11.

    12.

    580

    Mann CM, Kwon BK: An update on the pathophysiology of acute spinal cord injury. Semin Spine Surg 2007;
    19:272-279.
    This is a review of the pathophysiologic mechanisms
    that are activated in acute SCI, which are thought to
    play a role in secondary damage. This includes such
    things as ischemia, oxidative stress, excitotoxicity, inflammation, and apoptosis.
    Consortium for Spinal Cord Medicine/Paralyzed Veterans of America. Early Acute Management in Adults
    with Spinal Cord Injury: A Clinical Practice Guideline
    for Health Care Providers. Washington DC, Paralyzed
    Veterans of America, 2008.
    This is an exhaustive review of the literature on the management of acute SCI. It provides guidelines for such aspects as blood pressure management, surgical decompression, and pharmacologic treatment.
    Kwon BK, Curt A, Belanger LM, et al: Intrathecal pressure monitoring and cerebrospinal fluid drainage in
    acute spinal cord injury: A prospective randomized trial.
    J Neurosurg Spine 2009;10(3):181-193.
    In this study, acute SCI patients had lumbar intrathecal
    drains inserted and CSF pressure was evaluated over 72
    hours. The authors documented significant increases in
    CSF pressure after surgical decompression, and also during the acute postinjury period.
    Busch SA, Horn KP, Silver DJ, Silver J: Overcoming
    macrophage-mediated axonal dieback following CNS
    injury. J Neurosci 2009;29(32):9967-9976.
    In this study, the authors investigated the mechanisms
    by which the infiltration of macrophages into the injured spinal cord coincides with axonal retraction from
    the initial injury site. They provide interesting insights
    into the cellular and molecular mechanisms that are behind this macrophage-associated axonal dieback, such
    as the role of MMP-9.
    Hulsebosch CE, Hains BC, Crown ED, Carlton SM:
    Mechanisms of chronic central neuropathic pain after
    spinal cord injury. Brain Res Rev 2009;60(1):202-213.
    This is an excellent review of the genesis of neuropathic
    pain after SCI. In particular the role of posttraumatic inflammation and reactive oxygen species is outlined. A
    better understanding of the physiologic basis behind
    neuropathic pain would be very helpful in developing
    treatment strategies.
    Popovich P, McTigue D: Damage control in the nervous
    system: Beware the immune system in spinal cord injury.
    Nat Med 2009;15(7):736-737.
    This is an outstanding review of the role of inflammation in secondary injury after SCI. It highlights the complexity of the process, and how different elements of the
    inflammatory response at different time points after injury have unique effects.
    Rowland JW, Hawryluk GW, Kwon B, Fehlings MG:

    Orthopaedic Knowledge Update 10

    13.

    Fitch MT, Silver J: CNS injury, glial scars, and inflammation: Inhibitory extracellular matrices and regeneration failure. Exp Neurol 2008;209(2):294-301.
    This is an in-depth review of the inflammatory response
    to SCI and the development of the glial scar at the site
    of injury. It summarizes what is understood about how
    the glial scar impedes axonal regeneration.

    14.

    Rossignol S, Schwab M, Schwartz M, Fehlings MG: Spinal cord injury: Time to move? J Neurosci 2007;27(44):
    11782-11792.
    This is the summary of a symposium held at the 2006
    Society for Neuroscience meeting that reviewed a number of therapeutic strategies for SCI: diminishing the repulsive barriers to axonal regeneration, cell transplants
    to enhance immunologic mechanisms or remyelinate axons, surgical decompression, and rehabilitative training.

    15.

    Kakulas BA: A review of the neuropathology of human


    spinal cord injury with emphasis on special features.
    J Spinal Cord Med 1999;22(2):119-124.

    16.

    Guest JD, Hiester ED, Bunge RP: Demyelination and


    Schwann cell responses adjacent to injury epicenter cavities following chronic human spinal cord injury. Exp
    Neurol 2005;192(2):384-393.

    17.

    Sasaki M, Li B, Lankford KL, Radtke C, Kocsis JD: Remyelination of the injured spinal cord. Prog Brain Res
    2007;161:419-433.
    This is a review of various strategies to promote the remyelination of demyelinated axons within the injured
    cord. It is thought that some axons lose their myelin
    sheathes but are otherwise still intact across the injury
    site. Cells that remyelinate these axons might restore
    conduction and improve function.

    18.

    Bracken MB, Shepard MJ, Collins WF, et al: A randomized, controlled trial of methylprednisolone or naloxone
    in the treatment of acute spinal-cord injury: Results of
    the Second National Acute Spinal Cord Injury Study. N
    Engl J Med 1990;322(20):1405-1411.

    19.

    Bracken MB, Shepard MJ, Holford TR, et al: Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute
    spinal cord injury: Results of the Third National Acute
    Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. JAMA 1997;
    277(20):1597-1604.

    20.

    Akhtar AZ, Pippin JJ, Sandusky CB: Animal studies in


    spinal cord injury: A systematic review of methylprednisolone. Altern Lab Anim 2009;37(1):43-62.
    This is a systematic review of all of the available studies
    in which methylprednisolone was administered in an an-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 44: Spinal Cord Injury

    imal model of acute SCI. It was concluded that in over


    half of the studies, methylprednisolone had no effect (or
    even a deleterious effect). It dispels the widely held notion that methylprednisolone was routinely effective in
    animal studies of SCI a notion that biases clinicians
    into a more optimistic view of the benefits of the drug
    for human patients

    Bregman BS, Kunkel-Bagden E, Schnell L, Dai HN, Gao


    D, Schwab ME: Recovery from spinal cord injury mediated by antibodies to neurite growth inhibitors. Nature
    1995;378(6556):498-501.

    29.

    Freund P, Schmidlin E, Wannier T, et al: Anti-Nogo-A


    antibody treatment promotes recovery of manual dexterity after unilateral cervical lesion in adult primates:
    Re-examination and extension of behavioral data. Eur J
    Neurosci 2009;29(5):983-996.
    This was an important preclinical study in the development of the anti-Nogo-A antibody treatment for acute
    SCI. This antibody targets a protein that inhibits axonal
    regeneration, and here, the authors report that the intrathecal administration of this antibody in a nonhuman
    primate model of cervical SCI does promote recovery of
    hand function.

    30.

    Wannier-Morino P, Schmidlin E, Freund P, et al: Fate of


    rubrospinal neurons after unilateral section of the cervical spinal cord in adult macaque monkeys: Effects of an
    antibody treatment neutralizing Nogo-A. Brain Res
    2008;1217:96-109.
    This study, also in a nonhuman primate model of cervical SCI, found that the administration of the anti-Nogo
    antibody did not prevent rubrospinal neuron atrophy or
    death.

    31.

    McKerracher L, Higuchi H: Targeting Rho to stimulate


    repair after spinal cord injury. J Neurotrauma 2006;
    23(3-4):309-317.

    32.

    Dergham P, Ellezam B, Essagian C, Avedissian H, Lubell WD, McKerracher L: Rho signaling pathway targeted to promote spinal cord repair. J Neurosci 2002;
    22(15):6570-6577.

    33.

    Stirling DP, Koochesfahani KM, Steeves JD, Tetzlaff W:


    Minocycline as a neuroprotective agent. Neuroscientist
    2005;11(4):308-322.

    34.

    Yune TY, Lee JY, Jung GY, et al: Minocycline alleviates


    death of oligodendrocytes by inhibiting pro-nerve
    growth factor production in microglia after spinal cord
    injury. J Neurosci 2007;27(29):7751-7761.

    35.

    Caroni P, Schwab ME: Two membrane protein fractions


    from rat central myelin with inhibitory properties for
    neurite growth and fibroblast spreading. J Cell Biol
    1988;106(4):1281-1288.

    Stirling DP, Khodarahmi K, Liu J, et al: Minocycline


    treatment reduces delayed oligodendrocyte death, attenuates axonal dieback, and improves functional outcome
    after spinal cord injury. J Neurosci 2004;24(9):21822190.

    36.

    Caroni P, Schwab ME: Antibody against myelinassociated inhibitor of neurite growth neutralizes nonpermissive substrate properties of CNS white matter.
    Neuron 1988;1(1):85-96.

    Wells JE, Hurlbert RJ, Fehlings MG, Yong VW: Neuroprotection by minocycline facilitates significant recovery
    from spinal cord injury in mice. Brain 2003;126(Pt 7):
    1628-1637.

    37.

    Pinzon A, Marcillo A, Quintana A, et al: A reassessment of minocycline as a neuroprotective agent in


    a rat spinal cord contusion model. Brain Res 2008;
    1243:146-151.

    Nicholas JS, Selassie AW, Lineberry LA, Pickelsimer EE,


    Haines SJ: Use and determinants of the methylprednisolone protocol for traumatic spinal cord injury in South
    Carolina acute care hospitals. J Trauma 2009;66(5):
    1446-1450, discussion 1450.
    These authors sought to determine if emergency physicians in South Carolina had changed their practice of
    giving methylprednisolone to acute SCI patients, in light
    of the more recent criticisms of the NASCIS trials. They
    found that emergency rooms continued to have protocols for the use of steroids in acute SCI, but only one
    third of SCI patients who arrived at an emergency room
    with such a protocol ultimately received steroids.

    22.

    Suberviola B, Gonzlez-Castro A, Llorca J, Ortiz-Meln


    F, Miambres E: Early complications of high-dose
    methylprednisolone in acute spinal cord injury patients.
    Injury 2008;39(7):748-752.
    These Spanish investigators retrospecitvely reviewed patients with SCI between 1994 and 2005 and compared
    those treated with or without methylprednisolone. Although no improvement in neurologic outcome was
    seen with methylprednisolone, those treated with the
    drug had a significantly higher risk of infectious and
    metabolic complications during their intensive care unit
    stay.

    24.

    25.

    26.

    27.

    Hurlbert RJ, Hamilton MG: Methylprednisolone for


    acute spinal cord injury: 5-year practice reversal. Can J
    Neurol Sci 2008;35(1):41-45.
    In a survey of Canadian spine surgeons who treat acute
    SCI patients, approximately two thirds had abandoned
    the use of methylprednisolone. This was in stark contrast to a survey done by the same authors 5 years previously, in which two thirds of Canadian physicians did
    administer methylprednisolone for acute SCI. This highlights the fact that in the absence of a highly litiginous
    society, Canadian physicians feel free to stop using
    methylprednisolone.
    Eck JC, Nachtigall D, Humphreys SC, Hodges SD:
    Questionnaire survey of spine surgeons on the use of
    methylprednisolone for acute spinal cord injury. Spine
    (Phila Pa 1976) 2006;31(9):E250-E253.

    Schnell L, Schwab ME: Axonal regeneration in the rat


    spinal cord produced by an antibody against myelin-

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    5: Spine

    28.

    21.

    23.

    associated neurite growth inhibitors. Nature 1990;


    343(6255):269-272.

    581

    Section 5: Spine

    This is a replication of a previous study of minocycline


    in an animal model of SCI. In an effort to establish the
    robustness of preclinical evidence for novel therapies
    in animal models of SCI, the National Institutes of
    Health has funded a number of independent replication
    studies. This study was unable to replicate the effectiveness of minocycline in an animal model of SCI.
    38.

    39.

    Inamasu J, Ichikizaki K: Mild hypothermia in neurologic emergency: An update. Ann Emerg Med 2002;
    40(2):220-230.

    40.

    Kwon BK, Mann C, Sohn HM, et al; NASS Section on


    Biologics: Hypothermia for spinal cord injury. Spine J
    2008;8(6):859-874.
    This is an extensive review of the preclinical animal literature and the human literature on the use of both local and systemic hypothermia for acute SCI. At the time
    of this writing, there was no available human literature
    describing the use of systemic hypothermia in acute SCI.

    5: Spine

    41.

    42.

    Layden T: Kevin Everett, The Road Back. Sports Illustrated Dec 17, 2007;107(24):56-67.
    This is the description of Kevin Everetts cervical SCI
    suffered while playing football for the National Football
    Leagues Buffalo Bills. Mr. Everett was treated with systemic hypothermia afterward, raising tremendous interest in the possibility that this treatment influenced his
    significant neurologic recovery.
    Levi AD, Green BA, Wang MY, et al: Clinical application of modest hypothermia after spinal cord injury.
    J Neurotrauma 2009;26(3):407-415.
    This is the report of a small pilot study conducted at the
    University of Miami to study modest systemic hypothermia in acute SCI patients. There was no significant increase in complications associated with systemic hypothermia.

    43.

    Agrawal SK, Fehlings MG: The effect of the sodium


    channel blocker QX-314 on recovery after acute spinal
    cord injury. J Neurotrauma 1997;14(2):81-88.

    44.

    Ates O, Cayli SR, Gurses I, et al: Comparative neuroprotective effect of sodium channel blockers after experimental spinal cord injury. J Clin Neurosci 2007;14(7):
    658-665.
    This study evaluated three different sodium channel
    blockers (phenytoin, mexiletene, and riluzole), in a
    model of rodent thoracic SCI. It found that mexiletene
    and riluzole were both more effective than phenytoin, in
    terms of biochemical and histologic outcomes as well as
    in functional recovery.

    45.

    582

    Saganov K, Orendcov J, Czkov D, Vanick I: Limited minocycline neuroprotection after ballooncompression spinal cord injury in the rat. Neurosci Lett
    2008;433(3):246-249.
    This study found no benefit to using minocycline in a
    rodent model of compressive SCI, which stands in contrast to numerous other studies that do report a neuroprotective benefit.

    Schwartz G, Fehlings MG: Evaluation of the neuropro-

    Orthopaedic Knowledge Update 10

    tective effects of sodium channel blockers after spinal


    cord injury: Improved behavioral and neuroanatomical
    recovery with riluzole. J Neurosurg 2001;94(2, Suppl):
    245-256.
    46.

    Choi DW: Excitotoxic cell death. J Neurobiol 1992;


    23(9):1261-1276.

    47.

    Palmer GC: Neuroprotection by NMDA receptor antagonists in a variety of neuropathologies. Curr Drug Targets 2001;2(3):241-271.

    48.

    Gok B, Okutan O, Beskonakli E, Kilinc K: Effects of


    magnesium sulphate following spinal cord injury in rats.
    Chin J Physiol 2007;50(2):93-97.
    This study evaluated magnesium sulfate as an early neuroprotective agent in thoracic SCI. It reported a reduction in posttraumatic neutrophil invasion and improved
    hindlimb motor function with the administration of 600
    mg/kg magnesium sulfate.

    49.

    Wiseman DB, Dailey AT, Lundin D, et al: Magnesium


    efficacy in a rat spinal cord injury model. J Neurosurg
    Spine 2009;10(4):308-314.
    This study evaluated magnesium sulfate in a thoracic
    model of SCI. The authors report increased white matter sparing at the injury site and improved locomotor
    function in animals treated with magnesium sulfate.

    50.

    Kwon BK, Roy J, Lee JH, et al: Magnesium chloride in


    a polyethylene glycol formulation as a neuroprotective
    therapy for acute spinal cord injury: Preclinical refinement and optimization. J Neurotrauma 2009;26(8):
    1379-1393.
    This paper reports a series of experiments conducted to
    refine a magnesium chloride formulation with PEG, in
    preparation for human translation. It describes testing
    different doses and time windows of intervention, and
    reveals a time window of 4 to 8 hours for tissue neuroprotection.

    51.

    Keirstead HS, Nistor G, Bernal G, et al: Human embryonic stem cell-derived oligodendrocyte progenitor cell
    transplants remyelinate and restore locomotion after
    spinal cord injury. J Neurosci 2005;25(19):4694-4705.

    52.

    The Medical News. FDA places Geron Corporations


    IND for spinal cord injury on clinical hold. http://
    www.news-medical.net/news/20090819/FDA-placesGeron-Corporations-IND-for-spinal-cord-injury-onclinical-hold.aspx. Accessed August 19, 2009.
    This media report described the FDAs decision to put
    Geron on hold for its clinical trial. In January 2009, the
    approval to proceed with Geron was received. Of concern was the appearance of cystlike structures in preclinical models, prompting the need for longer term
    follow-up to rule out tumor formation.

    53.

    Geisler FH, Coleman WP, Grieco G, Poonian D; Sygen


    Study Group: The Sygen multicenter acute spinal cord
    injury study. Spine (Phila Pa 1976) 2001;26(24, suppl):
    S87-S98.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 44: Spinal Cord Injury

    54.

    Fawcett JW, Curt A, Steeves JD, et al: Guidelines for the


    conduct of clinical trials for spinal cord injury as developed by the ICCP panel: Spontaneous recovery after
    spinal cord injury and statistical power needed for therapeutic clinical trials. Spinal Cord 2007;45(3):190-205.

    55.

    Lammertse D, Tuszynski MH, Steeves JD, et al; International Campaign for Cures of Spinal Cord Injury Paralysis: Guidelines for the conduct of clinical trials for spinal cord injury as developed by the ICCP panel: Clinical
    trial design. Spinal Cord 2007;45(3):232-242.

    56.

    Steeves JD, Lammertse D, Curt A, et al; International


    Campaign for Cures of Spinal Cord Injury Paralysis:
    Guidelines for the conduct of clinical trials for spinal
    cord injury (SCI) as developed by the ICCP panel: Clinical trial outcome measures. Spinal Cord 2007;45(3):
    206-221.

    57.

    Tuszynski MH, Steeves JD, Fawcett JW, et al; International Campaign for Cures of Spinal Cord Injury Paralysis: Guidelines for the conduct of clinical trials for spinal cord injury as developed by the ICCP panel: Clinical
    trial inclusion/exclusion criteria and ethics. Spinal Cord
    2007;45(3):222-231.
    These four papers were produced by the International
    Campaign to Cure Paralysis to provide guidance to the
    SCI community around the conduct of clinical trials for
    SCI. They characterize the degree of spontaneous neurologic recovery and how this influences trial design. They
    outline how such trials should be designed, the types of
    inclusion/exclusion criteria that should be applied, and
    the types of outcome measures that should be used.
    These are important guidance documents for the field
    of SCI.

    5: Spine

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    583

    Chapter 45

    Adult Spinal Deformity


    Michael D. Daubs, MD

    Definition
    Adult spinal deformity is defined by the Scoliosis Research Society as a spinal deformity with any etiology in
    a skeletally mature patient. Scoliosis is defined as lateral
    deviation of the normal vertical line of the spine of
    greater than 10 when measured on radiographs. This
    definition covers a wide range of spinal disorders, including many that begin in childhood. The key component
    in the definition is the requirement for skeletal maturity.
    The various etiologies leading to deformity may have
    unique clinical presentations, but the resultant spinal
    deformities in a skeletally mature patient are evaluated
    in a similar methodic manner. Regardless of whether
    the primary deformity is scoliosis with coronal imbalance or failed arthrodesis with fixed sagittal imbalance,
    the overall treatment principles remain the same.

    Indications and Treatment Goals

    Dr. Daubs or an immediate family member serves as a


    paid consultant to or is an employee of Synthes and has
    received research or institutional support from Stryker.

    2011 American Academy of Orthopaedic Surgeons

    5: Spine

    The primary goals in treating adult spinal deformity are


    to gain spinal balance, halt the progression of deformity, reduce pain, and improve the patients healthrelated quality of life (HRQL). Treatment should improve the patients outcome above the natural history
    of the disease and avoid any deleterious long-term effects. The success of intervention is measured using validated HRQL measurement tools, which include both
    general health (Medical Outcomes Study 36-Item Short
    Form and the EuroQol-5) and disease specific (Scoliosis
    Research Society-30 and Oswestry Disability Index)
    outcome measures. To date, the treatment of adult scoliosis or adult deformity in general has not been evaluated with published randomized controlled trials with
    level I evidence. However, the clinical and radiologic
    factors that most significantly correlate with patient
    symptoms and functional outcomes have recently been
    elucidated in large case series.1,2
    The only study of the natural history of adult scoliosis evaluated patients with untreated adolescent idiopathic scoliosis.3 At a mean follow-up of 51 years
    (range, 44 to 61 years), the authors reported mean

    Cobb angles of 84, 89, and 49 for the thoracic, thoracolumbar, and lumbar spines, respectively. The study
    showed no difference in survival rates compared with
    the general population. More patients with scoliosis
    (77%) reported little to moderate low back pain than
    the control group (35%), but there was no overall difference in the ability to perform activities of daily living. Based on this study, it appears that many patients
    are able to tolerate high magnitudes of coronal deformity and maintain reasonable function. However, many
    patients with scoliosis have severe pain and functional
    impairment associated with curve progression and spinal imbalance. The indications for surgical treatment in
    adults with spinal deformity must be individualized and
    based on the patients symptoms, functional impairment, evidence of curve progression, and expectations.
    Although previous studies have shown that curves
    greater than 45 can progress after maturity,4 the results cannot be generalized. The best evidence for future curve progression is an individual patients documented history of progression.

    Patient Evaluation

    Clinical Evaluation
    Low back pain is the most common symptom reported
    by patients with adult spinal deformity. Symptoms of
    low back pain are also common in the general population and cannot be immediately attributed to scoliosis.
    A thorough history and examination is necessary to
    rule out other potential causes. In general, patients
    younger than 40 years with adult scoliosis present with
    symptoms similar to those of younger patients with adolescent idiopathic scoliosis. Typically, a patients primary concerns are the probability for curve progression
    and the potential for long-term sequelae, poor cosmesis, and low back pain. As patients with adult idiopathic scoliosis age, their presentation is similar to
    those with degenerative spinal conditions. Patients
    older than 40 years may more often report low back
    pain, radicular leg pain, and neurogenic claudication.
    The etiology of these symptoms should be evaluated in
    a manner similar to that used in evaluating patients
    without scoliosis. Psychosocial issues can impact the
    treatment of all patients, including those with a spinal
    deformity, and should be considered in the clinical evaluation.

    Orthopaedic Knowledge Update 10

    585

    Section 5: Spine

    Figure 1

    Illustration of the radiographic measurement for


    sagittal balance. C7PL = C7 plumb line.

    5: Spine

    In addition to a thorough neurologic evaluation, a


    physical examination should be performed to evaluate
    gait and standing balance. Observing the patients gait
    permits an evaluation of spinal balance while in motion. Many patients with scoliosis may stand erect in
    sagittal and coronal balance; however, ambulation
    causes fatigue, which may result in positive sagittal imbalance. Because patients with fixed sagittal imbalance
    often pitch forward progressively when ambulating any
    distance, hip and knee range of motion should be
    closely examined. Knees should be fully extended when
    evaluating standing balance. Hip range of motion
    should be evaluated to rule out hip flexion contractures
    as a contributing source of sagittal imbalance.
    In general, adults with spinal deformity should be
    clinically evaluated in a manner similar to that used for
    patients presenting with a spinal disorder. The source
    of the patients complaint, such as low back or leg pain,
    should be evaluated first. The unique dimensions of a
    deformity, whether it is scoliosis or fixed sagittal imbalance, should then be considered in the overall evaluation and treatment plan.

    Radiographic Evaluation
    Standing, 36-inch PA and lateral radiographs are
    needed to evaluate adult spinal deformity. The knees
    586

    Orthopaedic Knowledge Update 10

    Figure 2

    Illustration of the radiographic measurement


    for coronal balance. C7PL = C7 plumb line,
    CSVL = central sacral vertical line.

    should be fully extended for the lateral radiograph to


    ensure accurate assessment of sagittal balance. The cervical, thoracic, and lumbar spines as well as the pelvis
    and hip joints should be visible. Cobb angles, coronal
    and sagittal balance, and pelvic incidence should be
    measured and recorded (Figures 1 through 3). Supine
    AP and lateral full-length 36-inch radiographs are helpful in determining the flexibility of coronal and sagittal
    plane deformities. Radiographs taken with the patient
    bending can be used to assess the flexibility of coronal
    plane deformities and may aid in surgical decision making, especially in younger adults who can be classified
    with the Lenke system.5 CT with myelography may better assess spinal canal stenosis in patients with moderate to severe coronal deformity, whereas MRI may be
    adequate to assess patients with more minor curves.

    Types of Adult Spinal Deformity


    Any spinal disorder or disease that leads to scoliosis or
    coronal or sagittal imbalance in a skeletally mature patient is considered an adult spinal deformity. The most
    common categories are adult idiopathic scoliosis, adult
    de novo scoliosis, and fixed sagittal imbalance. Several

    2011 American Academy of Orthopaedic Surgeons

    Chapter 45: Adult Spinal Deformity

    neuromuscular disorders, such as cerebral palsy, spinal


    muscle atrophy, Duchenne muscular dystrophy, poliomyelitis, and posttraumatic conditions can cause spinal
    deformities in adulthood. Later onset adult diseases,
    such as Parkinson disease and multiple sclerosis, also
    can cause spinal deformity.

    Adult Scoliosis

    2011 American Academy of Orthopaedic Surgeons

    Figure 3

    Illustration showing the angles and measurements for pelvic incidence (a), sacral slope (b),
    and pelvic tilt (c). SS = sacral slope, PI = pelvic
    incidence, PT = pelvic tilt, VRL = vertical reference line, HRL = horizontal reference line.

    Patients who are surgically treated for scoliosis report


    increased preoperative low back and leg pain and
    greater loss of function when compared with those who
    were not surgically treated.13 In younger patients, curve
    magnitude is a more important factor in choosing surgical intervention.

    5: Spine

    Adult idiopathic scoliosis is defined as scoliosis in a


    skeletally mature patient that existed in childhood or
    adolescence. Adult de novo scoliosis, or degenerative
    scoliosis as it is commonly termed, is a condition that
    did not existent before skeletal maturity and developed
    in adulthood. The overall prevalence of adult scoliosis
    increases with age.6 Adult degenerative scoliosis predominantly develops in the thoracolumbar spine;7 however, compensatory curves can also develop in the thoracic spine. The incidence of low back pain in patients
    with untreated adolescent idiopathic scoliosis (mean
    age, 66 years) was higher than in a matched cohort
    (67% versus 35%). Most of the patients rated the intensity of pain as low or moderate.3 There was no difference in the incidence of low back pain symptoms between cohorts of patients with and without adult
    degenerative scoliosis.7,8 A separate cohort study evaluating scoliosis and nonscoliosis patients with low back
    pain reported that increased pain in the group with scoliosis correlated with greater curve magnitude and rotation.9 Loss of lumbar lordosis and thoracolumbar kyphosis also has been shown to correlate with a greater
    incidence of reported low back pain.10
    When evaluating HRQL outcome measures with radiographic parameters in adult scoliosis, curve magnitude was not found to be a significant factor, but patients with thoracolumbar and lumbar curves scored
    worse than patients with thoracic curves.1 This finding
    agrees with the natural history of untreated adolescent
    idiopathic scoliosis.3 A smaller series showed that
    worse patient-reported outcomes correlated with coronal imbalance greater than 5 cm, increased lateral listhesis (> 6 mm), and loss of lordosis.11 In the largest
    case series to date evaluating radiographic parameters,
    sagittal balance was the most reliable radiographic predictor of HRQL outcomes.1,2 Patients with positive sagittal balance greater than 5 cm reported worse pain,
    physical function, and self-image.
    In an attempt to better understand the factors that
    ultimately lead to surgical treatment for adult scoliosis,
    several studies12-15 have retrospectively reviewed radiographic, clinical, and HRQL measures comparing surgically and nonsurgically treated groups. Overall, the
    surgically treated group reported greater frequency of
    leg pain, moderate to severe low back pain, and curves
    of greater magnitude.
    As patients with adult scoliosis age, advancing degeneration leads to an increased incidence of low back
    pain of varying intensities. Lumbar and thoracolumbar
    curves are more symptomatic. HRQL measurements
    appear to be more influenced by the loss of lumbar lordosis and sagittal imbalance than by curve magnitude.

    Nonsurgical Treatment
    There is little consensus and only weak evidence for the
    effectiveness of any one nonsurgical treatment method
    for adult scoliosis and adult deformity in general.16
    Typically, the recommended nonsurgical treatment is
    based on the chief symptoms reported by the patient. If
    low back pain is the main symptom, a structured physical therapy program based on the patients physical capabilities is recommended, with emphasis on core
    strengthening and spinal balance. Radicular leg pain is
    often treated with selective nerve root injections, which
    can be helpful in localizing the pain generator; however, lumbar epidural injections for low back pain associated with scoliosis have poor lasting effectiveness.17
    Symptoms of neurogenic claudication associated with
    scoliosis and stenosis are seen in older patients with
    adult scoliosis. Nonsurgical treatment of lumbar stenosis is not as effective as surgical decompression.18
    Surgical Treatment
    The surgical decision-making process for adult scoliosis is difficult. The procedures are often complex, full

    Orthopaedic Knowledge Update 10

    587

    Section 5: Spine

    recovery can take up to 1 year, and complication rates


    as high as 20% have been reported in older patients.19
    Patients are often confused about their prognosis and
    fearful of the potential effects of scoliosis on their general health and appearance. Taking time to discuss the
    natural history of the condition and the risks for progression are helpful in alleviating the patients fear
    and anxiety. Properly informing patients of the treatment options, including a thorough discussion of potential complications, is crucial for shared decision
    making.
    The goals of surgical treatment are relief of leg and
    back pain, curve stabilization, and the achievement of
    spinal balance.
    Curve Correction
    Although there is evidence that coronal imbalance
    greater than 4 to 5 cm correlates with a reduced health
    status,1,11 there is no evidence that surgical correction
    of coronal imbalance correlates with improved outcomes. The most important predictor of outcomes is
    spinal sagittal balance; however, restoring lumbar lordosis to achieve sagittal balance often requires some degree of curve correction. In adults, thoracolumbar and
    lumbar curves are relatively more flexible than thoracic
    curves. As a result, overcorrection of the lumbar curve
    may result in coronal imbalance. It should be stressed
    that spinal balance is more important than radiographic curve correction. Intraoperative PA full-length
    radiographs, obtained after instrumentation and any
    corrective maneuvers are performed, are useful in determining if spinal balance was achieved.

    5: Spine

    Selection of Fusion Levels


    Selecting the appropriate cephalad and caudad levels
    for fusion remains an area of controversy. In a patient
    younger than 40 years with adult idiopathic scoliosis,
    the selection of fusion levels correlates more closely
    with recommendations for adolescent idiopathic scoliosis. The Lenke classification system can be applied and
    used as a general reference.5,20 As the patient ages,
    curves that were once nonstructural and minor become
    rigid and must be treated in adulthood as true double
    or triple major curves.
    In adults with thoracolumbar-lumbar curves, the
    decision-making process is more difficult. It has been
    commonly taught that a fusion should not end proximal to the thoracolumbar junction, but should cross
    the thoracolumbar junction and end in the lower thoracic spine.21 A recent report, however, questioned this
    principle, and showed no difference in outcomes or the
    incidence of proximal junctional-related complications,
    regardless of whether the proximal end level of fusion
    was at T9, T11, or L1.22 The authors recommended
    that fusions end proximally at the stable, neutral vertebrae, and that ending the fusion at the apex of the thoracic kyphosis should be avoided.
    In adults, determining the distal extent of the fusion
    typically involves the decision whether to fuse to L5 or
    the sacrum, and whether pelvic fixation should be used.
    588

    Orthopaedic Knowledge Update 10

    In a group of patients (mean age, 45 years) with long


    fusions to L5, advanced disk degeneration at the L5-S1
    disk developed in 69% of the patients, and 23% were
    subsequently treated with extension of the fusion to the
    sacrum. Extension to the sacrum was recommended in
    an additional 19% of patients, but medical morbidities
    prevented the procedure.23 The high rate of disk degeneration and subsequent forward shift in sagittal alignment associated with long fusions to L5 must be
    weighed against the added morbidity of sacropelvic fixation and fusion to the sacrum.24,25 Increased consensus
    on the indications for extending a long fusion to the sacrum include L5-S1 spondylolisthesis, L5-S1 stenosis,
    oblique takeoff of L5, prior L5-S1 laminectomy, and severe L5-S1 disk degeneration.26
    The addition of iliac screws to augment lumbosacral
    fixation when fusing to the sacrum has shown good results at 5-year follow-up with an overall successful fusion rate of 92%.27,28 Three of the five reported nonunions occurred in cases in which no anterior column
    support was used. With anterior column support, sacral
    and iliac screw fixation achieved a 96% fusion rate.28
    No sacral screw pull-outs, fractures, or loosening was
    reported; however, iliac screw loosening was reported in
    43% of patients and breakage in 5%. When extending
    a long fusion to the sacrum, the use of illiac screw fixation and anterior column support (anterior lumbar interbody fusion, posterior lumbar interbody fusion, or
    transforaminal lumbar interbody fusion) decreases the
    rate of sacral fixation failure and pseudarthrosis.28
    Approach
    In the traditional treatment of scoliosis, anterior release
    combined with or without anterior fusion was believed
    to improve curve correction and restore alignment, especially in patients with a rigid curve. However, the anterior thoracolumbar approach can be associated with
    morbidity. In one study, chronic pain was associated
    with an anterior thoracolumbar wound in 32% of patients, and 45% reported asymmetry and abdominal
    bulging.29 Recent trends have moved toward posteriorbased approaches, with rigid pedicle-based instrumentation and resection osteotomies. Recently published
    studies reported no difference in curve correction in
    adult patients treated with anterior release and a posterior instrumented fusion compared with patients treated
    with a posterior-only approach, including resection osteotomies when indicated.30-32 Although the added morbidity of an anterior approach has not been compared
    directly with the morbidity associated with posterior osteotomies in the treatment of adult scoliosis, anterior release for adult scoliosis may not be necessary to achieve
    comparable coronal correction and outcomes.
    Decompression
    Up to 64% of patients with adult scoliosis present with
    reports of leg pain associated with stenosis.17 Adequate
    neural decompression is the first treatment priority. A
    wide central decompression may provide adequate
    treatment in many patients, but a focal radiculopathy

    2011 American Academy of Orthopaedic Surgeons

    Chapter 45: Adult Spinal Deformity

    secondary to foraminal stenosis may require further intervention. Focal radiculopathy often occurs at the
    apex on the concave side of a lumbar curve where there
    is vertebral body rotation and translation. Partially correcting the curve with distraction and in situ rod bending, along with a wide foraminal decompression
    through the pars interarticularis, may adequately open
    the foramen. If this technique is not successful, an
    added posterior lumbar interbody fusion or transforaminal lumbar interbody fusion may be necessary to
    achieve and maintain foraminal patency. An anterior
    lumbar interbody fusion through a standard anterior
    retroperitoneal or a direct lateral transpsoas approach
    also may be effective.

    Fixed Sagittal Imbalance Syndrome


    Fixed sagittal imbalance is defined as radiographic sagittal imbalance of more than 5 cm. This syndrome has
    multiple etiologies (Table 1), all of which result in pos-

    2011 American Academy of Orthopaedic Surgeons

    Causes of Fixed Sagittal Imbalance


    Iatrogenic
    Fusion in hypolordosis
    Proximal junctional kyphosis (above a fused segment)
    Ankylosing spondylitis
    Congenital kyphosis
    Posttraumatic conditions
    Osteoporotic compression fractures
    Infection
    Neoplasm

    itive sagittal balance and the inability of the patient to


    stand upright. Aging is the most common cause of disk
    degeneration and height loss. With age, thoracic kyphosis increases and lumbar lordosis decreases. Most
    patients are able to maintain their sagittal balance with
    advancing age.37 Patients who become symptomatic are
    unable to compensate for the loss of lumbar lordosis
    through hip extension/pelvic retroversion and knee
    flexion, which eventually results in positive sagittal balance (Figure 1). Patients typically present with chronic
    low back pain that worsens with prolonged standing
    and a pitched forward posture with knees in flexion.
    Extensor muscle fatigue can cause diffuse back pain
    that may extend to the thoracic and cervical regions.
    Global sagittal balance is the result of the harmonious combination of lumbar lordosis, thoracic kyphosis,
    and cervical lordosis. Each anatomic region of the spine
    is interconnected; a change in curvature in one region
    causes a response in the other regions to balance the
    head and maintain the center of gravity over the pelvis.
    Because the pelvis is the foundation or base of the
    spine, its morphology influences the magnitude of curvature in the other regions. Pelvic incidence is a fixed,
    anatomic parameter of the pelvis that influences sagittal alignment. An understanding of pelvic incidence is
    critical in formulating the appropriate options for treating fixed sagittal imbalance.

    5: Spine

    Limited Decompression and Fusion


    The role for limited decompression without fusion and
    decompression with limited fusion in adult scoliosis is
    not well defined. Typically, the patient being considered
    for treatment with a limited approach is older, has unilateral or bilateral leg pain symptoms secondary to
    lumbar stenosis, and minimal or no back pain. The
    goal of a focused treatment is to address the primary
    symptomatic pathology (lumbar stenosis) without causing iatrogenic instability and rapid curve progression.
    The destabilizing effect of complete unilateral or bilateral facetectomy in the lumbar spine is well reported.33 Unilateral or bilateral limited laminotomy
    with partial facetectomy and preservation of the midline structures is less destabilizing;34 however, the relevancy of these biomechanical studies to effects in the
    deformed spine is unknown. A partial facetectomy
    may be sufficient to destabilize the apex segment of a
    curve.
    In general, a limited decompression may be considered in patients with leg pain only, lumbar curves of less
    than 20 minimal rotation, no radiographic instability
    (< 4 mm motion on dynamic radiographs and < 2 mm
    lateral translation), and no significant sagittal or coronal imbalance.35,36 Indications for decompression with
    limited fusion are even less clear. In curves less than
    20, with an unstable segment (degenerative spondylolisthesis), decompression and fusion of the unstable
    segment alone may be adequate. If the unstable segment is located outside of the major curve, limited fusion also can be considered.35,36 In general, ending a fusion adjacent to the apex of a coronal or sagittal curve
    is not recommended.
    There are no quality randomized or cohort studies
    comparing outcomes of the limited approach with the
    standard approach for treating adult scoliosis with associated stenosis. The previous discussion presented
    general guidelines; all patients should be counseled on
    the risks of progression and the possible need for additional surgery.

    Table 1

    Pelvic Incidence
    Pelvic incidence is defined as the angle between the line
    perpendicular to the middle of the sacral end plate and
    the line joining the middle of the sacral end plate to the
    center of the bicoxofemoral axis38 (Figure 3). Pelvic incidence correlates strongly with sacral slope, pelvic tilt,
    and lumbar lordosis.39 In simplified terms, pelvic incidence (a constant anatomic measurement determined
    by an individuals unique pelvic morphology) determines the sacral slope, which in turn determines the angle of take off of the lumbar spine in the sagittal plane
    and the resultant magnitude of lumbar lordosis. Normalized values for pelvic incidence, sacral slope, and
    pelvic tilt have been studied39,40 (Table 2). Adult females have slightly higher angles of pelvic incidence,

    Orthopaedic Knowledge Update 10

    589

    Section 5: Spine

    Table 2

    Normal Values for Pelvic Incidence, Sacral Slope, and Pelvic Tilt
    Population

    Radiographic Parameters (in degrees)


    Pelvic Incidence

    Sacral Slope

    Pelvic Tilt

    Children and adolescents (ages 3 to 18 years)


    Male

    49.2 11.2

    41.7 8.4

    49.2 11.2

    Female

    49.7 10.7

    41.2 8.0

    8.5 8.3

    Adults (ages 19 to 50 years)


    Male

    53.2 10.3

    41.9 8.7

    11.9 6.6

    Female

    48.2 7.0

    38.2 7.8

    10.3 4.8

    sacral slope, and lumbar lordosis than their male cohorts.


    Several studies, have confirmed the relationship between pelvic incidence, sacral slope, pelvic tilt, and
    global spinal balance.38,39,41-43 Each anatomic region of
    the spine and pelvis are interdependently connected to
    achieve spinal balance and upright posture. When a patient exhausts all compensatory mechanisms (pelvic retroversion, hip extension, knee flexion, thoracic
    hypokyphosis/extension) to stand upright, fixed sagittal
    imbalance syndrome ensues and the HRQL is negatively impacted.2,44

    5: Spine

    Treatment
    The recommended surgical treatment of fixed sagittal
    imbalance is dependent on the amount of positive sagittal imbalance, the degree of flexibility of the deformity, and whether the kyphosis is focal (limited to a
    few spinal segments; for example, posttraumatic kyphosis) or multilevel (involving several spinal segments;
    for example, Scheuermann kyphosis). Pelvic incidence
    is also important in determining the amount of correction that is needed45 (a patient with a higher pelvic incidence may need more lumbar lordosis to adequately
    correct sagittal balance). In general, fixed sagittal imbalance is surgically treated with four proceduresan
    interbody fusion, a Smith-Petersen osteotomy, a pedicle
    subtraction osteotomy, and a vertebral column resection.46
    Interbody Fusion
    Interbody fusion is limited to use in patients with minor sagittal imbalance (6 to 8 cm). Two thirds of lumbar lordosis occurs through the L4-L5 and the L5-S1
    segments. Lumbar lordosis can be improved by restoring the disk height at L4-L5 and L5-S1 through the use
    of structural interbody allograft or cages. Because of
    the technical challenges and potential complications of
    inserting larger grafts or cages through the posterior
    approaches (transforaminal or posterior lumbar interbody fusions), anterior lumbar interbody fusion is pre590

    Orthopaedic Knowledge Update 10

    ferred by many surgeons as a more effective method of


    regaining lordosis. For example, in a patient with a
    prior thoracolumbar fusion extending to L4 with disk
    degeneration and sagittal imbalance of 8 cm, an anterior lumbar interbody fusion at L4-L5 and L5-S1 may
    restore enough lordosis to obtain sagittal balance.
    Smith-Petersen Osteotomy
    Smith-Petersen osteotomies are usually performed at
    multiple levels and can restore as much as 10 of lordosis per level depending on the amount of disk mobility.
    A Smith-Petersen osteotomy will not be successful if
    there is anterior fusion, and/or will provide minimal
    correction if there is minimal disk height associated
    with large osteophytes. Less correction per level can be
    expected in the thoracic spine because less disk mobility is typical in this area. Smith-Petersen osteotomies
    can be added to the anterior lumbar interbody fusion
    or used in conjunction with a pedicle subtraction osteotomy to increase the magnitude of lordosis correction. Smith-Petersen osteotomies are commonly used to
    treat Scheuermann kyphosis, lesser degrees of thoracolumbar kyphosis, and can be used as a method of restoring lordosis and improving correction in thoracolumbar scoliosis.
    Pedicle Subtraction Osteotomy
    A pedicle subtraction osteotomy is indicated in patients
    with more severe sagittal imbalance (> 12 cm).46 A correction of 30 to 35 can be expected in the lumbar
    spine and 25 in the thoracic spine.47 These osteotomies
    are effective in treating focal kyphosis and can be used
    to treat severe scoliosis, with an asymmetric correction
    in the sagittal and coronal planes (Figure 4). Pedicle
    subtraction osteotomy can also be used when a prior
    circumferential fusion has been performed. A recent
    study (minimum 5-year follow-up) on the use of pedicle
    subtraction osteotomies for fixed sagittal imbalance reported no loss of regional correction in lordosis, and
    only a minor increase in positive sagittal balance.48 The
    pseudarthrosis rate was 29%; no instances of pseudar-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 45: Adult Spinal Deformity

    5: Spine

    Figure 4

    A 52-year-old woman with progressive adult idiopathic thoracolumbar kyphoscoliosis was treated with an asymmetric L1 pedicle subtraction osteotomy and a T3 to L5 thoracic and lumbar fusion. A, Preoperative AP radiograph.
    B, Preoperative AP clinical photograph. C, Preoperative lateral radiograph. D, Preoperative lateral clinical photograph. E, Postoperative AP radiograph. F, Postoperative AP clinical photograph. G, Postoperative lateral radiograph. H, Postoperative lateral clinical photograph.

    throsis occurred at the osteotomy site, with most occurring at the thoracolumbar junction. The neurologic
    complications of pedicle subtraction osteotomies were
    evaluated in 108 patients with 10-year follow-ups.49
    The overall rate of neurologic deficits (defined as
    bowel/bladder loss, or motor loss of two or more

    2011 American Academy of Orthopaedic Surgeons

    grades) was 11%, with permanent deficits in only 3%


    of patients. The mean correction in sagittal balance was
    11 cm.
    Vertebral Column Resection
    Vertebral column resections are indicated for the cor-

    Orthopaedic Knowledge Update 10

    591

    Section 5: Spine

    rection of rigid, angular kyphosis in the thoracic spine;


    severe rigid scoliosis; congenital kyphosis; hemivertebrae resection in the thoracic and lumbar spines; and
    kyphotic deformity associated with tumor, fracture, or
    infection in the thoracic spine. Vertebral column resections are more commonly performed in the thoracic
    spine and provide more correction than pedicle subtraction osteotomies. Resections also can be performed
    in the lumbar spine, but are more technically difficult
    because of the position of the lumbar nerve root. In one
    report, the mean correction with a vertebral column resection was 62 in the coronal plane and 45 in the sagittal plane.50 Vertebral column resection is an effective
    treatment of severe, rigid deformities. Neurologic monitoring is highly recommended. In a study of 43 patients treated with vertebral column resection (93% at
    the spinal cord level), 18% of patients lost motorevoked potentials during the procedure, but all returned to normal baseline values with surgical intervention; no permanent injuries were reported.51

    Neuromuscular Adult Scoliosis

    5: Spine

    Neuromuscular adult scoliosis covers a broad range of


    conditions, including cerebral palsy, spinal muscle atrophy, Duchenne muscular dystrophy, poliomyelitis, and
    paraplegia. Adult-onset conditions such as multiple
    sclerosis and Parkinson disease, which cause general
    weakness and balance problems, can also cause
    neuromuscular-type deformities. Adults typically present with pain and/or progressive deformity. The deformity can occur in any region of the spine, with the patient presenting with kyphosis, lordosis, and/or sagittal
    and coronal imbalance. Often, there is a long sweepingtype deformity, which may be flexible in the young
    adult patient. The deformities associated with multiple
    sclerosis and Parkinson disease may be flexible at the
    early onset of the disease in middle-aged and older
    adults but may become progressively rigid with time.
    Reducing pain, halting deformity progression, and
    achieving spinal balance are the goals of treatment. In a
    patient who is confined to a wheelchair, sitting balance
    is key to allowing efficient use of the upper extremities
    and preventing skin breakdown. Because a high rate of
    surgical complications occurs in this group of patients,
    proper counseling regarding expected outcomes is important. In one of the few studies evaluating spinal surgery in patients with Parkinson disease, the rate of revision surgery was 86% and the infection rate was
    14%.52

    showed that changes in transcranial electric motorevoked potentials were detected earlier than changes in
    somatosensory-evoked potentials.53 Twenty-six patients
    had decreases in amplitude of 65% in transcranial electric motor-evoked potentials during posterior instrumentation and corrective maneuvers. Nine (35%) of
    these patients (0.8% of the study group) had a transient motor or sensory deficit postoperatively, all of
    which were detected by transcranial electric motorevoked potentials. Changes in somatosensory-evoked
    potentials occurred, on average, 5 minutes after the initial changes detected by the transcranial electric motorevoked potentials, and somatosensory-evoked potentials failed to detect a motor deficit in 4 of 7 patients.
    With early detection and subsequent changes in the surgical course of action, all deficits resolved by 90 days
    postoperatively. Although the results of this study cannot be generalized to the treatment of adult deformity,
    especially with regard to the rate of neurologic recovery
    following corrective maneuvers, it does provide excellent evidence of the potential benefits of transcranial
    electric motor-evoked potentials and intraoperative
    neurophysiologic monitoring of the spinal cord. The
    January 2009 position statement of the Scoliosis Research Society (www.srs.org) recommends the use of intraoperative neurophysiologic monitoring during the
    surgical correction of spinal deformity and considers it
    the preferred method for the early detection of impending or evolving spinal cord deficits.
    The evidence for monitoring intraoperative nerve
    root function with electromyography is less clear and is
    controversial. The effective use of electromyography
    for evaluating pedicle screw placement in the thoracic54
    and lumbar55 spine has been reported. Its role in preventing or detecting intraoperative nerve root injury is
    less clear.49,56 In a large series of adult patients treated
    with lumbar pedicle subtraction osteotomy for adult
    deformity, electromyography failed to detect any of the
    reported nerve root injuries.49 In many patients with
    adult deformity, even in surgery primarily involving the
    lumbar spine, the procedure involves manipulation or
    instrumentation of the upper lumbar or thoracolumbar
    region where the cord and/or conus may be affected.
    Intraoperative neurophysiologic monitoring is widely
    used and preferred in most surgical procedures for
    adult spinal deformity.

    Challenges

    The Aging Spine


    Intraoperative Neurophysiologic Monitoring
    The evidence in support of the routine use of intraoperative neurophysiologic monitoring during the treatment of spinal deformity has strengthened. Its use aids
    in the early detection of impending spinal cord injury
    and may prevent worsening postoperative morbidity. A
    study of more than 1,000 patients (mean age, 14 years)
    surgically treated for adolescent idiopathic scoliosis
    592

    Orthopaedic Knowledge Update 10

    The rate of complications in adult deformity surgery increase as the complexity of the surgery increases. As the
    population ages, there has been an increase in the number of older patients who are being surgically treated
    for major spinal deformities. Many complications are
    related to medical comorbidities and osteoporosis. The
    rate of major complications in patients older than 60
    years was 20% in one series, with the rate of complications significantly increasing in patients older than 69

    2011 American Academy of Orthopaedic Surgeons

    Chapter 45: Adult Spinal Deformity

    years.19 Aggressive medical treatment and newer pharmacotherapies may reduce the risks of spinal implant
    failure in the osteoporotic spine. Methylmethacrylate
    augmentation of pedicle screw fixation improves pullout strength and is a viable option in severe cases.57-59
    Despite the higher risk of complications, older patients
    have significant improvement in HRQL when compared with those treated nonsurgically.19,60

    Corrective Osteotomies
    Pedicle subtraction osteotomies and vertebral column
    resections allow the correction of rigid sagittal and coronal deformities, but there are increased risks with
    these techniques. The incidence of neurologic deficits
    was as high as 11% in one study, but most of the injuries were limited to the nerve root levels and eventually
    resolved.49 The rate of pseudarthrosis with pedicle subtraction osteotomies was reported as high as 28% at
    5-year follow-up; however, after revision surgery the
    HRQL measures improved and were not significantly
    different from those of patients without psuedoarthosis.48 Vertebral column resections are associated with a
    higher rate of neurologic deficits and intraoperative
    neurophysiologic monitoring changes.50,51 With monitoring, the detection of potential spinal cord deficits
    can be detected early and permanent deficits can be
    avoided.51 Intraoperative neurophysiologic monitoring
    is highly recommended for these procedures.

    with fewer associated costs and complications. Drugcoated eluting devices are a future possible development. Less invasive surgical methods, such as the lateral lumbar and transpsoas interbody fusion
    approaches and percutaneously placed instrumentation
    systems, may have a role in adult deformity surgery.64
    Genetic research may allow the personalization of
    treatment options and early intervention to prevent the
    onset of severe deformity or may eradicate spinal disease through gene therapy.65
    The treatment of adult spinal deformity is complex.
    The indications for surgical treatment should not be
    based on radiographs alone. Many patients can tolerate
    high magnitude curves and function well.3 Treatment
    recommendations should be individualized and the impact of the deformity on the patients daily function
    and quality of life should be considered.

    Annotated References
    Glassman SD, Berven S, Bridwell K, Horton W, Dimar
    JR: Correlation of radiographic parameters and clinical
    symptoms in adult scoliosis. Spine (Phila Pa 1976)
    2005;30(6):682-688.

    2.

    Glassman SD, Bridwell K, Dimar JR, Horton W, Berven


    S, Schwab F: The impact of positive sagittal balance in
    adult spinal deformity. Spine (Phila Pa 1976) 2005;
    30(18):2024-2029.

    3.

    Weinstein SL, Dolan LA, Spratt KF, Peterson KK, Spoonamore MJ, Ponseti IV: Health and function of patients
    with untreated idiopathic scoliosis: A 50-year natural
    history study. JAMA 2003;289(5):559-567.

    4.

    Weinstein SL, Ponseti IV: Curve progression in idiopathic scoliosis. J Bone Joint Surg Am 1983;65(4):
    447-455.

    5.

    Lenke LG, Edwards CC II, Bridwell KH: The Lenke


    classification of adolescent idiopathic scoliosis: How it
    organizes curve patterns as a template to perform selective fusions of the spine. Spine (Phila Pa 1976) 2003;
    28(20):S199-S207.

    6.

    Schwab F, Dubey A, Gamez L, et al: Adult scoliosis:


    Prevalence, SF-36, and nutritional parameters in an elderly volunteer population. Spine (Phila Pa 1976) 2005;
    30(9):1082-1085.

    7.

    Kobayashi T, Atsuta Y, Takemitsu M, Matsuno T,


    Takeda N: A prospective study of de novo scoliosis in a
    community based cohort. Spine (Phila Pa 1976) 2006;
    31(2):178-182.

    8.

    Robin GC, Span Y, Steinberg R, Makin M, Menczel J:


    Scoliosis in the elderly: A follow-up study. Spine (Phila
    Pa 1976) 1982;7(4):355-359.

    9.

    Gremeaux V, Casillas JM, Fabbro-Peray P, Pelissier J,


    Herisson C, Perennou D: Analysis of low back pain in

    Pseudarthrosis
    Pseudarthrosis continues to be a major challenge and is
    one of the main complications in multilevel, adult deformity surgery. With longer term follow-up, the rate of
    pseudarthrosis increases. It has been reported to be
    17% in one large series61 and as high as 24% in a recent report,62 with only 25% of the cases of pseudarthrosis detected within the 2-year follow-up period.
    Bone morphogenetic protein (recombinant human bone
    morphogenetic protein-2) mixed with tricalcium
    phosphate/hydroxyapatite crystals in multilevel, adult
    deformity surgery was found to be an adequate replacement for autogenous bone graft, with rates of fusion as
    high as 100% at 2-year follow-up.63 This is an encouraging result, but longer-term follow-up is needed.

    Future Directions
    Over the next several years there will be a demand for
    better-quality scientific evidence that surgical treatment
    in adult spinal deformity is making a clinically significant improvement in the lives of patients. Large clinical
    series have shown that sagittal balance is a key predictor of improvement in HRQL. As the understanding of
    the role of pelvic parameters in determining sagittal
    balance increases, orthopaedic surgeons may become
    more adept at individualizing surgical interventions to
    restore spinal balance. Biologic proteins to improve fusion rates will continue to be discovered along with
    better delivery systems that may require lower doses

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    5: Spine

    1.

    593

    Section 5: Spine

    adults with scoliosis. Spine (Phila Pa 1976) 2008;33(4):


    402-405.
    This cohort study evaluated patients with lumbar scoliosis and chronic low back pain, and a group without
    scoliosis. There was no difference between the groups in
    regard to severity or duration of pain. Pain was increased in patients with scoliosis with a larger magnitude curve and increased rotatory olisthesis. Level of evidence: III.
    10.

    11.

    5: Spine

    12.

    13.

    14.

    594

    Oswestry Disability Index for walking compared with


    the nonsurgical group. Level of evidence: III.
    15.

    Smith JS, Fu KM, Urban P, Shaffrey CI: Neurological


    symptoms and deficits in adults with scoliosis who present to a surgical clinic: Incidence and association with
    the choice of operative versus nonoperative management. J Neurosurg Spine 2008;9(4):326-331.
    Patients who underwent surgery had higher Oswestry
    Disability Index scores and a greater incidence of severe
    radiculopathy, weakness, and neurogenic claudication
    symptoms preoperatively compared with the nonsurgical group. Level of evidence: III.

    16.

    Everett CR, Patel RK: A systematic literature review of


    nonsurgical treatment in adult scoliosis. Spine (Phila Pa
    1976) 2007;32(19, suppl)S130-S134.
    This systematic literature review concluded there was
    very little evidence for any type of nonsurgical care in
    the treatment of adult scoliosis. Level of evidence: IV.

    17.

    Smith JS, Shaffrey CI, Berven S, et al; Spinal Deformity


    Study Group: Operative versus nonoperative treatment
    of leg pain in adults with scoliosis: A retrospective review of a prospective multicenter database with twoyear follow-up. Spine (Phila Pa 1976) 2009;34(16):
    1693-1698.
    Two hundred eight patients with leg pain and adult scoliosis were evaluated. One hundred twelve were treated
    nonsurgically and 96 were treated with surgery. At
    2-year follow-up, surgically treated patients had significantly less leg pain than the nonsurgically treated group.
    Level of evidence: III.

    18.

    Weinstein JN, Tosteson TD, Lurie JD, et al; SPORT Investigators: Surgical versus nonsurgical therapy for lumbar spinal stenosis. N Engl J Med 2008;358(8):794-810.
    A prospective, randomized study evaluating the treatment of lumbar spinal stenosis is presented. In the astreated analysis, patients who underwent surgery had
    significantly more improvement in all primary outcomes
    than did patients who were treated nonsurgically. Level
    of evidence: I.

    19.

    Daubs MD, Lenke LG, Cheh G, Stobbs G, Bridwell KH:


    Adult spinal deformity surgery: Complications and outcomes in patients over age 60. Spine (Phila Pa 1976)
    2007;32(20):2238-2244.
    The rate of major complications was 20%, and increasing age was a significant factor in predicting the presence of a complication. Patients older than 69 years had
    significantly more complications. Level of evidence: IV.

    20.

    Lenke LG: Lenke classification system of adolescent idiopathic scoliosis: Treatment recommendations. Instr
    Course Lect 2005;54:537-542.

    21.

    Kuklo TR: Principles for selecting fusion levels in adult


    spinal deformity with particular attention to lumbar
    curves and double major curves. Spine (Phila Pa 1976)
    2006;31(19, suppl):S132-S138.

    22.

    Kim YJ, Bridwell KH, Lenke LG, Rhim S, Kim YW: Is

    Schwab FJ, Smith VA, Biserni M, Gamez L, Farcy JP,


    Pagala M: Adult scoliosis: A quantitative radiographic
    and clinical analysis. Spine (Phila Pa 1976) 2002;27(4):
    387-392.
    Ploumis A, Liu H, Mehbod AA, Transfeldt EE, Winter
    RB: A correlation of radiographic and functional measurements in adult degenerative scoliosis. Spine (Phila
    Pa 1976) 2009;34(15):1581-1584.
    A retrospective review was performed on 58 patients
    with de novo scoliosis to evaluate the correlation of
    symptoms and radiographic findings. Coronal imbalance greater than 5 cm and loss of lordosis correlated
    with poorer health status. Bodily pain was higher in patients with more than 6 mm of lateral olisthesis. Level of
    evidence: IV.
    Bess S, Boachie-Adjei O, Burton D, et al; International
    Spine Study Group: Pain and disability determine treatment modality for older patients with adult scoliosis,
    while deformity guides treatment for younger patients.
    Spine (Phila Pa 1976) 2009;34(20):2186-2190.
    This retrospective, multicenter database review of 290
    patients with adult scoliosis evaluated the determinants
    of surgery. Age, comorbidities, and sagittal balance did
    not influence the treatment modality. In younger patients, surgical treatment was determined by coronal
    plane deformity. Level of evidence: III.
    Glassman SD, Schwab FJ, Bridwell KH, Ondra SL, Berven S, Lenke LG: The selection of operative versus nonoperative treatment in patients with adult scoliosis.
    Spine (Phila Pa 1976) 2007;32(1):93-97.
    This retrospective case-controlled matched series compared patients treated surgically and nonsurgically to
    determine the factors that may have predicted one treatment over the other. Patients in the surgical group had
    larger curves in the thoracic and thoracolumbar/lumbar
    spine, greater frequency of leg pain, and a higher frequency and level of back pain compared to the patients
    treated nonsurgically. Level of evidence: III.
    Pekmezci M, Berven SH, Hu SS, Deviren V: The factors
    that play a role in the decision-making process of adult
    deformity patients. Spine (Phila Pa 1976) 2009;34(8):
    813-817.
    The authors present a retrospective review evaluating
    the differences between patients with adult spinal deformity who underwent surgery and those who did not.
    There was no difference in preoperative pain levels or
    magnitude of back or leg pain. Patients who underwent
    surgery had worse scores on the Scoliosis Research
    Society-30 Patient Questionnaire for vitality, and on the

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 45: Adult Spinal Deformity

    the T9, T11, or L1 the more reliable proximal level after


    adult lumbar or lumbosacral instrumented fusion to L5
    or S1? Spine (Phila Pa 1976) 2007;32(24):2653-2661.
    This retrospective study found no difference in revision
    rates, proximal junctional kyphosis, or Scoliosis Research Society outcomes when stopping the proximal fusion level at T9, T11, or L1 in a long instrumented fusion to L5 or S1. Level of evidence: IV.
    23.

    Kuhns CA, Bridwell KH, Lenke LG, et al: Thoracolumbar deformity arthrodesis stopping at L5: Fate of the
    L5-S1 disc, minimum 5-year follow-up. Spine (Phila Pa
    1976) 2007;32(24):2771-2776.
    Sixty-nine percent of patients had advanced disk degeneration at L5-S1 at 5-year follow-up following a thoracolumbar fusion that stopped at L5. Twenty-three percent had subsequent extension of their fusion to the
    sacrum. Level of evidence: IV.

    24.

    Kwon BK, Elgafy H, Keynan O, et al: Progressive junctional kyphosis at the caudal end of lumbar instrumented fusion: Etiology, predictors, and treatment.
    Spine (Phila Pa 1976) 2006;31(17):1943-1951.

    25.

    Edwards CC II , Bridwell KH, Patel A, Rinella AS, Berra


    A, Lenke LG: Long adult deformity fusions to L5 and
    the sacrum: A matched cohort analysis. Spine (Phila Pa
    1976) 2004;29(18):1996-2005.

    26.

    27.

    29.

    30.

    Kuklo TR, Bridwell KH, Lewis SJ, et al: Minimum


    2-year analysis of sacropelvic fixation and L5-S1 fusion
    using S1 and iliac screws. Spine (Phila Pa 1976) 2001;
    26(18):1976-1983.
    Tsuchiya K, Bridwell KH, Kuklo TR, Lenke LG, Baldus
    C: Minimum 5-year analysis of L5-S1 fusion using sacropelvic fixation (bilateral S1 and iliac screws) for spinal deformity. Spine (Phila Pa 1976) 2006;31(3):
    303-308.
    Kim YB, Lenke LG, Kim YJ, et al: The morbidity of an
    anterior thoracolumbar approach: Adult spinal deformity patients with greater than five-year follow-up.
    Spine (Phila Pa 1976) 2009;34(8):822-826.
    At 5-year follow-up, patients undergoing an anterior
    thoracolumbar approach complained of postoperative
    pain (32.3%), bulging (43.5%), and functional disturbance (24.2%). Level of evidence: IV.
    Pateder DB, Kebaish KM, Cascio BM, Neubaeur P,
    Matusz DM, Kostuik JP: Posterior only versus combined anterior and posterior approaches to lumbar scoliosis in adults: A radiographic analysis. Spine (Phila Pa
    1976) 2007;32(14):1551-1554.
    A retrospective, case-based comparison of posterior
    only versus a combined anterior and posterior approach
    for adult scoliosis is discussed. There were no significant

    2011 American Academy of Orthopaedic Surgeons

    31.

    Rose PS, Lenke LG, Bridwell KH, et al: Pedicle screw instrumentation for adult idiopathic scoliosis: An improvement over hook/hybrid fixation. Spine (Phila Pa
    1976) 2009;34(8):852-857, discussion 858.
    This retrospective cohort study found significantly improved correction of the major curve, and a lower revision rate with the use of pedicle screw constructs in the
    treatment of adolescent idiopathic scoliosis. There were
    no differences in Scoliosis Research Society scores between the groups. Level of evidence: III.

    32.

    Kim YB, Lenke LG, Kim YJ, Kim YW, Bridwell KH,
    Stobbs G: Surgical treatment of adult scoliosis: Is anterior apical release and fusion necessary for the lumbar
    curve? Spine (Phila Pa 1976) 2008;33(10):1125-1132.
    This is a retrospective, cohort study of 48 patients, 25
    who underwent posterior instrumented fusion without
    an anterior apical release and 23 who underwent apical
    release followed by a posterior spinal fusion. There was
    no difference in the amount of correction, and the overall Scoliosis Research Society outcome scores were better in the group without the anterior apical relaease.
    Level of evidence: III.

    33.

    Abumi K, Panjabi MM, Kramer KM, Duranceau J, Oxland T, Crisco JJ: Biomechanical evaluation of lumbar
    spinal stability after graded facetectomies. Spine (Phila
    Pa 1976) 1990;15(11):1142-1147.

    34.

    Lu WW, Luk KD, Ruan DK, Fei ZQ, Leong JC: Stability of the whole lumbar spine after multilevel fenestration and discectomy. Spine (Phila Pa 1976) 1999;
    24(13):1277-1282.

    35.

    Weidenbaum M: Considerations for focused surgical intervention in the presence of adult spinal deformity.
    Spine (Phila Pa 1976) 2006;31(19, suppl)S139-S143.

    36.

    Ploumis A, Transfledt EE, Denis F: Degenerative lumbar


    scoliosis associated with spinal stenosis. Spine J 2007;
    7(4):428-436.
    This review paper evaluated the treatment of degenerative scoliosis with stenosis. The authors also introduce
    an algorithm for the treatment of degenerative scoliosis
    with stenosis. Level of evidence: IV.

    37.

    Gelb DE, Lenke LG, Bridwell KH, Blanke K, McEnery


    KW: An analysis of sagittal spinal alignment in 100
    asymptomatic middle and older aged volunteers. Spine
    (Phila Pa 1976) 1995;20(12):1351-1358.

    38.

    Legaye J, Duval-Beaupre G, Hecquet J, Marty C: Pelvic


    incidence: A fundamental pelvic parameter for threedimensional regulation of spinal sagittal curves. Eur
    Spine J 1998;7(2):99-103.

    39.

    Vialle R, Levassor N, Rillardon L, Templier A, Skalli W,


    Guigui P: Radiographic analysis of the sagittal alignment and balance of the spine in asymptomatic subjects.
    J Bone Joint Surg Am 2005;87(2):260-267.

    Orthopaedic Knowledge Update 10

    5: Spine

    28.

    Bridwell KH: Selection of instrumentation and fusion


    levels for scoliosis: Where to start and where to stop. Invited submission from the Joint Section Meeting on Disorders of the Spine and Peripheral Nerves, March 2004.
    J Neurosurg Spine 2004;1(1):1-8.

    differences in spinal balance or sagittal and coronal


    plane curve correction between the two groups.

    595

    Section 5: Spine

    40.

    41.

    Legaye J, Duval-Beaupre G: Sagittal plane alignment of


    the spine and gravity: A radiological and clinical evaluation. Acta Orthop Belg 2005;71(2):213-220.

    42.

    Berthonnaud E, Dimnet J, Roussouly P, Labelle H:


    Analysis of the sagittal balance of the spine and pelvis
    using shape and orientation parameters. J Spinal Disord
    Tech 2005;18(1):40-47.

    43.

    Roussouly P, Gollogly S, Berthonnaud E, Dimnet J:


    Classification of the normal variation in the sagittal
    alignment of the human lumbar spine and pelvis in the
    standing position. Spine (Phila Pa 1976) 2005;30(3):
    346-353.

    44.

    Lafage V, Schwab F, Patel A, Hawkinson N, Farcy JP:


    Pelvic tilt and truncal inclination: Two key radiographic
    parameters in the setting of adults with spinal deformity. Spine (Phila Pa 1976) 2009;34(17):E599-E606.
    This study evaluated 125 patients with adult deformity.
    Radiographic parameters were correlated with the SF-12,
    the Oswestry Disability Index, and the Scoliosis Research
    Society-30 Patient Questionnaire. Increased pelvic tilt correlated with worse outcome scores, suggesting that patients who were compensating for sagittal imbalance related worse health status. Level of evidence: III.
    Rose PS, Bridwell KH, Lenke LG, et al: Role of pelvic
    incidence, thoracic kyphosis, and patient factors on sagittal plane correction following pedicle subtraction osteotomy. Spine (Phila Pa 1976) 2009;34(8):785-791.
    Forty patients who were treated with a pedicle subtraction osteotomy were reviewed to evaluate the role of
    pelvic incidence and thoracic kyphosis on the amount of
    lumbar lordosis needed for the restoration of sagittal
    balance. They arrived at a formula: PI + LL + TK < or =
    45, to help determine the amount of lumbar lordosis
    correction that is necessary. Level of evidence: IV.

    46.

    Bridwell KH: Decision making regarding Smith-Petersen


    vs. pedicle subtraction osteotomy vs. vertebral column
    resection for spinal deformity. Spine (Phila Pa 1976)
    2006;31(19, suppl):S171-S178.

    47.

    Bridwell KH, Lewis SJ, Lenke LG, Baldus C, Blanke K:


    Pedicle subtraction osteotomy for the treatment of fixed
    sagittal imbalance. J Bone Joint Surg Am 2003;85(3):
    454-463.

    5: Spine

    45.

    48.

    596

    Mac-Thiong JM, Berthonnaud E, Dimar JR II, Betz RR,


    Labelle H: Sagittal alignment of the spine and pelvis
    during growth. Spine (Phila Pa 1976) 2004;29(15):
    1642-1647.

    Kim YJ, Bridwell KH, Lenke LG, Cheh G, Baldus C:


    Results of lumbar pedicle subtraction osteotomies for
    fixed sagittal imbalance: A minimum 5-year follow-up
    study. Spine (Phila Pa 1976) 2007;32(20):2189-2197.
    Thirty-five consecutive patients with sagittal imbalance
    treated with lumbar pedicle subtraction osteotomies
    were retrospectively analyzed during an average
    follow-up of 5.8 years. Scoliosis Research Society outcome scores were maintained at the 5-year follow-up.

    Orthopaedic Knowledge Update 10

    The pseudoarthorsis rate was 29%. Level of evidence:


    IV.
    49.

    Buchowski JM, Bridwell KH, Lenke LG, et al: Neurologic complications of lumbar pedicle subtraction osteotomy: A 10-year assessment. Spine (Phila Pa 1976)
    2007;32(20):2245-2252.
    One hundred eight patients who underwent a pedicle
    subtraction osteotomy were reviewed to determine the
    incidence of neurologic complications with this procedure. The rate of neurologic complications was 11%,
    with only 3% resulting in a permanent deficit. Level of
    evidence: IV.

    50.

    Suk SI, Kim JH, Kim WJ, Lee SM, Chung ER, Nah KH:
    Posterior vertebral column resection for severe spinal
    deformities. Spine (Phila Pa 1976) 2002;27(21):23742382.

    51.

    Lenke LG, Sides BA, Koester LA, Hensley M, Blanke


    KM: Vertebral column resection for the treatment of severe spinal deformity. Clin Orthop Relat Res 2010;
    468(3):687-699.
    This is a retrospective review of 43 patients that underwent a vertebral column resection for the treatment of
    severe spinal deformity. Level of evidence: IV.

    52.

    Babat LB, McLain RF, Bingaman W, Kalfas I, Young P,


    Rufo-Smith C: Spinal surgery in patients with Parkinsons disease: Construct failure and progressive deformity. Spine (Phila Pa 1976) 2004;29(18):2006-2012.

    53.

    Schwartz DM, Auerbach JD, Dormans JP, et al: Neurophysiological detection of impending spinal cord injury
    during scoliosis surgery. J Bone Joint Surg Am 2007;
    89(11):2440-2449.
    One thousand one hundred twenty-one patients who
    were monitored intraoperatively with motor-evoked potentials and somatosensory-evoked potentials and who
    underwent surgery for adolescent idiopathic scoliosis
    were reviewed. A significant amplitiude change in monitoring was reported in 3.4% of the patients. Transcranial electric motor-evoked potentials were more sensitive to altered spinal cord blood flow because of
    hypotension or a vascular insult. Changes in motorevoked potentials are detected earlier than changes in
    somatosensory-evoked potentials and result in a more
    rapid identification of impending spinal cord injury.
    Level of evidence: IV.

    54.

    Raynor BL, Lenke LG, Kim Y, et al: Can triggered electromyograph thresholds predict safe thoracic pedicle
    screw placement? Spine (Phila Pa 1976) 2002;27(18):
    2030-2035.

    55.

    Glassman SD, Dimar JR, Puno RM, Johnson JR, Shields


    CB, Linden RD: A prospective analysis of intraoperative
    electromyographic monitoring of pedicle screw placement with computed tomographic scan confirmation.
    Spine (Phila Pa 1976) 1995;20(12):1375-1379.

    56.

    Gunnarsson T, Krassioukov AV, Sarjeant R, Fehlings


    MG: Real-time continuous intraoperative electromyo-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 45: Adult Spinal Deformity

    SF-12, EQ5D, and Oswestry Disability Index scores between those treated surgically and nonsurgically. Patients treated with surgery had significantly less pain;
    better health, self-image, and mental health; and were
    more satisfied with their treatment than patients treated
    nonsurgically. Level of evidence: III.

    graphic and somatosensory evoked potential recordings


    in spinal surgery: Correlation of clinical and electrophysiologic findings in a prospective, consecutive series
    of 213 cases. Spine (Phila Pa 1976) 2004;29(6):677684.
    57.

    58.

    59.

    Aydogan M, Ozturk C, Karatoprak O, Tezer M, Aksu


    N, Hamzaoglu A: The pedicle screw fixation with vertebroplasty augmentation in the surgical treatment of the
    severe osteoporotic spines. J Spinal Disord Tech 2009;
    22(6):444-447.
    Forty-nine patients who underwent pedicle screw augmentation with polymethylmethacrylate were reviewed.
    All patients had the T-score value of less than 2.5.
    There were no proximal or distal junctional segment
    fractures at a minimum follow-up of 24 months. Level
    of evidence: IV.
    Chang MC, Liu CL, Chen TH: Polymethylmethacrylate
    augmentation of pedicle screw for osteoporotic spinal
    surgery: A novel technique. Spine (Phila Pa 1976) 2008;
    33(10):E317-E324.
    Forty-one patients with osteoporosis who underwent
    spinal decompression and pedicle screw instrumentation
    with polymethylmethacrylate augmentation were studied. There were no reported instrumentation failures or
    adjacent-level fractures. Level of evidence: IV.
    Li G, Passias P, Kozanek M, et al: Adult scoliosis in patients over sixty-five years of age: Outcomes of operative versus nonoperative treatment at a minimum twoyear follow-up. Spine (Phila Pa 1976) 2009;34(20):
    2165-2170.
    This is a retrospective cohort review of 83 patients older
    than 65 years with adult scoliosis. The study compared
    the Scoliosis Research Society-22 Patient Questionnaire,

    2011 American Academy of Orthopaedic Surgeons

    61.

    Kim YJ, Bridwell KH, Lenke LG, Cho KJ, Edwards CC II, Rinella AS: Pseudarthrosis in adult spinal
    deformity following multisegmental instrumentation
    and arthrodesis. J Bone Joint Surg Am 2006;88(4):
    721-728.

    62.

    Weistroffer JK, Perra JH, Lonstein JE, et al: Complications in long fusions to the sacrum for adult scoliosis:
    Minimum five-year analysis of fifty patients. Spine
    (Phila Pa 1976) 2008;33(13):1478-1483.
    The authors report on a retrospective study of complications in 50 adult patients with scoliosis who were
    treated with long fusions to the sacrum. Pseudarthrosis
    was reported in 24% of the patients.

    63.

    Mulconrey DS, Bridwell KH, Flynn J, Cronen GA, Rose


    PS: Bone morphogenetic protein (RhBMP-2) as a substitute for iliac crest bone graft in multilevel adult spinal
    deformity surgery: Minimum two-year evaluation of fusion. Spine (Phila Pa 1976) 2008;33(20):2153-2159.
    Ninety-eight patients who underwent adult deformity
    surgery supplemented with the use of bone morphogenetic protein (RhBMP-2) were prospectively followed
    for a minimum of 24 months. The overall fusion rate
    was 95%. Level of evidence: III.

    64.

    Anand N, Baron EM, Thaiyananthan G, Khalsa K,


    Goldstein TB: Minimally invasive multilevel percutaneous correction and fusion for adult lumbar degenerative
    scoliosis: A technique and feasibility study. J Spinal Disord Tech 2008;21(7):459-467.
    Twelve patients were treated with a transpsoas anterior
    approach for an anterior fusion using a PEEK
    (polyether-ether ketone) cage followed by percutaneous
    posterior pedicle screw fixation. The mean Cobb angle
    preoperatively was 19 and 6 postoperatively. Level of
    evidence: IV.

    65.

    Ogilvie JW, Braun J, Argyle V, Nelson L, Meade M,


    Ward K: The search for idiopathic scoliosis genes. Spine
    (Phila Pa 1976) 2006;31(6):679-681.

    Orthopaedic Knowledge Update 10

    5: Spine

    60.

    Burval DJ, McLain RF, Milks R, Inceoglu S: Primary


    pedicle screw augmentation in osteoporotic lumbar vertebrae: Biomechanical analysis of pedicle fixation
    strength. Spine (Phila Pa 1976) 2007;32(10):10771083.
    Pedicle screw augmentation with polymethylmethacrylate in cadaver vertebrae was found to improve the initial fixation strength and fatigue strength of instrumentation in osteoporotic vertebrae. Pedicle screws
    augmented with polymethylmethacrylate had significantly greater pullout strength than those placed in
    healthy control vertebrae with no augmentation. Level
    of evidence: III.

    597

    Chapter 46

    Lumbar Degenerative Disease


    Wellington K. Hsu, MD

    Introduction
    Degenerative disorders of the lumbar spine are prevalent, affect quality of life, and are a major health care
    concern of the general population. These conditions
    lead to back, buttocks, and lower extremity symptoms
    that result in lost work days, permanent disability, and
    psychological sequelae. The evolution of the orthopaedic literature has provided algorithms for surgeons to
    prescribe nonsurgical and surgical care in common conditions such as lumbar disk herniation, spinal stenosis,
    and discogenic pain. It is important to review current
    concepts regarding the diagnosis, management, and
    treatment of these conditions.

    is most commonly caused by osteophyte formation and


    overgrowth of the superior articular facet, and foraminal stenosis usually results from a foraminal disk protrusion, posterior osteophyte formation, or loss of vertical height from degenerative collapse of the disk. The
    extraforaminal zone, which is defined as the area lateral to the intervertebral foramen, is most often affected by far-lateral disk and osteophyte pathology.
    Mild to moderate stenosis commonly leads to symptoms related to the dynamic position of the spine. Studies have shown that during terminal extension of the
    lumbar spine, the central canal and foraminal diameter
    decreases by 20% compared to its position in terminal
    flexion. For this reason, patients who experience symptoms with the spine in extension (standing and walking) that are relieved with sitting should be evaluated

    Lumbar Spinal Stenosis

    Pathoanatomy/Pathophysiology

    Dr. Hsu or an immediate family member serves as a paid


    consultant to or is an employee of Stryker and has received research or institutional support from Medtronic
    Sofamor Danek, Baxter Northwestern Alliance, and Pioneer Surgical.

    2011 American Academy of Orthopaedic Surgeons

    5: Spine

    Lumbar spinal stenosis is defined as the narrowing of


    the spinal canal in the lumbar region that is a consequence of several pathologic conditions, the most common of which is chronic degenerative spondylosis. Narrowing of the spinal canal can occur centrally or
    laterally, and although either can lead to a different set
    of symptoms, patients often present with a combination of both. Absolute stenosis has been defined as a
    decrease in the midsagittal lumbar canal diameter of
    less than 10 mm on MRI. Furthermore, where a normal
    cross-sectional area of the spinal canal on an axial MRI
    is defined as 150 to 200 mm2, measurements of less
    than 100 mm2 have been established as central spinal
    stenosis. However, despite these definitions, stenosis diagnosed with radiographs often does not lead to clinically significant symptoms. Common causes of central
    stenosis include congenital anomalies such as short
    pedicle length, ligamentum flavum hypertrophy, and
    broad-based disk-osteophyte complexes
    Lateral stenosis can be further classified into three
    distinct zones: the lateral recess, foraminal zone, and
    extraforaminal zone (Figure 1). Lateral recess stenosis

    Figure 1

    Illustration of lateral recess stenosis in which the


    superior articular process impinges on the traversing lumbar nerve root. The coronal section
    shows the relative positions of the central canal,
    lateral recess, foraminal zone, and extraforaminal zone. (Reproduced from Rao RD, David KS:
    Lumbar degenerative disorders, in Vaccaro AR,
    ed: Orthopaedic Knowledge Update 8. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2005, pp 539-551.)

    Orthopaedic Knowledge Update 10

    599

    Section 5: Spine

    Table 1

    Distinguishing Features of Neurogenic and Vascular Claudication


    Findings

    Neurogenic Claudication

    Vascular Claudication

    Pain location

    Back, buttocks, posterior thighs

    Posterior calfs, heels

    Radiation

    Proximal to distal

    Distal to proximal

    Gait

    Flexed posture

    Upright, normal posture

    Exacerbating activities

    Lumbar extension, standing, walking

    Any lower extremity activity

    Relieving activities

    Lumbar flexion, sitting

    Cessation of lower extremity activity

    Lower extremity examination

    Normal pulses, appearance

    Diminished pulses, hair loss, diffuse


    edema, nail atrophy

    5: Spine

    for lumbar stenosis. These characteristics suggest that


    spinal stenosis is a threshold disease (having a critical
    spinal canal size before which patients are asymptomatic and beyond which the condition becomes apparent). Severe spinal stenosis can lead to pain that is not
    relieved with sitting. In these patients, the pathology
    may be so severe that the threshold of clinical symptoms is exceeded regardless of the position of the spine.
    The symptoms associated with lumbar spinal stenosis are likely due to both mechanical and inflammatory
    causes. Mechanical compression results in local neural
    ischemia that can then lead to neuritis, reduced axonal
    transport, and decreased nutritional support. Because
    at least 50% of the vascular supply is dependent on cerebrospinal fluid diffusion, mild compression can significantly affect the local homeostasis of the involved
    nerve roots. Furthermore, increased neural tension can
    also lead to a host inflammatory response that can
    cause nerve irritation. Local release of inflammatory
    cytokines can lead to nerve root dysfunction and dorsal
    root ganglion irritation. There is evidence to support
    that a more rapid onset of canal compression leads to
    more severe symptoms than a chronic condition.

    Clinical Presentation
    Neurogenic claudication is classically described as
    back, buttocks, and/or posterior thigh pain that worsens with lumbar extension and is relieved by flexion.
    Unlike vascular claudication, pain is often more proximal in the lower extremities and is not relieved with
    standing (Table 1). Another common distinguishing
    factor between vascular and neurogenic claudication is
    the characteristic flexed posture on gait with lumbar
    stenosis that is typically not seen with peripheral vascular disease. Although central canal stenosis classically
    presents with bilateral lower extremity symptoms, lateral recess and foraminal stenosis can often lead to unilateral radicular pain that is worsened with extension
    and rotation to the affected side. Unlike radiculopathy
    from an acute disk herniation, pain from stenosis is not
    typically aggravated by sciatic tension signs such as a
    straight leg raise or sitting for prolonged periods of
    time.
    Lumbar stenosis patients are also predisposed to developing concomitant pathologic changes in the cervi600

    Orthopaedic Knowledge Update 10

    cal spine. The prevalence of tandem spinal stenosis in


    the lumbar stenosis patient population has been reported from 5% to 25%. A recent cadaver study reported a positive predictive value of 15.3% for the
    presence of cervical stenosis when lumbar stenosis was
    observed.1 In cadavers with lumbar stenosis, the odds
    ratio for the presence of cervical stenosis was 3.58 as
    compared to those without lumbar findings. These
    studies indicate that surgeons should be keenly aware
    of the potential for significant and possibly asymptomatic cervical pathology during the evaluation of patients with lumbar degenerative conditions. All patients
    with symptomatic lumbar spinal stenosis should be
    questioned thoroughly on any potential symptoms of
    cervical myelopathy, with subsequent workup as appropriate.

    Management
    After the initial diagnostic evaluation with upright AP
    and lateral lumbar spine plain radiographs, MRI is the
    recommended advanced imaging modality to evaluate
    lumbar spinal stenosis. MRI has been shown to exhibit
    substantial interobserver and intraobserver reliability in
    the diagnosis of lumbar spinal stenosis.2 When MRI is
    not possible because of the presence of ferromagnetic
    implants, CT myelography can be used in its place. CT
    is also more proficient at demonstrating bony changes,
    and may better demonstrate neurologic compression resulting from bony osteophytes. Although advanced imaging studies such as MRI and CT are primarily used in
    the diagnosis of lumbar stenosis, plain radiographs
    should also be carefully scrutinized to assess for degenerative instability, sagittal and coronal plane imbalance,
    and overall bone quality, as these conditions all are relevant in the management of this disorder.
    Nonsurgical treatment with anti-inflammatory
    drugs, activity modification, exercise therapy, and epidural steroid injections is widely accepted as the first
    choice for management of lumbar spinal stenosis. Although the symptoms from lumbar stenosis often
    worsen with aging and the progression of spondylosis,
    a recent study has indicated that nonsurgical treatment
    can lead to maintenance of activities of daily living in
    most patients after 5-year follow-up.3 Epidural steroid
    and/or selective nerve root injections can provide signif-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 46: Lumbar Degenerative Disease

    Figure 2

    In a fenestration procedure, the interspinous ligament and spinous processes are preserved while
    the laminotomy is performed of the upper and
    lower lumbar segments (A). Through this limited
    approach, the undersurface of the spinous process can be resected toward the midline. Contralateral decompression after adequate dural retraction can also be performed (B). (Reproduced
    with permission from Singh K, Samartzis D, An
    H: Surgical techniques: Lumbar spinal stenosis. J
    Am Acad Orthop Surg 2008;16: pp 171-176.)

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    5: Spine

    icant relief of the symptoms from spinal stenosis and


    delay the need for surgery for many patients. However,
    patients often experience only transient relief and require multiple injections to benefit on a long-term basis.
    Surgical treatment is offered to those patients in
    whom initial nonsurgical therapies fail and who have
    significant symptoms that affect quality of life. The
    foundation of surgery for the treatment of lumbar spinal stenosis is an adequate decompression of the neural
    elements involved. Lumbar decompression usually involves resection of at least 50% of the cephalad and
    caudad spinous processes and associated lamina, which
    provides greater space for the neural elements at the
    level of the disk space. When advanced multilevel
    stenosis is diagnosed, more extensive laminectomy is
    required to decompress the neural elements behind the
    vertebral body. Care must be taken to preserve at least
    50% of the facet anatomy bilaterally during decompression to avoid iatrogenic instability. Novel surgical
    techniques aim to preserve the midline structures such
    as the spinous processes and interspinous ligaments
    during decompression with the hope of offering longterm stability to the surgically treated lumbar segment.
    These techniques, often termed microdecompression,
    limited laminotomy, or fenestration, involve laminotomies and foraminotomies bilaterally that thoroughly
    decompress the nerve roots and cauda equina without
    resecting the superficial anatomic structures (Figure 2).
    Mild to moderate lumbar stenosis can often be treated
    adequately in this manner.
    The results of surgical decompression were recently
    compared with those of nonsurgical treatment in a
    landmark study as part of the Spine Patient Outcomes
    Randomized Trial (SPORT).4 In a clinical trial involving 654 patients, with both a randomized and observational cohort, surgical candidates with a history of at

    least 12 weeks of symptoms of spinal stenosis were enrolled. Patients with spondylolisthesis were excluded.
    Because of the high level of crossover in both patient
    cohorts (37% to 42%), an as-treated statistical data
    analysis was performed to compare clinical outcomes
    at various posttreatment time points from 6 weeks to 2
    years. Evaluation of bodily pain and physical function
    scores on the Medical Outcomes Study 36-Item Short
    Form (SF-36) and modified Oswestry Disability Index
    scores demonstrated that patients who underwent surgery for lumbar spinal stenosis had a far better outcome than those treated nonsurgically as early as 6
    weeks after treatment that persisted to final follow-up
    (2 years). The benefits from surgical treatment in spinal
    stenosis were significantly greater than those seen with
    intervertebral disk herniation from the same SPORT
    data because nonsurgical treatment was less effective in
    patients with stenosis. The significantly improved clinical outcomes from surgical treatment in comparison to
    nonsurgical therapies for lumbar spinal stenosis was
    also reported, where the effects were maintained 2
    years after treatment.5
    The indications to add a fusion procedure to surgical
    decompression in the treatment of lumbar spinal stenosis are the presence of degenerative spondylolisthesis,
    radiographic signs of instability such as scoliosis or vertebral body listhesis, or iatrogenic instability such as
    that created when greater than 50% of bilateral facets
    are removed. Recent studies in the patient population
    with spinal stenosis have suggested that those patients
    who achieve a successful lumbar fusion have superior
    outcomes compared to patients with pseudarthrosis.6
    Because the use of instrumentation in lumbar fusion
    has improved arthrodesis rates, it is thought by many
    authors that this leads to improved long-term clinical
    results. Clinical outcomes after lumbar fusion were recently stratified by diagnosis in a report of 327 patients.7 In this study, evaluation of health-related quality of life data revealed the most substantial clinical
    improvement in those patients with a diagnosis of either spondylolisthesis or scoliosis. In comparison, patients with a diagnosis of adjacent segment disease with
    pseudarthrosis and postdiskectomy revision registered
    improvements in Oswestry Disability Index scores, but
    with smaller magnitudes of recovery.
    Because lumbar spinal stenosis often affects patients
    older than 60 years, the associated risks and complications must be thoroughly considered before deciding on
    surgical treatment. As many recent studies have demonstrated the significant increase in complication risk in
    octogenarians, these patients must be made aware of
    the possible medical sequelae from surgical treatment.
    However, recent evidence has suggested that despite being exposed to this additional risk, patients age 60
    years and older who undergo lumbar spine surgery
    have a reduced mortality compared to matched control
    subjects in the general population. In a cohort of 1,015
    patients who underwent spine surgery for the diagnosis
    of lumbar spinal stenosis, Kaplan-Meier analyses revealed 10-year survival rates of 87.8% in patients age
    60 to 70 years and 83.8% in those age 70 to 85 years,
    601

    Section 5: Spine

    Figure 4
    Figure 3

    Schematic of different types of disk herniations. A,


    Protrusion with broad-based continuity between
    herniated and parent disk material. B, Inferior
    migration of disk material under the posterior
    longitudinal ligament. C, Sequestered disk fragment detached from and inferior to an extruded
    disk herniation. (Reproduced with permission
    from Fardon DF, Milette PC: Nomenclature and
    classification of lumbar disk pathology. Spine
    2001;26:E93-E113.)

    5: Spine

    which were similar to that for joint arthroplasty surgery.8 Furthermore, although total joint arthroplasty
    has been well accepted as an efficacious and costeffective intervention, until recently, reports on the improvement in quality of life after surgical treatment of
    spinal stenosis have been lacking. In a study of 90 patients with a spinal decompression with or without fusion for lumbar spinal stenosis, quality-of-life measures
    as defined by SF-36 mental and physical component
    scores were compared to those after total hip and knee
    arthroplasty.9 At 1- and 2-year follow-up, clinical improvement as measured by SF-36 questionnaires was
    comparable for patients treated surgically for spinal
    stenosis and joint osteoarthritis. Because total hip and
    knee arthroplasty patients reportedly have some of the
    highest self-reported quality-of-life scores in any surgical procedure, these clinical results are favorable for the
    surgical treatment of spinal stenosis.

    Lumbar Disk Herniation

    Pathoanatomy
    A lumbar disk herniation is defined as a local displacement of disk contents beyond the circumferential borders of the intervertebral disk space that can lead to
    compression of the neural elements posteriorly.10 A herniated disk may present as a protrusion, defined as a
    broad-based displacement where disk material is continuous with that of the intervertebral disk space, or
    extrusion, when the diameter of the disk material in the
    canal is greater than the distance between the edges of
    the base (Figure 3). Extrusions are termed sequestrations if no continuity exists between disk material in
    the spinal canal and the parent disk. Fragments can
    also migrate in any direction away from the site of extrusion.
    602

    Orthopaedic Knowledge Update 10

    Disk herniations classified by relationship to the


    thecal sac. A, T2 axial MRI demonstrating a posterolateral disk herniation (arrow) typically compressing the traversing nerve root. B, T1 axial
    MRI showing a far-lateral or extraforaminal disk
    herniation affecting the exiting nerve root
    (arrows).

    Herniations are also categorized based on location


    of the disk fragment in relationship to the thecal sac:
    central, posterolateral, foraminal, or extraforaminal.
    Posterolateral disk herniations commonly compress the
    traversing nerve root at a particular level (for example,
    the L5 root at the L4-5 level) while the foraminal and
    extraforaminal (far-lateral) disk fragments affect the
    exiting nerve root (for example, the L4 root at the L4-5
    level) (Figure 4). The type of disk herniation has potential implications on outcome; however, a recent study
    comparing lumbar disk herniation morphology on MRI
    between clinicians and radiologists revealed only fair
    agreement.2

    Pathophysiology
    The pathways by which a disk herniation can lead to
    radicular pain likely involve both mechanical and
    chemical irritation of the nerve root. Mechanical compression can lead to nerve root deformation, local ischemia, and subsequent radiating neuritis. A compounding factor with a disk herniation is the chemical
    effect of nucleus pulposus material directly on the nerve
    root that leads to the release of several inflammatory
    cytokines. Tumor necrosis factor- (TNF-), which is
    produced by intervertebral disk cells, has been implicated in this process. TNF- has been demonstrated to
    increase localized sodium channel accretion, which predisposes nerve roots to irritation from mechanical compression. These theories are supported by animal studies that have demonstrated increased edema, fibrosis,
    and demyelination after exposing nerve tissue to nucleus pulposus extracts. Other cytokines have been implicated in the cause of radicular pain such as
    interleukin-1, interleukin-6, prostaglandin-E2, and
    phospholipase-A2, which have been found in high concentrations around the nerve root and dorsal root ganglion. These factors likely act as chemical modulators
    of pain.11

    2011 American Academy of Orthopaedic Surgeons

    Chapter 46: Lumbar Degenerative Disease

    Clinical Presentation

    Management
    Because most patients improve clinically within a 6-week
    period after the onset of back pain and radiculopathy,
    nonsurgical modalities are the initial mainstays of treatment. These include activity modification, physical therapy, anti-inflammatory medications, and epidural steroid
    injections. Although none of these treatments have been
    shown to alter the natural history of a lumbar disk herniation, they provide relief while the radicular symptoms
    can dissipate naturally. Most surgeons advocate for nonsurgical treatment of at least 6 weeks before considering
    other more invasive measures.
    Epidural steroid injections are a low-risk alternative
    to surgical treatment of lumbar disk herniation. A ran-

    2011 American Academy of Orthopaedic Surgeons

    domized controlled trial demonstrated that 50% of patients who received an epidural steroid injection to
    treat a lumbar disk herniation avoided surgical intervention.13 Although this study showed a higher satisfaction rate for patients who underwent diskectomy, the
    results suggest that for those who wish to avoid surgery, epidural injections can confer some pain relief and
    in some cases help the patient avoid a surgical procedure. Other studies of outcomes after selective nerve
    root injections reveal similar results in patients with
    lumbar radiculopathy.
    The surgical treatment of a lumbar disk herniation
    isa diskectomy and laminotomy. Recent studies from
    SPORT investigators have demonstrated the improved
    clinical outcomes after surgery in comparison with
    nonsurgical treatment.12 Because of the inherent difficulties of randomized clinical trials in a surgical patient
    population, high rates of nonadherence to treatment assignment have led to several difficulties in the interpretation of the intent-to-treat statistical analyses for the
    SPORT studies. High crossover rates lead to a bias toward the null hypothesis in intent-to-treat analyses that
    inherently underestimates the true effect of surgery.
    However, as-treated analyses of outcome measures
    have suggested the advantages of surgical treatment
    when compared to the nonsurgical cohort. The 4-year
    results after continued follow-up of the randomized
    and observational SPORT trial revealed greater improvement in pain, function, satisfaction, and self-rated
    progress in the diskectomy group when compared to
    those treated nonsurgically. These significant improvements were seen as early as 6 weeks after surgery and
    reached maximum benefit by 6 months. At the 4-year
    time point, improvement was seen in all primary and
    secondary outcome measures except for work status.
    These authors conclude that after initial nonsurgical
    treatment of 6 weeks, surgery was superior to nonsurgical care in improving functional status and treating
    radiculopathy.12
    Amid concerns of the surgical costs of care for spinal
    disorders, a follow-up study on the same patient population evaluated the cost effectiveness of surgical treatment of a lumbar disk herniation.14 Quality-adjusted
    life-years (QALY), which account for both quality and
    length of life, have been used for the assessment of the
    value of interventions in health and medicine across
    many subspecialties. Although surgery was initially
    more costly than nonsurgical treatment, clinical outcomes assessed at 2-year follow-up were superior in the
    surgical group. The cost per QALY gained for the surgical group was estimated at $34,355 and $69,403 for
    the Medicare and general populations, respectively.14
    As the authors pointed out, this cost ratio compares favorably with accepted medical interventions such as
    that for hypertension in 60-year-old men ($59,500 per
    QALY).
    Although diskectomy technique has changed over
    the past two decades, recent studies have suggested that
    a simple sequestrectemy, or a removal of only the disk
    fragments in the spinal canal and not in the disk space,
    can lead to excellent if not better clinical and radio-

    Orthopaedic Knowledge Update 10

    5: Spine

    Lumbar disk herniations usually lead to radicular complaints including pain, paresthesias, and weakness
    down the lower extremity in a dermatomal distribution. Referred pain, or sclerotomal pain, is characterized by pain in the low back, buttocks, or posterior
    thigh and originates from mesodermal tissue such as
    muscles, ligaments, or periosteum. Ninety-three percent
    of all disk herniations occur at either the L4-L5 or
    L5-S1 level.12
    Patients sometimes report worsening symptoms with
    sitting, which places tension on the lower lumbar nerve
    roots. The straight leg raise test is positive when concordant, lower extremity radiculopathy is re-created
    with leg elevation of 35 to 70. This test, which has
    demonstrated a high sensitivity but low specificity, is
    believed to manually stretch the L5 and S1 nerve roots
    on the unilateral side. The straight leg raise test on the
    contralateral side, which produces concordant leg
    symptoms with contralateral leg elevation, has a lower
    sensitivity but higher specificity for L4-L5 and L5-S1
    disk herniations. The femoral stretch test is useful for
    pathology of the upper lumbar roots (L1-4), which is
    performed with ipsilateral hip extension and knee flexion. This test is confirmatory when it reproduces anterior thigh pain.
    Severe compression of the nerve roots in the lumbosacral spine by a large disk herniation can lead to
    cauda equina syndrome, which is characterized by saddle anesthesia, urinary retention and overflow incontinence, impotence, bilateral leg pain, and lower extremity weakness. The severity of these symptoms increases
    the urgency of surgical decompression. Although clinical studies have disagreed on the exact recommendation for the timing of decompression for cauda equina
    syndrome, evidence suggests that longer duration and
    increased severity of significant symptoms lead to an
    increased risk of poor results. Consequently, most surgeons would advocate for decompression as soon as
    possible to optimize outcome. Patients with cauda
    equina syndrome with surgical decompression more
    than 48 hours after demonstrating symptoms are at
    greater risk for permanent urologic and sexual dysfunction, leg weakness, and chronic pain than those treated
    within 48 hours of symptom onset.

    603

    Section 5: Spine

    5: Spine

    graphic results than a conventional surgical protocol.


    In a study that compared the 2-year outcomes of patients who underwent a sequestrectomy, or a standard
    diskectomy in which disk tissue was removed from the
    intervertebral disk space, both cohorts significantly improved similarly within a 6-month period.15 However,
    with measurements of parameters such as overall outcome, health-related quality-of-life scores, and analgesic use, the sequestrectomy group demonstrated significantly better outcomes. Furthermore, reherniation rates
    in both groups were not significantly different at 2
    years. The authors postulated that more extensive removal of disk tissue can lead to pathologic changes that
    may manifest as increased low back pain at long-term
    follow-up, which can lead to significantly worse clinical
    outcome. A follow-up study of the same patient cohorts demonstrated significantly greater disk height loss
    and degeneration in the diskectomy patients at 2-year
    follow-up.16 These conclusions were supported by an
    evidence-based review of the literature that compared
    conservative and aggressive approaches during a diskectomy.17 An aggressive approach was defined as a
    complete removal of disk fragments with curettage of
    the disk space whereas a conservative diskectomy used
    a smaller incision with little invasion of the disk space.
    Similarly, these authors concluded that a more conservative approach to disk removal can lead to shorter
    surgical times, faster return to work, and decreased
    long-term back pain. However, this review did reveal a
    higher incidence of recurrent disk herniation in this
    group when compared to an aggressive approach.
    The ability to access the neural elements through
    small incisions and tubular retractor systems has
    spawned several minimally invasive surgical techniques,
    with the hope that muscle-splitting approaches will result in less tissue damage and reduced postoperative
    morbidity compared to conventional open approaches.
    Earlier studies have suggested similar clinical outcomes
    in both of these patient groups. However, a doubleblinded, randomized controlled trial in 328 patients
    comparing the two techniques demonstrated significantly better clinical outcomes in self-reported leg pain,
    back pain, and recovery rates in the conventional diskectomy cohort at 2-year follow-up.18 The reason for
    these results are unclear; however, incomplete decompression of the neural elements from limited visualization in a tubular approach remains a concern for the
    use of this technique.

    Outcomes
    Although the symptoms and morphologic features of
    lumbar disk herniations have been studied for years,
    there are controversies regarding the significance of
    these characteristics. For example, although lumbar
    diskectomy has been widely thought to successfully relieve radicular pain, postoperative outcomes of low
    back pain are unclear. Historically, it has been thought
    that degenerative changes within the disk are the cause
    of axial symptoms that could not be relieved by nerve
    root decompression. However, as part of the SPORT
    604

    Orthopaedic Knowledge Update 10

    study, a greater, more statistically significant improvement in back pain was reported as measured on a sixpoint scale in the diskectomy group as compared to the
    nonsurgical cohort.19 Furthermore, this study demonstrated that central disk herniations were associated
    with more severe axial back pain than posterolateral
    extrusions and that after diskectomy, these patients had
    as successful a clinical outcome as the overall surgical
    cohort.
    Although most lumbar disk herniations occur at the
    L4-L5 or L5-S1 level, significant disk pathology is also
    seen at the upper lumbar segments (L2-L3 and L3-L4).
    The greatest treatment effects from surgery were reported at these upper lumbar levels (L2-L3 and L3-L4)
    when compared to those seen at L4-L5 and L5-S1.20
    The authors pointed out that the primary reason for
    this finding was not the absolute improvement in the
    surgical cohort but rather the paucity of success of nonsurgical treatment in the upper lumbar level group.
    One possible explanation for this finding is that the
    cross-sectional area for the spinal canal at the upper
    lumbar levels is significantly smaller than the lower segments, leading to a greater intensity of symptoms. The
    authors also noted that upper lumbar herniations were
    more likely to appear in the far lateral and foraminal
    positions, which may be less likely to respond to nonsurgical care.

    Discogenic Low Back Pain


    A degenerated intervertebral disk is characterized by
    hydration loss, disk space narrowing, annular tears,
    and, ultimately, ankylosis across the lumbar segment.
    Discogenic pain refers to axial midline low back pain
    without radicular symptoms attributable to the arthritic disk pathology. However, the ubiquitous nature
    of degenerative disk disease and of low back pain in the
    general population has led to significant controversy in
    the diagnosis and management of this condition. Degenerative changes of the spine are prevalent in all age
    groups and are demonstrated in over 75% of the population older than 60 years.21 Although 80% of the US
    population will experience an episode of low back pain
    at some point in their lifetime, only 1% of these patients will require long-term treatment. Because most
    individuals will not require prolonged treatment of low
    back pain even in the setting of lumbar degenerative
    spondylosis, there is difficulty in attributing back pain
    to degenerative disks.

    Diagnostic Imaging
    Plain AP and lateral radiographs are initial, inexpensive
    imaging tests in the assessment of discogenic pain.
    These images may show various signs of spondylosis,
    including disk space narrowing, endplate sclerosis, marginal osteophytes, instability, and facet degeneration.
    Flexion and extension lumbar radiographs may demonstrate further mobility across a lumbar segment; however, the tradeoff of additional irradiation for clinical

    2011 American Academy of Orthopaedic Surgeons

    Chapter 46: Lumbar Degenerative Disease

    Figure 5

    Grading system for the assessment of lumbar disk degeneration. Grade I (A) refers to a homogenous, hyperintense
    signal intensity within the disk space with normal height. Grade II (B) changes are defined as inhomogenous white
    signals with normal height. An intermediate gray signal intensity within the nucleus pulposus (C) is a grade III disk.
    Grade IV (D) changes are characterized by hypointense dark gray signals with mild loss of disc height. Grade V (E)
    disks have space collapse with complete loss of height. (Adapted with permission from Pfirrmann CW, Metzdorf A,
    Zanetti M, et al: Magnetic resonance classification of lumbar intervertebral disc degeneration. Spine 2001;26:
    1873-1878.)

    2011 American Academy of Orthopaedic Surgeons

    Table 2

    Modic Classification of Signal Changes on MRI


    in the Vertebral Body Marrow Adjacent to End
    Plates
    Stage

    Vertebral Body Changes

    Type I

    T1 decreased signal
    T2 increased signal

    Type II

    T1 increased signal
    T2 increased signal

    Type III

    T1 decreased signal
    T2 decreased signal

    5: Spine

    utility has led many authors to question the routine use


    of these images.22
    MRI provides a much more detailed view of intervertebral disk pathology and is highly sensitive to
    degenerative changes. Internal disk disruption, which
    often cannot be seen on plain radiography, can be diagnosed on MRI with loss of signal intensity on T2weighted images, suggesting loss of water content (Figure 5). Furthermore, annular tears can also be seen in
    the form of high-intensity zones, which is another sign
    of internal disk derangement. Bone marrow changes as
    a result of vertebral end plate changes have been associated with degenerative intervertebral disk disease.
    These changes have been classified into three types on
    the basis of chronicity of the degeneration (Table 2).
    Type I lesions are characterized by early fissuring of the
    cartilaginous end plate and acute vascularity within the
    subchondral bone (Figure 6, A and B). Type II changes
    demonstrate fatty degeneration of the adjacent bone
    marrow (Figure 6, C and D). Type III Modic findings
    reflect an advanced form of arthritis associated with
    subchondral bone sclerosis and loss of cancellous bone.
    Despite the inherent value of the anatomic detail
    from MRI, the clinical significance of these findings is
    difficult to determine. Although the presence of highintensity zones has been thought by many to correlate
    with chronic back pain, recent studies have suggested
    that this lesion does not reliably lead to a diagnosis of
    internal disk disruption.23,24
    Epidemiologic studies on the relationship between
    lumbar spondylosis and back pain cite many confounding factors of outcome including abnormal psychomet-

    ric testing, cigarette smoking, personality disorders, ongoing litigation, associated workers compensation
    claims, job satisfaction, and body habitus. Furthermore, several studies have sought to correlate the presence of Modic changes with clinical symptoms; however, the results are controversial. One recent study has
    demonstrated that both Modic type I lesions and those
    changes that are seen at the L5-S1 segment are more
    likely to be associated with significant pain symptoms.25 The results suggest that type I lesions may represent an early derangement phase in a pain condition
    that may later stabilize as disk degeneration progresses.
    Provocative diskography has historically been used
    in confirming the diagnosis of discogenic pain. A positive result is defined as a concordant pain response elic-

    Orthopaedic Knowledge Update 10

    605

    Section 5: Spine

    Figure 6

    Typical Modic type I (A, B) and type II (C, D) changes in lumbar degenerative disk disease. Type I changes are characterized by a low intensity signal on T1-weighted (A) and high intensity signal on T2-weighted images (B). More advanced Modic type II changes are defined as high intensity signals on both T2-weighted (C) and T1-weighted (D)
    sagittal images. (Reproduced with permission from Albert HB, Kjaer P, Jensen TS, et al: Modic changes, possible
    causes, and relation to low back pain. Med Hypothesis 2008;70:361-368. http://www.sciencedirect.com/science/
    journal/03069877.)

    5: Spine

    ited from the patient with the injection of an intervertebral disk with abnormal morphology in the setting of
    negative control lumbar levels. It stands to reason that
    patients with a positive diskogram suffer from discogenic low back pain and have a higher likelihood of
    clinical success from a lumbar fusion. However, significant controversy in the evaluation of diskography as a
    diagnostic tool exists because of its operator-dependent
    nature, the heterogeneity of the study subjects involved,
    and conflicting clinical outcomes. A series of studies
    evaluating diskography have shown high false-positive
    rates (25%) in asymptomatic patients, high falsenegative rates (30%) in patients with chronic low back
    pain, and poor positive predictive values. Furthermore,
    a recent study suggests that disk levels exposed to diskography result in accelerated disk degeneration, disk
    herniation, and end plate changes compared to
    matched control subjects as seen on MRI at 10-year
    follow-up.26 The literature refutes diskography as a
    stand-alone diagnostic measure with poor predictive
    value, and at best, supports its use as either a confirmatory test or one piece of a complex diagnostic puzzle.

    Clinical Features
    Lumbar discogenic pain is classically described as a
    deep, aching low back pain that is mechanical in nature. Sitting, standing, bending, and axial loading are
    thought to exacerbate these symptoms, while rest and a
    supine position may provide relief. Patients often experience pain in both flexion and extension and have decreased range of motion compared to asymptomatic
    patients. Physical examination findings are often non606

    Orthopaedic Knowledge Update 10

    specific and of little use in the diagnosis. Some have


    postulated that because instability of a lumbar motion
    segment is one cause of low back pain, disk degeneration may lead to micromotion that is the root cause of
    axial pain in these patients. However, because no diagnostic methods exist that can help elucidate this hypothesis, it remains an area for future study.

    Management/Treatment
    A multifaceted approach to nonsurgical care in the
    form of anti-inflammatory medications, fitness programs, weight loss, and functional rehabilitation remains the first-line treatment of discogenic back pain.
    For most patients with this condition, these measures
    are often effective in managing symptoms until the episode resolves. Other nonsurgical measures such as acupuncture, behavioral therapy, and exercise therapy
    have also demonstrated modest improvement in symptoms.27 Although multiple different physical therapy
    modalities have been compared, no single program has
    demonstrated greater efficacy over another. Transcutaneous electrical nerve stimulation, muscle stimulation
    protocols, traction, and chiropractic treatment have not
    demonstrated long-term efficacy in the management of
    low back pain.27
    When multiple modalities of nonsurgical management fail in patients diagnosed with discogenic low
    back pain, there are limited options for further treatment. Surgical treatment is considered a last-resort option for the patient who endures intractable symptoms
    for a 6-month period; however, controversy remains
    among experienced practitioners regarding the exact

    2011 American Academy of Orthopaedic Surgeons

    Chapter 46: Lumbar Degenerative Disease

    2011 American Academy of Orthopaedic Surgeons

    The authors concluded that although patients with an


    indication of spondylolisthesis experienced the best
    outcomes, fusion for the diagnosis of degenerative disk
    disease can lead to improved clinical outcomes.30

    Annotated References
    1.

    Lee MJ, Garcia R, Cassinelli EH, Furey C, Riew KD:


    Tandem stenosis: A cadaveric study in osseous morphology. Spine J 2008;8(6):1003-1006.
    The midsagittal canal diameter of cervical and lumbar
    spines of 440 adult skeletons from the Hamann-Todd
    Collection at the Cleveland Museum of Natural History
    was measured with digital calipers. The study demonstrated that the presence of lumbar spinal stenosis has a
    15.3% positive predictive value for cervical stenosis.
    Level of evidence: IV.

    2.

    Lurie JD, Doman DM, Spratt KF, Tosteson AN, Weinstein JN: Magnetic resonance imaging interpretation in
    patients with symptomatic lumbar spine disc herniations: Comparison of clinician and radiologist readings.
    Spine (Phila Pa 1976) 2009;34(7):701-705.
    Examination of the radiology reports from 396 patients
    as part of the SPORT trial demonstrated that in 42.2%
    of cases, the radiology reports did not clearly describe
    the morphology of the disk herniation. Although agreement of MRI readings between clinicians and radiologists was excellent for level and location of the disk herniation, it was only fair comparing herniation
    morphology. Level of evidence: IV.

    3.

    Miyamoto H, Sumi M, Uno K, Tadokoro K, Mizuno K:


    Clinical outcome of nonoperative treatment for lumbar
    spinal stenosis, and predictive factors relating to prognosis, in a 5-year minimum follow-up. J Spinal Disord
    Tech 2008;21(8):563-568.
    A prospective study of 120 patients who received inpatient treatment of lumbar spinal stenosis in the form of
    anti-inflammatory medications and caudal blocks was
    conducted for a minimum of 5 years. In 52.5% of patients, clinical outcome was the same or better at final
    follow-up with patients classified as radicular type exhibiting better results than other subjects. Level of evidence: IV.

    4.

    Weinstein JN, Tosteson TD, Lurie JD, et al; SPORT Investigators: Surgical versus nonsurgical therapy for lumbar spinal stenosis. N Engl J Med 2008;358(8):794-810.
    In an as-treated statistical analysis of 289 patients in a
    randomized cohort and 365 patients in an observational
    cohort with lumbar spinal stenosis, patients who underwent decompressive surgery demonstrated a significant
    advantage by 3 months for all primary outcome measures that remained significant at 2 years compared to
    nonsurgical care. Level of evidence: II.

    5.

    Malmivaara A, Sltis P, Helivaara M, et al; Finnish


    Lumbar Spinal Research Group: Surgical or nonoperative treatment for lumbar spinal stenosis? A randomized
    controlled trial. Spine (Phila Pa 1976) 2007;32(1):1-8.

    Orthopaedic Knowledge Update 10

    5: Spine

    surgical indications. Lumbar fusion has historically


    been used in the surgical treatment of degenerative disk
    disease; however, reported clinical outcomes are widely
    variable. An individual patients response to surgery
    can be affected by association with workers compensation, psychosocial comorbidities, and unrealistic expectations.
    The advantages of an anterior lumbar interbody fusion (ALIF) include the avoidance of posterior muscle
    dissection and improved access to remove the lumbar
    disk resulting in increased surface area for bony healing. The potential disadvantages are the need for an access surgeon, risk of great vessel damage, and retrograde ejaculation. A recent study reported the clinical
    and radiographic outcomes of patients who underwent
    a stand-alone ALIF for the diagnosis of degenerative
    disk disease at the L4-L5 or L5-S1 levels with at least
    six-year follow-up.28 In this study, patients were treated
    with recombinant human bone morphogenetic
    protein-2 and titanium-tapered cages at a single lumbar
    level. At the 6-year time point, 128 of 130 patients had
    a radiographically solid fusion. Clinical outcomes as
    determined by Oswestry Disability Index, SF-36, and
    back and leg pain scores demonstrated significant improvement as early as 6 weeks after surgery and sustained benefit at 6 years. The secondary surgery rate
    was 10% over the life of the study; however, there were
    no reports of vessel damage, retrograde ejaculation, or
    long-term complications. Lumbar total disk arthroplasty has been studied as an alternative to ALIF for the
    treatment of discogenic back pain; lumbar disk arthroplasty is also discussed in chapter 45.
    From a posterior approach, in addition to an intertransverse fusion, either a transforaminal lumbar interbody fusion (TLIF) or a posterior lumbar interbody fusion can be performed. Both of these techniques allow
    for the direct decompression of the neural elements, removal of disk, and screw instrumentation through a
    single posterior approach. Used with posterior pedicle
    screw instrumentation, interbody fusions provide a
    360 fusion construct that may enhance lumbar fusion
    rates compared to a posterolateral fusion alone. TLIF
    has demonstrated a lower incidence of postoperative
    radiculitis because of less neural retraction as compared
    to a posterior lumbar interbody fusion. In a retrospective analysis of 167 patients, TLIF was compared to
    anterior-posterior reconstructive surgery in the treatment of several degenerative conditions in the lumbar
    spine.29 The authors concluded that an anteriorposterior procedure leads to significantly longer surgical and hospitalization time, increased blood loss, and
    twice the complication rate as does TLIF.
    The outcomes of lumbar fusion for degenerative disk
    disease vary based upon source, patient selection criteria, outcome measures, and comorbidities. A wide
    spread of clinical outcomes has been reported in the literature. However, studies published in the past decade
    have increased understanding of the importance of patient selection and expectations from a surgical procedure. A recent systematic review compiled the literature
    reporting outcomes from fusion for several diagnoses.

    607

    Section 5: Spine

    In a randomized controlled trial of 94 patients for the


    surgical and nonsurgical treatment of spinal stenosis,
    those undergoing decompressive surgery reported
    greater improvement regarding leg pain, back pain, and
    overall disability compared with those patients who received nonsurgical care. Level of evidence: I.
    6.

    Kornblum MB, Fischgrund JS, Herkowitz HN, Abraham DA, Berkower DL, Ditkoff JS: Degenerative lumbar spondylolisthesis with spinal stenosis: A prospective
    long-term study comparing fusion and pseudarthrosis.
    Spine (Phila Pa 1976) 2004;29(7):726-733, discussion
    733-734.

    7.

    Glassman SD, Carreon LY, Djurasovic M, et al: Lumbar


    fusion outcomes stratified by specific diagnostic indication. Spine J 2009;9(1):13-21.
    In a prospective study in 327 patients with a decompression and posterolateral lumbar fusion, overall clinical
    outcome was stratified by and correlated to initial diagnosis. The greatest improvement in Oswestry Disability
    Index scores were seen in patients with spondylolisthesis
    and scoliosis, whereas patients with disk pathology,
    postdiskectomy revision, instability, stenosis, and adjacent segment degeneration had a smaller magnitude of
    improvement. Level of evidence: II.

    5: Spine

    8.

    608

    Kim HJ, Lee HM, Kim HS, et al: Life expectancy after
    lumbar spine surgery: One- to eleven-year follow-up of
    1015 patients. Spine (Phila Pa 1976) 2008;33(19):21162121, discussion 2122-2123.
    The 10-year survival of 1,015 elderly patients older than
    50 years was documented following spine surgery for
    lumbar spinal stenosis. The overall 10-year survival rate
    in patients 60 to 70 years old was 87.7%, and 83.8% in
    patients 70 to 85 years old. These patients had reduced
    mortality in comparison with the corresponding portion
    of the general population. Level of evidence: III.

    9.

    Rampersaud YR, Ravi B, Lewis SJ, et al: Assessment of


    health-related quality of life after surgical treatment of
    focal symptomatic spinal stenosis compared with osteoarthritis of the hip or knee. Spine J 2008;8(2):296-304.
    Patients who underwent surgical treatment for spinal
    stenosis were compared with a matched cohort of patients who underwent total hip or total knee arthroplasty for osteoarthritis. Clinical outcomes at 1- and
    2-year follow-up demonstrate that spinal stenosis surgery can lead to improvement in self-reported qualityof-life scores comparable to those of total hip and knee
    arthroplasty patients. Level of evidence: III.

    10.

    Fardon DF, Milette PC; Combined Task Forces of the


    North American Spine Society, American Society of
    Spine Radiology, and American Society of Neuroradiology: Nomenclature and classification of lumbar disc pathology: Recommendations of the Combined Task
    Forces of the North American Spine Society, American
    Society of Spine Radiology, and American Society of
    Neuroradiology. Spine (Phila Pa 1976) 2001;26(5):E93E113.

    11.

    Doita M, Kanatani T, Harada T, Mizuno K: Immunohistologic study of the ruptured intervertebral disc of
    the lumbar spine. Spine 1996;21:235-241.

    Orthopaedic Knowledge Update 10

    12.

    Weinstein JN, Lurie JD, Tosteson TD, et al: Surgical versus nonoperative treatment for lumbar disc herniation:
    Four-year results for the Spine Patient Outcomes Research Trial (SPORT). Spine (Phila Pa 1976) 2008;
    33(25):2789-2800.
    Five hundred one participants enrolled in a prospective,
    randomized controlled trial and 743 patients in an observational cohort were treated for lumbar disk herniation with either standard open diskectomy or nonsurgical care. As-treated statistical analysis 4 years after
    treatment demonstrated greater improvement in all primary and secondary outcome measures after surgical
    treatment for lumbar disk herniation except work status. Level of evidence: II.

    13.

    Buttermann GR: Treatment of lumbar disc herniation:


    Epidural steroid injection compared with discectomy. A
    prospective randomized study. J Bone Joint Surg Am
    2004;86:670-679.

    14.

    Tosteson AN, Skinner JS, Tosteson TD, et al: The cost


    effectiveness of surgical versus nonoperative treatment
    for lumbar disc herniation over two years: Evidence
    from the Spine Patient Outcomes Research Trial
    (SPORT). Spine (Phila Pa 1976) 2008;33(19):21082115.
    Using discounted cost per QALY, cost effectiveness of
    surgical treatment compared with nonsurgical treatment
    for lumbar disk herniation was evaluated. Using the patient population from the SPORT randomized and observational cohorts, at 2 years, although surgical treatment was cost effective when compared with
    nonsurgical treatment, the estimated economic value of
    surgery varied according to method of surgical cost assignment. Level of evidence: III.

    15.

    Barth M, Weiss C, Thom C: Two-year outcome after


    lumbar microdiscectomy versus microscopic sequestrectomy: Part 1. Evaluation of clinical outcome. Spine
    (Phila Pa 1976) 2008;33(3):265-272.
    Eighty-four patients with lumbar disk herniations randomized to either treatment with microdiskectomy or
    microscopic sequestrectomy were evaluated for clinical
    outcome with at least 2-year follow-up. Although both
    patient groups dramatically improved immediately after
    surgery, self-rated assessment scores continued to improve within 2 years after sequestrectomy as opposed to
    deterioration in the microdiskectomy group. Reherniation rates were not significantly different between the
    two groups. Level of evidence: I.

    16.

    Barth M, Diepers M, Weiss C, Thom C: Two-year outcome after lumbar microdiscectomy versus microscopic
    sequestrectomy: Part 2. Radiographic evaluation and
    correlation with clinical outcome. Spine (Phila Pa 1976)
    2008;33(3):273-279.
    Eighty-four patients with lumbar disk herniations randomized to treatment with either microdiskectomy or
    simple fracture excision (sequestrectomy) underwent repeat MRI of the lumbar spine at 2-year follow-up.
    Modic-type end plate changes correlated with unfavorable clinical outcome after surgical treatment, and sequestrectomy demonstrated significantly less postoperative disk degeneration than standard microdiskectomy
    at final follow-up. Level of evidence: II.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 46: Lumbar Degenerative Disease

    17.

    18.

    Watters WC III, McGirt MJ: An evidence-based review


    of the literature on the consequences of conservative
    versus aggressive discectomy for the treatment of primary disc herniation with radiculopathy. Spine J 2009;
    9(3):240-257.
    A systematic evidence-based review of all published
    studies of outcomes after aggressive or conservative diskectomy was performed. Although there were no level I
    studies reviewed, the authors concluded that conservative diskectomy may lead to shorter surgery time,
    quicker return to work, and decreased incidence of
    long-term low back pain. However, conservative diskectomy may also lead to increased incidence of recurrent
    disk herniation. Level of evidence: III.
    Arts MP, Brand R, van den Akker ME, Koes BW, Bartels RH, Peul WC; Leiden-The Hague Spine Intervention Prognostic Study Group (SIPS): Tubular diskectomy vs conventional microdiskectomy for sciatica: A
    randomized controlled trial. JAMA 2009;302(2):149158.
    A prospective controlled trial of 328 patients with radiculopathy from a lumbar disk herniation was randomized to treatment with either a tubular or conventional
    microdiskectomy. Using clinical outcome scores for up
    to 1 year after randomization, patients who underwent
    tubular diskectomy reported less favorable results for
    self-reported leg pain, back pain, and recovery. Level of
    evidence: I.
    Pearson AM, Blood EA, Frymoyer JW, et al: SPORT
    lumbar intervertebral disk herniation and back pain:
    Does treatment, location, or morphology matter? Spine
    (Phila Pa 1976) 2008;33(4):428-435.
    A combined analysis of 1,191 patients enrolled in the
    SPORT study randomized to surgical or nonsurgical
    treatment of lumbar disk herniations reported a significant improvement in back pain in the surgical group
    compared with those treated nonsurgically at 2-year
    follow-up. Level of evidence: III.

    20.

    Lurie JD, Faucett SC, Hanscom B, et al: Lumbar discectomy outcomes vary by herniation level in the Spine Patient Outcomes Research Trial. J Bone Joint Surg Am
    2008;90(9):1811-1819.
    A retrospective review of 1,190 patients enrolled in the
    SPORT study for lumbar disk herniations correlated
    level of herniation to clinical outcome. At 2-year followup, patients with upper lumbar herniations (L3-4 and
    L2-3) showed a significantly greater treatment effect
    from surgery than did patients with L5-S1 disk herniations. This finding may have been a result of less improvement from nonsurgical treatment in the upper
    lumbar herniation group. Level of evidence: III.

    21.

    Muraki S, Oka H, Akune T, et al: Prevalence of radiographic lumbar spondylosis and its association with low
    back pain in elderly subjects of population-based cohorts: The ROAD study. Ann Rheum Dis 2009;68(9):
    1401-1406.
    The Research on Osteoarthritis Against Disability
    (ROAD) study evaluated 2, 288 patients age 60 years or
    older. Clinically significant spondylosis was diagnosied
    in 75.8% of patients in the study, with age and body

    2011 American Academy of Orthopaedic Surgeons

    22.

    Hammouri QM, Haims AH, Simpson AK, Alqaqa A,


    Grauer JN: The utility of dynamic flexion-extension radiographs in the initial evaluation of the degenerative
    lumbar spine. Spine (Phila Pa 1976) 2007;32(21):23612364.
    Of 342 plain radiographic series in the initial evaluation
    of the degenerative lumbar spine including flexion and
    extension films, only 2 had new findings not appreciated on the AP and lateral films. The authors concluded
    that dynamic radiographs did not significantly alter the
    initial course of clinical management. Level of evidence:
    IV.

    23.

    Kleinstck F, Dvorak J, Mannion AF: Are structural


    abnormalities on magnetic resonance imaging a contraindication to the successful surgical treatment of
    chronic nonspecific low back pain? Spine 2006;31(19):
    2250-2257.

    24.

    Jarvik JJ, Hollingworth W, Heagerty P, Haynor DR,


    Deyo RA: The Longitudinal Assessment of Imaging and
    Disability of the Back (LAIDBack) Study: Baseline data.
    Spine 2001;26:1158-1166.

    25.

    Kuisma M, Karppinen J, Niinimki J, et al: Modic


    changes in endplates of lumbar vertebral bodies: Prevalence and association with low back and sciatic pain
    among middle-aged male workers. Spine (Phila Pa
    1976) 2007;32(10):1116-1122.
    In a cross-sectional study comparing self-reported low
    back pain symptoms and Modic changes on MRI in 228
    middle-aged male workers (159 train engineers and 69
    sedentary control subjects), Modic type I lesions and
    significant end plate changes seen at the L5-S1 level
    were more likely to be associated with low back pain
    than that seen at other lumbar levels. Level of evidence:
    III.

    26.

    Carragee EJ, Don AS, Hurwitz EL, Cuellar JM, Carrino


    JA, Herzog R: 2009 ISSLS Prize Winner: Does discography cause accelerated progression of degeneration
    changes in the lumbar disc. A ten-year matched cohort
    study. Spine (Phila Pa 1976) 2009;34(21):2338-2345.
    The authors concluded that modern diskography techniques resulted in accelerated disk degeneration, disk
    herniation, loss of disk height and signal, and the development of end plate changes.

    27.

    Keller A, Hayden J, Bombardier C, van Tulder M: Effect


    sizes of non-surgical treatments of non-specific lowback pain. Eur Spine J 2007;16(11):1776-1788.
    In a review of randomized controlled trials from systematic reviews of treatment of acute low back pain, there
    was a modest effect size of NSAIDs and manipulation,
    and for chronic low back pain, acupuncture, behavioral
    therapy, exercise therapy, and NSAIDs had the largest
    effect sizes. Level of evidence: II.

    28.

    Burkus JK, Gornet MF, Schuler TC, Kleeman TJ, Zdeblick TA: Six-year outcomes of anterior lumbar interbody arthrodesis with use of interbody fusion cages and

    Orthopaedic Knowledge Update 10

    5: Spine

    19.

    mass index as risk factors for developing arthritic


    changes. Level of evidence: IV.

    609

    Section 5: Spine

    recombinant human bone morphogenetic protein-2.


    J Bone Joint Surg Am 2009;91(5):1181-1189.
    At 6-year follow-up of 130 patients treated with recombinant human bone morphogenetic protein-2 and standalone fusion cages, 128 patients had successful fusion.
    Significant improvements in Oswestry Disability Index
    and SF-36 scores that were seen as early as 6 weeks after
    surgery were maintained at 6-year follow-up. Level of
    evidence: IV.
    Villavicencio AT, Burneikiene S, Bulsara KR, Thramann
    JJ: Perioperative complications in transforaminal lumbar interbody fusion versus anterior-posterior reconstruction for lumbar disc degeneration and instability.
    J Spinal Disord Tech 2006;19(2):92-97.

    Carreon LY, Glassman SD, Howard J: Fusion and nonsurgical treatment for symptomatic lumbar degenerative
    disease: A systematic review of Oswestry Disability Index and MOS Short Form-36 outcomes. Spine J 2008;
    8(5):747-755.
    A systematic review of prospective randomized controlled clinical trials in patients with low back pain of at
    least 12 weeks duration was performed. In an evaluation of 25 studies, substantial improvement can be expected in patients treated with fusion when an established indication such as spondylolisthesis or
    degenerative disk disease is given. For patients with
    chronic low back pain, there is less improvement. Level
    of evidence: II.

    5: Spine

    29.

    30.

    610

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 47

    Cervical Degenerative Disease


    John M. Rhee, MD

    K. Daniel Riew, MD

    Introduction
    Degenerative, or spondylotic, conditions of the cervical
    spine constitute a spectrum of disorders. In most cases,
    the underlying mechanism is thought to begin with degeneration of the cervical disk, which can subsequently
    set off a cascade of secondary degenerative events. Depending on the presence and location of neurologic
    compression, the patient may present with pure axial
    pain, radiculopathy due to root compression, myelopathy due to cord compression, or a combination of all
    three conditions.

    segmental instability (Figure 1). Degenerative disks may


    lead to diffuse, poorly localized neck pain associated
    with other symptoms such as occipital headaches or radiation into the shoulder and scapula. Symptomatic
    facet arthrosis usually presents as a localized pain over
    the involved joint, particularly in extension. A welldescribed cause of axial neck pain is atlanto-axial osteoarthrosis2 (Figure 2). Patients with this disorder are
    typically older (70 years or older) than those with subaxial arthrosis and present with pain localized to the
    occipitocervical junction that is typically exacerbated
    by rotation to the symptomatic side but not by sagittal

    Axial Neck Pain Without Radiculopathy


    or Myelopathy

    Clinical Evaluation

    Dr. Rhee or an immediate family member has received


    royalties from Biomet; is a member of a speakers bureau or has made paid presentations on behalf of
    Biomet and Synthes; serves as a paid consultant to or is
    an employee of Synthes; has received research or institutional support from Synthes and Medtronic Sofamor
    Danek; and has stock or stock options held in Phygen.
    Dr. Riew or an immediate family member serves as a
    board member, owner, officer, or committee member of
    the Cervical Spine Research Society, the Scoliosis Research Society, and the Korean American Spine Society;
    has received royalties from Biomet, Medtronic, Amedica,
    Osprey, and is working on an artificial disc that may
    generate royalties in several years; serves as a paid consultant to or is an employee of Biomet and Medtronic;
    has received research or institutional support from
    Medtronic Sofamor Danek; and has stock or stock options held in Spinal Kinetics, Amedica, Nexgen Spine, Osprey, SpineMedica, Vertiflex, Benvenue, Paradigm Spine,
    PSD, and Spineology.

    2011 American Academy of Orthopaedic Surgeons

    5: Spine

    Axial neck pain is a very common problem, with an estimated lifetime prevalence of 66% in one series.1 Most
    cases of axial pain arise from soft-tissue sprains and
    muscle strains, and are overwhelmingly benign, selflimited disorders. A smaller but still substantial population may have axial pain as a manifestation of cervical
    spondylosis, arising from entities such as disk degeneration, facet arthrosis, kyphosis, and less commonly,

    Figure 1

    Cervical spondylolisthesis in a 47-year-old woman


    with cervical myelopathy caused by a grade II
    spondylolisthesis at C4-5. Associated spinal cord
    compression is present from the resulting narrowing of the spinal canal. Note also the buckling inward of the ligamentum flavum (arrow),
    which causes dorsal spinal cord compression.
    This patient also has significant disk degeneration at C5-6 and C6-7, although she has no neck
    pain. She was treated with anterior and posterior decompression and fusion, with complete
    resolution of myelopathy and solid fusion.

    Orthopaedic Knowledge Update 10

    611

    Section 5: Spine

    history of any injury and its mechanism should be determined. Nonspine causes of neck and shoulder pain,
    such as gallbladder, coronary, rotator cuff, or brachial
    plexusrelated problems, should be investigated.

    Radiographic Evaluation

    Figure 2

    C1-2 facet arthrosis in a 75-year-old woman with


    severe left-sided neck pain occurring with rotation to the left. Open mouth odontoid view
    demonstrates severe facet arthrosis on the left
    side at C1-2 (arrows). Significant loss of joint
    space is evident on the left.

    5: Spine

    plane motion. Kyphosis may also be associated with


    neck pain. Kyphosis may occur secondary to the degenerative cascade, after multilevel cervical laminectomy,
    or due to myopathies that affect the cervical extensor
    musculature. Patients with kyphosis describe pain related to extensor muscle fatigue, as these muscles must
    overcome the negative biomechanical consequences of
    kyphosis to maintain forward gaze.
    Physical examination of all patients should assess
    limitations in range of motion of the neck. Localized
    tenderness over a facet joint may be elicited in patients
    with symptomatic facet arthrosis, whether subaxial or
    atlantoaxial. In patients with atlantoaxial arthrosis, rotation to the affected side may reproduce pain, especially over the initial arc of motion when C1-2 rotation
    predominates over any subaxial contribution to rotation. Performing the same maneuver in the supine position with gentle traction on the cervical spine may reduce symptoms as the arthritic C1-2 facets are
    unloaded.
    In addition to degenerative cervical spine etiologies,
    the differential diagnosis of isolated axial neck pain includes fractures, dislocations, inflammatory arthritides
    (for example, rheumatoid arthritis, ankylosing spondylitis), infections (for example, diskitis, osteomyelitis,
    epidural abscess), tumors (intradural, extradural), and
    nonspine sources. Although making a specific diagnosis
    can be difficult in the patient with axial neck pain,
    these potentially dangerous causes of neck pain should
    be ruled out before embarking on treatment of cervical
    spondylosis or neck strain/ sprain. A detailed history
    often provides the essential information. Constant, unremitting pain that worsens at night and is associated
    with constitutional symptoms such as fever, malaise,
    and weight loss are suggestive of tumor or infection. A
    612

    Orthopaedic Knowledge Update 10

    Indications for obtaining radiographs include a history


    of trauma, prolonged duration of symptoms (longer
    than 1 month), presence of constitutional symptoms,
    suspected infection or malignancy, or known systemic
    disease (such as cancer or inflammatory arthritis). Plain
    radiographs are a reasonable initial test in the patient
    with axial neck pain, and perhaps are most useful in
    demonstrating the absence of more dangerous pathology rather than showing conditions such as degenerative disks, spurs, and other spondylotic changes that
    are universal during the course of normal aging.3 If atlantoaxial arthrosis is suspected, an open mouth odontoid view may demonstrate arthritic changes in the
    C1-2 joints. Flexion-extension views may assist in evaluating potential instability. If tumor or infection is suspected, or if pain persists despite benign radiographs
    and a trial of nonsurgical treatment, MRI and/or CT
    may be helpful. Although imaging studies are helpful in
    evaluating patients with neck pain, care must be exercised in attributing symptoms to radiographic findings,
    as degenerative changes are more often the rule rather
    than the exception in the general population.

    Other Diagnostic Studies


    Despite clinical and radiologic studies, the exact pain
    generator may remain unclear in a large percentage of
    patients with axial pain. In such situations, more invasive tests such as diagnostic injections or diskography
    can be considered to further elucidate the diagnosis.
    However, these modalities are reserved for those in
    whom an initial trial of less invasive nonsurgical options has failed, which in many cases may result in resolution of symptoms despite the absence of a specific
    diagnosis. Facet injections may help provide both diagnostic information and therapeutic benefit in those
    with suspected symptomatic facet joint arthrosis. Cervical diskography can be used to identify symptomatic
    disk degeneration, but its true utility in predicting surgical outcomes remains controversial and is also associated with potential risks such as discitis or injury to the
    soft-tissue structures of the neck.

    Treatment
    In most patients for whom axial neck pain can be attributed to cervical spondylosis, conservative treatment
    is preferred because of a favorable natural history, and
    it is often difficult, if not sometimes impossible, to determine the exact pain generator for surgical treatment.
    Nonsteroidal anti-inflammatory drugs are favored over
    narcotic-based medications. Short-term collar immobilization may help decrease pain in those with acute
    symptoms. Active physical therapy, such as cervical
    muscle strengthening exercise, is generally preferred
    over passive treatment once the acute pain has im-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 47: Cervical Degenerative Disease

    Cervical Spondylotic Radiculopathy

    Clinical Evaluation
    Patients with cervical spondylotic radiculopathy report
    pain and/or neurologic dysfunction along a nerve root
    distribution as a result of compression of the involved
    root(s). The amount of weakness, numbness, or pain
    experienced varies. It is important to keep in mind,
    however, that not all patients with cervical radiculopathy have classic radiating arm pain symptoms. Not
    infrequently, radiculopathic pain is localized to one side
    of the neck and shoulder girdle and does not run down
    the arm. Trapezial and periscapular pain can be associated with radiculopathy arising from virtually any cervical level.
    The two most common causes of cervical radiculopathy are soft and hard disk pathology (Figure 3). Soft
    disk pathologies represent acute ruptures with extrusion of nuclear material into the epidural space. Osteophytes in association with bulging disks may be referred to as hard disks. Disk height loss and bulging of

    2011 American Academy of Orthopaedic Surgeons

    Figure 3

    Soft disk herniation versus spondylotic radiculopathy and oblique radiograph. A, Axial MRI demonstrating a foraminal soft disk herniation. B,
    Axial MRI of a different patient demonstrating
    bilateral foraminal stenosis from uncinate hypertrophy, which is also demonstrated on C, the
    oblique radiograph (arrow, in the C5-6
    foramen).

    the anulus fibrosus associated with degeneration can


    also cause radiculopathy by decreasing the space available for the nerve root either within or as it enters the
    neuroforamen.
    Table 1 lists typical pain and neurologic patterns associated with radiculopathies of the cervical nerve
    roots. The most common levels of root involvement are
    C6 and C7. High cervical radiculopathies (C2, C3, C4)
    are less common but may present with unilateral upper
    trapezial pain, neck pain, and headaches.
    A careful physical examination should be performed
    to identify the nerve root involved, with the caveat that
    crossover within myotomes and dermatomes may be
    present. In contrast to the lumbar spine, posterolateral
    disk herniations and foraminal stenosis in the cervical
    spine tend to produce radiculopathy of the nerve root
    exiting at the same level. For example, both a C5-C6
    disk herniation and C5-C6 foraminal stenosis typically
    produce a C6 radiculopathy. A large central to midlateral disk herniation or stenosis may, however, cause a
    radiculopathy of the next lower nerve root.
    Several provocative tests may elicit or reproduce
    symptoms of radiculopathy. A Spurling maneuver may
    reproduce the radicular symptoms in a patient with a
    foraminal disk or stenosis. The neck is maximally extended and rotated to the side of the pathology. Concomitant adduction of the shoulder with extension of
    the elbow and wrist may accentuate the Spurling sign,
    as these maneuvers not only narrow the foramen but
    also stretch the root. Improvement of symptoms may

    Orthopaedic Knowledge Update 10

    5: Spine

    proved. Epidural injections for degenerative disks and


    facet joint injections for symptomatic arthrosis have
    been reported to provide pain relief4,5 and may be considered if other less invasive forms of nonsurgical treatment fail. However, their true efficacy in controlled
    studies is lacking, and it seems doubtful that they will
    have any effect on the long-term natural history of
    these conditions.
    For patients with symptomatic facet arthrosis in
    whom nonsurgical treatment fails, surgical fusion may
    yield reliable results if a specific facet joint can be implicated,2 either in the subaxial or atlantoaxial spine. In
    addition, those with more readily identifiable pain generators such as kyphosis have also been shown to benefit from surgery, particularly if the kyphosis is associated with myelopathy or significant functional
    impairments such as loss of horizontal gaze or difficulty eating. However, considerable controversy arises
    in the surgical management of patients whose pain is
    thought to be mediated by a degenerative disk, as one
    of the biggest challenges in this population lies in identifying the correct pain generator because there is no
    unequivocal method for doing so. Furthermore, because radiographic changes of spondylosis are so prevalent, no radiographic modality alone can be relied
    upon to make the diagnosis. Despite these obstacles,
    authors have reported favorable results with anterior
    cervical diskectomy and fusion in patients with degenerative disks, primary reports of axial neck pain, and
    concordant diskograms.6,7 However, both surgeon and
    patient must be aware that much more consistent results are achievable when surgically managing neural
    compressive pathologies, such as radiculopathy and
    myelopathy, instead. In the setting of radiculopathy or
    myelopathy, associated headaches have been shown to
    improve after anterior cervical diskectomy and fusion
    or cervical arthroplasty.8

    613

    Section 5: Spine

    Table 1

    Common Cervical Radiculopathy Patterns


    Root Symptoms Motor Reflex
    C2

    Posterior occipital headaches, temporal pain

    C3

    Occipital headache, retro-orbital or


    retroauricular pain

    C4

    Base of neck, trapezial pain

    C5

    Lateral arm

    Deltoid

    Biceps

    C6

    Radial forearm, thumb, and index fingers

    Biceps, wrist extension

    Brachioradialis

    C7

    Middle finger

    Triceps, wrist flexion

    Triceps

    C8

    Ring and little fingers

    Finger flexors

    T1

    Ulnar forearm

    Hand intrinsics

    tests may help differentiate radiculopathy from peripheral entrapment neuropathies, although they are rarely
    needed as primary diagnostic modalities. In addition,
    because electrodiagnostic studies are highly operator
    dependent, they must be interpreted in light of the entire clinical and radiographic picture.

    5: Spine

    Radiographic Evaluation

    Figure 4

    ACDF 1 year after surgery. Flexion (A) and extension (B) radiographs 1 year after single-level
    ACDF with allograft and plate, demonstrating
    solid fusion and no motion across the spinous
    processes at C5-6.

    occur if the patient subsequently flexes and rotates the


    neck to the other side and abducts the shoulder with
    the hand behind the neck, as these maneuvers both
    open up the foramen and relax the root. The presence
    of a Spurling sign is very helpful in determining a cervical spine origin of symptoms, as the reproduction of
    pain with a Spurling sign is unlikely if the cause of the
    pain is outside of the cervical spine.
    The differential diagnosis of cervical spondylotic radiculopathy is similar to that for axial neck pain. In addition, peripheral nerve entrapment syndromes (for example, carpal or cubital tunnel syndromes) and
    tendinopathies of the shoulder, elbow, and wrist must
    be considered. Selective cervical nerve root injections
    can be useful in confirming the source of symptoms
    and may also be therapeutic, although it is uncertain
    whether they affect the long-term natural history of radiculopathy. Electromyography and nerve conduction
    614

    Orthopaedic Knowledge Update 10

    Osteophytes causing radiculopathy can often be seen


    on AP, lateral, and oblique radiographs. However, definitive confirmation generally requires MRI or CT myelograms. MRI is noninvasive and may be better at
    identifying disk herniations (particularly those that are
    intraforaminal and thus lateral to the root sleeve seen
    on myelography) and parenchymal cord lesions,
    whereas CT myelography may be better at detecting
    bony foraminal stenosis and delineating whether root
    compression arises from soft disk herniations versus
    hard pathology such as osteophytes.

    Treatment
    The natural history of cervical spondylotic radiculopathy is generally favorable. Many patients with disk herniations achieve resolution of symptoms over time
    without surgical intervention. Furthermore, it is not
    common for patients with radiculopathy to progress to
    myelopathy.9 Thus, in the absence of severe or progressive neurologic findings or incapacitating pain, the initial management of cervical spondylotic radiculopathy
    is usually nonsurgical and may include antiinflammatory medications, physical therapy, short term
    immobilization, oral steroid tapers, and nerve root injections.

    Surgical Treatment Options


    Anterior Cervical Diskectomy and
    Fusion or Arthroplasty
    Indications for surgery include severe or progressive
    neurologic deficit (weakness or numbness) or significant pain that fails to respond to nonsurgical treatment. Depending on the pathology, cervical spondylotic

    2011 American Academy of Orthopaedic Surgeons

    Chapter 47: Cervical Degenerative Disease

    2011 American Academy of Orthopaedic Surgeons

    Figure 5

    Total disk replacement. Flexion (A) and extension


    (B) radiographs after cervical disk replacement
    for radiculopathy. The patient has incidental,
    asymptomatic upper cervical kyphosis due to an
    old traumatic injury. Note maintenance of motion at the level of disk replacement.

    and thus potential for osteophytic regrowth. Accordingly, a more thorough decompression is necessary
    when performing arthroplasty over ACDF, including
    bilateral foraminal decompressions and removal of all
    potential impinging pathology (even that which is currently asymptomatic).
    Posterior Decompression
    Posterior laminoforaminotomy is an alternative option
    in patients with radiculopathy caused by foraminal disk
    herniations or uncinate spurs. The ideal indication is in
    the patient with foraminal root compression who obtains excellent arm symptom relief by flexing the neck
    and rotating away from the symptomatic side (a reverse Spurling sign). This position essentially mimics
    the neuroforaminal enlargement resulting from a
    foraminotomy when the medial half of the facet joint is
    resected. In such cases, the offending anterior osteophyte or disk herniation can but does not necessarily
    need to be removed to alleviate symptoms. However,
    poor symptom relief with the reverse Spurling maneuver may indicate the need to remove the anterior osteophyte or herniation, which may be difficult to accomplish from a posterior approach in certain cases. If so,
    an anterior approach may be preferable.
    Major advantages of posterior foraminotomy are
    that it can be performed with minimal patient morbidity and it avoids both fusion and placement of an artificial disk. However, disadvantages include the possibility for incomplete decompression in the setting of
    anterior compressive lesions, as well as the potential for
    deterioration of results with time as the degenerative
    process continues in the absence of a fusion.17 Despite
    these potential limitations, large series, including those
    using laminoforaminotomy through a minimally invasive approach, have reported arm pain relief in 90% to
    97% of patients.17-20

    Orthopaedic Knowledge Update 10

    5: Spine

    radiculopathy may be surgically addressed anteriorly or


    posteriorly. Anterior cervical diskectomy and fusion
    (ACDF) is currently the most common procedure in the
    surgical treatment of cervical radiculopathy (Figure 4).
    Although initially described with autograft and no instrumentation, many surgeons currently use allograft
    and a plate to avoid complications related to iliac crest
    autograft harvest while still achieving satisfactory arthrodesis rates and maintenance of segmental lordosis.
    Reported outcomes for relief of arm pain, as well as improvements in motor and sensory function are typically
    in the 90% range.10 Benefits of ACDF include the direct
    removal of most lesions causing cervical radiculopathy
    (such as herniated disks or uncovertebral spurs)
    without requiring intraoperative neural retraction, restoration or improvement in overall cervical alignment,
    indirect foraminal decompression resulting from restoration of interbody height with the graft, and improvement in spondylotic neck pain with fusion. There are
    extremely low rates of infection or wound complications, cosmetically preferable interior scars compared
    to posterior incisions, and mild perioperative pain in
    most cases. Potential drawbacks of ACDF include
    pseudarthrosis (rate varies widely according to graft
    type and use of plate, but modern data report 5% to
    10% for a single-level ACDF),11-13 persistent speech and
    swallowing complications related to the anterior approach,14,15 and the potential for accelerated adjacent
    segment degeneration with fusion.
    Recently, cervical arthroplasty has become available
    for the treatment of cervical radiculopathy (Figure 5).
    Arthroplasty appears to enjoy the same set of anterior
    approach-related advantages as ACDF, but one major
    advantage over ACDF is preservation of motion and
    thus potentially less adjacent segment disease. Longterm studies are currently not available to determine
    whether arthroplasty can indeed decrease the rate of
    symptomatic adjacent segment disease requiring repeat
    surgery,16 and debate continues as to whether adjacent
    segment disease is actually accelerated in those who
    have undergone fusion. However, The US Food and
    Drug Administration (FDA) Investigational Device Exemption (IDE) trial data for three different cervical arthroplasty devices have been favorable at 2-year
    follow-up, with at least equivalent clinical outcomes to
    ACDF in terms of relief of neck and arm pain. Reported device-related complications have been few, and
    the short-term reoperation rate may be lower than that
    of ACDF. Currently, the best indication for arthroplasty
    appears to be radiculopathy in relatively younger patients with reasonable motion at the involved segment.
    Potential contraindications include poor bone quality
    that could compromise implant stability, kyphosis, and
    segments that do not demonstrate significant motion
    preoperatively. Other contraindications include boneforming arthropathies such as ossification of the posterior longitudinal ligament (OPLL) and diffuse idiopathic skeletal hyperostosis, instability, and neck pain
    due to facet arthrosis. It remains to be seen whether arthroplasty may lead to a higher rate of recurrent disease over time at the index level due to ongoing motion

    615

    Section 5: Spine

    Physical Examination
    Although a detailed neurologic and physical examination should be performed (Table 2), a normal neurologic examination does not exclude the diagnosis of
    myelopathy, just as the absence of neck or arm pain
    similarly does not rule out the diagnosis.21

    Differential Diagnosis

    Figure 6

    MRI studies demonstrating a massive herniated


    nucleus pulposus. Axial (A) and sagittal (B)
    views of the cervical spine of a 42-year-old
    man with severe cervical myelopathy due to a
    massive soft disk herniation, manifested as gait
    instability, bilateral hand numbness, burning
    dysesthesias in the arms, and hand clumsiness
    but minimal to no radiating neck or arm pain.
    Note the cord signal changes present on B.

    Cervical Spondylotic Myelopathy

    History

    5: Spine

    Cervical myelopathy describes the condition caused by


    compression of the spinal cord (Figure 6). Upper extremity symptoms include a generalized feeling of clumsiness of the arms and hands, dropping things, inability
    to manipulate fine objects such as coins or buttons,
    trouble with handwriting, and diffuse (typically nondermatomal) numbness. Lower extremity complaints
    include gait instability and imbalance, leading to a
    drunken gait. Patients with severe cord compression
    may also report symptoms of Lhermitte sign: electric
    shocklike sensations that radiate down the spine or into
    the extremities with certain offending positions of the
    neck.
    Contrary to what the unsuspecting clinician might
    expect, patients with myelopathy often may not present
    with many of the symptoms commonly attributed to
    spinal column degeneration. For example, despite advanced degrees of spondylosis, many floridly myelopathic patients have no neck pain. Although radicular complaints such as radiating arm pain may coexist
    with myelopathy if the patient also has symptomatic
    nerve root compression, many myelopathic patients
    have no radicular symptoms or signs despite imaging
    studies that clearly demonstrate root compression. It is
    this patient with no pain in whom myelopathy may be
    undiagnosed until it becomes severe. Many patients
    with myelopathy also deny any loss of motor strength
    until the condition progresses to the later stages. Subtle
    bowel and bladder symptoms, such as urinary urgency,
    can be elicited with a careful history, but frank incontinence is relatively rare and typically occurs during later
    stages of disease.
    616

    Orthopaedic Knowledge Update 10

    The most common cause of cervical myelopathy in patients older than 50 years is spondylosis (degenerative
    changes), leading to the condition known as cervical
    spondylotic myelopathy (CSM). Anterior structures,
    such as bulging, ossified, or herniated disks, as well as
    osteophytic bone spurs, are the most common causes of
    cord compression in CSM. Degenerative spondylolisthesis of the cervical spine can also exacerbate or cause
    compression (Figure 1). Less commonly than their anterior counterparts, posterior structures, such as ligamentum flavum hypertrophy or, rarely, ossification of
    the ligamentum flavum, may also contribute to cord
    compression.
    CSM commonly arises in the setting of a congenitally narrowed spinal canal. In these patients, the cord
    may have had sufficient space and escaped compression
    during the patients relative youth until the accumulation of a threshold amount of space-occupying degenerative changes. Although CSM tends to be a disorder
    seen in the older patient, depending on the degree of
    congenital stenosis and the magnitude of the accumulated spondylotic changes, it can be seen in patients
    younger than 50 years.
    OPLL is another major cause of cervical myelopathy
    (Figure 7). The cause of OPLL remains unclear but is
    most likely multifactorial, with both genetic and metabolic factors involved, including diabetes and obesity.
    Other causes of cervical myelopathy include various
    etiologies of cervical cord compression, such as tumor,
    epidural abscess, osteomyelitis/ diskitis, and trauma.
    Kyphosis, whether primary or occurring after laminectomy, can also cause cord compression and myelopathy. Whenever evaluating patients with myelopathic
    complaints, it is important that a broad differential diagnosis, including nonspinal conditions such as stroke,
    movement disorders, vitamin B12 deficiency, amyotrophic lateral sclerosis, and multiple sclerosis, be kept
    in mind.

    Radiographic Evaluation
    The lateral radiograph can be used to determine the degree of congenital cervical stenosis present. A Pavlov
    ratio (AP diameter of canal/AP diameter of vertebral
    body) of less than 0.8 suggests a congenitally narrow
    spinal canal predisposing to stenosis and cord compression. A space available for the cord of 13 mm or less
    also suggests a narrow sagittal diameter of the spinal
    canal and has been shown to correlate with neurologic
    injury after trauma.
    To confirm spinal cord compression, advanced imaging in the form of MRI or CT myelography is necessary. MRI is noninvasive and provides adequate imag-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 47: Cervical Degenerative Disease

    Table 2

    Physical Findings in Cervical Myelopathy


    Test

    Finding

    Significance

    Motor examination

    Weakness

    Grip and intrinsic strength not uncommonly


    affected

    Sensory examination

    Alteration to touch or pinprick

    Sensory levels are rarely seen, compared to


    thoracic myelopathy

    Reflexes

    Hyperreflexia

    May be normal or even diminished in the


    presence of conditions affecting peripheral
    nerves (for example, diabetes, neuropathy,
    root compression)

    Gait

    Unsteady gait

    May be seen with either cervical or thoracic


    myelopathy

    Hoffman sign

    Flicking the middle finger distal phalanx


    results in pathologic flexion of the thumb
    and index finger

    Upper motor neuron sign

    Inverted radial reflex

    Diminished brachioradialis reflex with


    contraction of the finger flexors instead

    Classically due to cord and root compression at


    C56, but may arise from compression at other
    levels

    Clonus

    Sustained (>3) beats

    Upper motor neuron sign

    Babinski

    Upgoing toe

    Upper motor neuron sign, may indicate poorer


    prognosis

    Finger escape sign

    Inability to maintain the ulnar digits in an


    extended and adducted position

    Consistent with cervical myelopathy

    Scapulohumeral reflex

    Tapping the tip of the scapula results in brisk


    scapular elevation and humeral abduction

    Consistent with upper cervical myelopathy

    Jaw jerk

    Tapping lower jaw leads to a brisk jerk

    Origin of upper motor neuron findings may be


    in brain rather than spinal cord

    Treatment
    Unlike cervical spondylotic radiculopathy, cervical
    spondylotic myelopathy tends to be progressive and
    rarely improves in the long term without surgical management.22 The typical progression is a stepwise clinical
    deterioration puctuating stable periods. Continued impingement by the spondylotic spine results in cord ischemia by compressing the anterior spinal artery and
    also may have a direct mechanical effect on the cord.

    2011 American Academy of Orthopaedic Surgeons

    5: Spine

    ing characteristics in most patients. A closed MRI is


    preferred over an open study whenever possible because of its superior image quality. Signal changes
    within the cord may be demonstrated on MRI and are
    suggestive of severe compression. Signal changes seen
    on T1-weighted images correlate with a poorer prognosis for neurologic recovery following surgical decompression. When necessary, CT myelograms provide outstanding resolution of both bony and neural anatomy
    for surgical planning. Alternatively, if a high-quality
    MRI is present but questions remain regarding bony
    anatomy for the purposes of surgical planning, a noncontrast CT can be obtained to provide complementary
    information. OPLL and osteophytes are much easier to
    identify on CT than MRI.

    Surgical management has been shown to improve functional outcomes, pain, and neurologic status compared
    to nonsurgical treatment.23 It has also been suggested
    that early intervention improves prognosis before permanent destructive changes occur in the spinal cord.24
    Therefore, nonsurgical treatment should be reserved for
    patients with mild cases or those who pose a prohibitive surgical risk. If nonsurgical treatment is elected,
    patients are instructed to report any progression in
    symptoms. An orthosis, anti-inflammatory medications, and neck strengthening exercises can be considered along with physical therapy for balance and gait
    training. Traction and chiropractic manipulation
    should probably be avoided in these patients, as they
    are unlikely to be of much benefit but do carry a small
    risk of harm.
    It is not so clear, however, how best to treat patients
    with imaging evidence of cord compression but no clinical symptoms of myelopathy. This scenario not infrequently occurs, for example, in patients who obtained
    an MRI for an episode of axial neck pain that subsequently resolved. On the one hand, asymptomatic cord
    compression may eventually become symptomatic, particularly if the compression is severe or the patient sustains an injury. On the other hand, it is possible, espe-

    Orthopaedic Knowledge Update 10

    617

    Section 5: Spine

    Figure 7

    Radiograph of the cervical spine of a 72-year-old


    woman with cervical myelopathy due to massive
    OPLL (arrow). Note that the OPLL extends from
    C2-4 and is thick enough to be seen on plain
    radiographs. She was treated with multilevel
    laminectomy and fusion with excellent improvement in myelopathy and neck pain.

    5: Spine

    cially with milder degrees of stenosis, that the patient


    may never develop problems. Ultimately, this decision
    rests in the informed consent of the patient and an understanding of the risks and benefits of surgical versus
    nonsurgical care. Depending on the degree of cord
    compression or presence of spinal cord signal changes,
    it can be entirely reasonable to recommend surgery
    even in the absence of symptoms.

    Surgical Treatment Options


    Although there is consensus regarding the need for surgical treatment of cervical myelopathy, considerable debate exists regarding the optimal surgical approach.
    There are several options, including anterior decompression and fusion or arthroplasty, laminectomy,
    laminectomy and fusion, and laminoplasty. Each approach has its own set of advantages and disadvantages, and there is no one procedure that is clearly favorable in all circumstances. Considerations that may
    favor one approach over another include the number of
    stenotic levels present, patient factors such as comorbidities, and a desire to either limit or preserve motion.
    Anterior Decompression and Fusion
    The major advantage of the anterior approach for cervical myelopathy is the ability to directly decompress
    structures most commonly responsible for cord compression, such as herniated disks, spondylotic bars, and
    OPLL. Anterior decompression, in contrast to posterior
    618

    Orthopaedic Knowledge Update 10

    approaches, can also directly relieve neural compression resulting from kyphosis by removing the vertebral
    bodies over which the cord may be draped. In addition,
    the fusion procedure associated with anterior decompression helps to relieve spondylotic neck pain, can correct and improve kyphosis, immobilizes and therefore
    protects the segment of decompressed cord, and prevents recurrent disease over the fused segments. Anterior surgery also enjoys a low rate of infection and relatively mild postoperative pain. However, it is
    important to keep in mind that all anterior operations
    carry relatively small but real risks intrinsic to the anterior approach, such as persistent speech and swallowing disturbance, airway obstruction, esophageal injury,
    and vertebral artery injury.
    Overall excellent neurologic recovery rates and outcomes have been reported with anterior surgery for myelopathy.25 For those with myelopathy arising from one
    to two disk segments, the anterior approach is generally the one of choice, as it provides excellent outcomes
    with relatively little morbidity. The traditional approach has been ACDF. Recently, however, anterior diskectomy and total disk replacement has been reported
    with success in patients with single-level myelopathy,
    although the role of arthroplasty in myelopathy remains to be defined and currently may be best suited
    for those with myelopathy due to soft disk herniation
    rather than severe spondylosis.
    The supremacy of the anterior approach is not so
    clear in those requiring multilevel anterior surgery.
    Multilevel fusions are more prone to nonunion (11%
    to 40% reported in the literature) and graft/plate complications.26 In particular, long corpectomy reconstructions tend to be biomechanically unsound, even when
    plated, and carry a relatively high risk of graft kickout
    (up to 20% reported in the literature).26 If an anterior
    approach is necessary in a patient with multilevel myelopathy and the pattern of cord compression allows, it
    may be preferable to perform multilevel ACDF. Alternatively, single-level corpectomy can be done at levels
    of retrovertebral compression along with diskectomy(ies) at level(s) of disk-based compression to avoid
    the pitfalls of long multilevel corpectomy.
    Laminectomy Alone or With Fusion
    Although laminectomy without fusion for the treatment of cervical myelopathy is still performed, especially by neurosurgeons, there are numerous drawbacks
    to its use (Figure 8). Postlaminectomy kyphosis can occur after laminectomy and, although the true incidence
    in the adult population is unknown, estimates range
    from 11% to 47%.27,28 Postlaminectomy kyphosis can
    lead to potential recurrent myelopathy if the cord becomes draped and compressed over the kyphotic area.29
    In addition to potential neurologic sequelae, the kyphosis itself can be a source of neck pain or deformity. If an
    aggressive facetectomy is performed along with laminectomy, spondylolisthesis can also develop and contribute
    to cord compression. Furthermore, if a patient requires
    a subsequent posterior operation, the exposed dura

    2011 American Academy of Orthopaedic Surgeons

    Chapter 47: Cervical Degenerative Disease

    over the length of the laminectomy can make the revision more tedious, difficult, and risky to perform.
    A posterior fusion can be added to avoid the pitfalls
    of laminectomy alone. Laminectomy and fusion are
    typically performed along with lateral mass screw instrumentation. Fusion has several potential benefits, including improvement of spondylotic neck pain, better
    maintenance of cervical alignment, and prevention of
    postlaminectomy kyphosis. In addition, mild amounts
    of preexisting kyphosis can be improved after laminectomy by positioning the neck in extension before securing the instrumentation. However, in those with significant or fixed kyphosis, anterior, anterior-posterior, or
    osteotomy based approaches may be needed to achieve
    satisfactory correction. For those in whom a posterior
    approach is desirable due to the number of levels involved but fusion is not necessary, laminoplasty may be
    a better choice.

    2011 American Academy of Orthopaedic Surgeons

    Figure 8

    Postlaminectomy kyphosis. Radiograph of the cervical spine of an elderly woman with postlaminectomy kyphosis who had undergone multiple anterior and posterior procedures,
    including laminectomy without fusion, as well
    as laminectomy with attempted fusion and
    eventual removal of rods. She has multiple nonunions both anteriorly and posteriorly, as well
    as severe cervical kyphosis. It is imperative to
    prevent this sort of deformity from developing
    by avoiding cervical laminectomy alone in patients who present initially with kyphosis.

    12%.33 It most commonly affects the C5 root, resulting


    in deltoid and biceps weakness, although other roots
    can also be affected. Although typically associated with
    laminoplasty, root palsies appear to occur with similar
    frequency after all types of spinal cord decompression
    procedures (such as anterior surgery or laminectomy).
    Neck pain is often reported to be an issue in patients
    who have had laminoplasty. Controversy exists as to
    whether laminoplasty-associated neck pain is simply a
    persistence of the patients preoperative spondylotic
    neck pain or a de novo pain arising postoperatively.
    However, laminoplasty is not the procedure of choice
    in those with significant preoperative axial neck pain.
    The patient with preoperative kyphosis also presents a
    relative contraindication to laminoplasty. Most of the
    compressive structures that lead to cervical myelopathy,
    such as disk herniations, spondylotic bars, and OPLL,
    arise anteriorly. Thus, laminoplasty and other
    posteriorly-based procedures for spinal cord decompression rely on the ability of the cord to drift away
    from the anterior lesions as a result of releasing the
    posterior tethers (laminae, ligamentum flavum). Although such drifting reliably occurs in a lordotic or
    neutral cervical spine, it may not occur in the setting of
    significant kyphosis. Laminoplasty has been shown to
    produce acceptable neurologic recovery rates in patients with up to 13 of kyphosis.34 However, because
    some loss of lordosis occurs even with laminoplasty,
    laminoplasty in patients with preexisting kyphosis may

    Orthopaedic Knowledge Update 10

    5: Spine

    Laminoplasty
    Laminoplasty was designed as a procedure to achieve
    multilevel posterior cord decompression while avoiding
    postlaminectomy kyphosis, a major problem associated
    with laminectomy. There are many ways of performing
    laminoplasty, but the open door and French door techniques are the most common. The common theme in all
    variations of laminoplasty is the creation of a hinge at
    the junction of the lateral mass and lamina by thinning
    the dorsal cortex but not cutting completely through
    the ventral cortex, thereby allowing the creation of
    greenstick fractures. In the open door technique, the
    hinge is created unilaterally; in the French door version,
    the hinge is created bilaterally. The opening is performed on the opposite lateral mass-laminar junction in
    an open door procedure, or in the midline with the
    French door variation. Opening the laminoplasty increases the space available for the spinal cord, which
    drifts away from compressive lesions into the space created. The opening can then be held patent with bone
    (eg, autologous spinous process or rib allograft), sutures, suture-anchors, or specially designed plates30
    (Figure 9).
    In addition to its benefits over laminectomy, laminoplasty possesses several distinct advantages over anterior surgery. First, because an indirect decompression is
    performed, it is in general a technically easier and
    quicker operation to perform than multilevel anterior
    corpectomy, particularly in patients with severe stenosis
    or OPLL. Second, laminoplasty is a motion-preserving
    procedure. In contrast to anterior surgery, no fusion is
    required with laminoplasty. The theoretical advantages
    of laminoplasty have been borne out in head-to-head
    clinical trials with multilevel anterior corpectomy.
    Laminoplasty and anterior surgery have similiar rates
    of neurologic improvement, but laminoplasty has a
    much lower complication rate.31,32
    Laminoplasty is clearly not a perfect operation, is
    not appropriate in all cases, and does have its disadvantages. Segmental rootlevel palsy remains a concern,
    with an incidence postoperatively ranging from 5% to

    619

    Section 5: Spine

    Figure 9

    Laminoplasty. AP (A) and lateral (B) radiographs after open door laminoplasty with plate fixation. This 40-year-old
    woman had multilevel myelopathy with no axial neck pain and preserved lordosis, making her an ideal candidate
    for this operation. Partial inferior laminectomy of C3 and superior laminectomy of C7 were also performed to decompress the cord at the C3-4 and C6-7 disk spaces, respectively, while at the same time preserving the extensor
    muscular attachments as much as possible, which in turn may lessen the incidence of postoperative neck pain and
    loss of lordosis that can occur even with laminoplasty.

    5: Spine

    lead to acceleration of kyphosis, which in turn might


    cause neck pain and recurrent cord compression. In kyphotic patients with multilevel myelopathy, laminectomy with fusion may be a better alternative if the kyphosis is flexible. If the kyphosis is not flexible but
    instead fixed or ankylosed, the anterior approach with
    or without supplemental posterior surgery will likely
    lead to the best outcomes.
    Combined Anterior and Posterior Surgery
    Combined approaches are strongly recommended in
    patients with postlaminectomy kyphosis. In this setting,
    if a multilevel corpectomy is performed to decompress
    the cord, an extremely unstable biomechanical environment results due to the preexisting laminectomy: in essence, the right and left sides of the spine become disconnected from each other. Supplemental posterior
    fixation is recommended to improve construct stability.35 Likewise, in patients needing multilevel fusion (
    four motion segments) or those with significant kyphosis, especially in the setting of poor bone quality, supplemental posterior fixation and fusion should be considered.

    2.

    Ghanayem AJ, Leventhal M, Bohlman HH: Osteoarthrosis of the atlanto-axial joints. Long-term follow-up
    after treatment with arthrodesis. J Bone Joint Surg Am
    1996;78(9):1300-1307.

    3.

    Boden SD, McCowin PR, Davis DO, Dina TS, Mark


    AS, Wiesel S: Abnormal magnetic-resonance scans of
    the cervical spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg Am 1990;72(8):
    1178-1184.

    4.

    Hession WG, Stanczak JD, Davis KW, Choi JJ: Epidural


    steroid injections. Semin Roentgenol 2004;39(1):7-23.

    5.

    Silbergleit R, Mehta BA, Sanders WP, Talati SJ:


    Imaging-guided injection techniques with fluoroscopy
    and CT for spinal pain management. Radiographics
    2001;21(4):927-939, discussion 940-942.

    6.

    Palit M, Schofferman J, Goldthwaite N, et al: Anterior


    discectomy and fusion for the management of neck
    pain. Spine (Phila Pa 1976) 1999;24(21):2224-2228.

    7.

    Garvey TA, Transfeldt EE, Malcolm JR, Kos P: Outcome of anterior cervical discectomy and fusion as perceived by patients treated for dominant axialmechanical cervical spine pain. Spine (Phila Pa 1976)
    2002;27(17):1887-1895, discussion 1895.

    8.

    Riina J, Anderson PA, Holly LT, Flint K, Davis KE,


    Riew KD: The effect of an anterior cervical operation
    for cervical radiculopathy or myelopathy on associated
    headaches. J Bone Joint Surg Am 2009;91(8):19191923.

    Annotated References
    1.

    620

    Ct P, Cassidy JD, Carroll L: The Saskatchewan


    Health and Back Pain Survey: The prevalence of neck
    pain and related disability in Saskatchewan adults.
    Spine (Phila Pa 1976) 1998;23(15):1689-1698.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 47: Cervical Degenerative Disease

    Eight hundred three patients who had single-level ACDF


    or cervical arthroplasty in FDA IDE trials were evaluated post hoc for improvement in associated headaches.
    Both groups had significant improvement at 24 months
    after surgery. Level of evidence: I.
    9.

    Lees F, Turner JW: Natural history and prognosis of


    cervical spondylosis. Br Med J 1963;2(5373):16071610.

    10.

    Bohlman HH, Emery SE, Goodfellow DB, Jones PK:


    Robinson anterior cervical discectomy and arthrodesis
    for cervical radiculopathy: Long-term follow-up of one
    hundred and twenty-two patients. J Bone Joint Surg Am
    1993;75(9):1298-1307.

    11.

    Wang JC, McDonough PW, Endow K, Kanim LE, Delamarter RB: The effect of cervical plating on single-level
    anterior cervical discectomy and fusion. J Spinal Disord
    1999;12(6):467-471.

    12.

    13.

    Martin GJ Jr, Haid RW Jr, MacMillan M, Rodts GE Jr,


    Berkman R: Anterior cervical discectomy with freezedried fibula allograft: Overview of 317 cases and literature review. Spine (Phila Pa 1976) 1999;24(9):852-858,
    discussion 858-859.
    Samartzis D, Shen FH, Goldberg EJ, An HS: Is autograft the gold standard in achieving radiographic fusion in one-level anterior cervical discectomy and fusion
    with rigid anterior plate fixation? Spine (Phila Pa 1976)
    2005;30(15):1756-1761.
    Bazaz R, Lee MJ, Yoo JU: Incidence of dysphagia after
    anterior cervical spine surgery: A prospective study.
    Spine (Phila Pa 1976) 2002;27(22):2453-2458.

    15.

    Winslow CP, Winslow TJ, Wax MK: Dysphonia and


    dysphagia following the anterior approach to the cervical spine. Arch Otolaryngol Head Neck Surg 2001;
    127(1):51-55.

    16.

    Hilibrand AS, Carlson GD, Palumbo MA, Jones PK,


    Bohlman HH: Radiculopathy and myelopathy at segments adjacent to the site of a previous anterior cervical
    arthrodesis. J Bone Joint Surg Am 1999;81(4):519-528.

    17.

    Herkowitz HN, Kurz LT, Overholt DP: Surgical management of cervical soft disc herniation. A comparison
    between the anterior and posterior approach. Spine
    (Phila Pa 1976) 1990;15(10):1026-1030.

    18.

    19.

    20.

    Henderson CM, Hennessy RG, Shuey HM Jr, Shackelford EG: Posterior-lateral foraminotomy as an exclusive
    operative technique for cervical radiculopathy: A review
    of 846 consecutively operated cases. Neurosurgery
    1983;13(5):504-512.
    Zeidman SM, Ducker TB: Posterior cervical laminoforaminotomy for radiculopathy: Review of 172 cases.
    Neurosurgery 1993;33(3):356-362.
    Adamson

    TE:

    Microendoscopic

    posterior

    2011 American Academy of Orthopaedic Surgeons

    cervical

    21.

    Rhee JM, Heflin JA, Hamasaki T, Freedman B: Prevalence of physical signs in cervical myelopathy: A prospective, controlled study. Spine 2009;34(9):890-895.
    In a prospective evaluation of 39 patients with cervical
    myelopathy who were compared with 37 control subjects, myelopathic physical signs were substantially
    more prevalent in the myelopathy group. However,
    21% of myelopathy patients (as evidenced by myelopathic symptoms, correlative spinal cord compression on imaging, and improvement in myelopathy after
    decompression) did not show any physical signs. Thus,
    the absence of myelopathic signs does not preclude the
    diagnosis of cervical myelopathy or its successful surgical treatment.

    22.

    Nurick S: The pathogenesis of the spinal cord disorder


    associated with cervical spondylosis. Brain 1972;95(1):
    87-100.

    23.

    Sampath P, Bendebba M, Davis JD, Ducker TB: Outcome of patients treated for cervical myelopathy: A prospective, multicenter study with independent clinical review. Spine (Phila Pa 1976) 2000;25(6):670-676.

    24.

    Emery SE, Smith MD, Bohlman HH: Upper-airway obstruction after multilevel cervical corpectomy for myelopathy. J Bone Joint Surg Am 1991;73(4):544-551.

    25.

    Emery SE, Bohlman HH, Bolesta MJ, Jones PK: Anterior cervical decompression and arthrodesis for the
    treatment of cervical spondylotic myelopathy: Two to
    seventeen-year follow-up. J Bone Joint Surg Am 1998;
    80(7):941-951.

    26.

    Rhee JM: Posterior surgery for cervical spondylotic myelopathy. Semin Spine Surg 2004;16:255-263.

    27.

    Kato Y, Iwasaki M, Fuji T, Yonenobu K, Ochi T: Longterm follow-up results of laminectomy for cervical myelopathy caused by ossification of the posterior longitudinal ligament. J Neurosurg 1998;89(2):217-223.

    28.

    Mikawa Y, Shikata J, Yamamuro T: Spinal deformity


    and instability after multilevel cervical laminectomy.
    Spine (Phila Pa 1976) 1987;12(1):6-11.

    29.

    Guigui P, Benoist M, Deburge A: Spinal deformity and


    instability after multilevel cervical laminectomy for
    spondylotic myelopathy. Spine (Phila Pa 1976) 1998;
    23(4):440-447.

    30.

    Park AE, Heller JG: Cervical laminoplasty: Use of a


    novel titanium plate to maintain canal expansionsurgical technique. J Spinal Disord Tech 2004;17(4):265271.

    31.

    Yonenobu K, Hosono N, Iwasaki M, Asano M, Ono K:


    Laminoplasty versus subtotal corpectomy: A comparative study of results in multisegmental cervical spondy-

    Orthopaedic Knowledge Update 10

    5: Spine

    14.

    laminoforaminotomy for unilateral radiculopathy: Results of a new technique in 100 cases. J Neurosurg
    2001;95(1, suppl)51-57.

    621

    Section 5: Spine

    lotic myelopathy. Spine (Phila Pa 1976) 1992;17(11):


    1281-1284.
    32.

    Uematsu Y, Tokuhashi Y, Matsuzaki H: Radiculopathy


    after laminoplasty of the cervical spine. Spine (Phila Pa
    1976) 1998;23(19):2057-2062.

    Suda K, Abumi K, Ito M, Shono Y, Kaneda K, Fujiya


    M: Local kyphosis reduces surgical outcomes of expansive open-door laminoplasty for cervical spondylotic
    myelopathy. Spine (Phila Pa 1976) 2003;28(12):12581262.

    35.

    Riew KD, Hilibrand AS, Palumbo MA, Bohlman HH:


    Anterior cervical corpectomy in patients previously
    managed with a laminectomy: Short-term complications. J Bone Joint Surg Am 1999;81(7):950-957.

    5: Spine

    33.

    Edwards CC II, Heller JG, Murakami H: Corpectomy


    versus laminoplasty for multilevel cervical myelopathy:
    An independent matched-cohort analysis. Spine (Phila
    Pa 1976) 2002;27(11):1168-1175.

    34.

    622

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 48

    Cervical Spine Trauma


    Jens R. Chapman, MD

    Richard J. Bransford, MD

    Epidemiologic Factors
    Cervical spine injuries are particularly challenging to
    treat despite dramatic improvements in diagnostic and
    treatment capabilities. The cervical spine allows considerable head motion while it protects the spinal cord,
    the exiting nerve roots, and the accompanying vascular
    structures. The exposed position, high carrying load,
    expansive range of motion, and limited intrinsic bony
    stability of the spine in the neck region mean that it is
    exposed to a wide range of injuries, from soft-tissue
    sprains to severe fracture-dislocations with associated
    neurovascular injury. Cervical spine trauma is estimated to lead to 25,000 new fractures per year in the
    United States, affecting 2% to 3% of all patients with
    blunt trauma.1 The estimated incidence is 10 to 50 fractures per 1 million population. The leading injury
    mechanisms are motor vehicle crashes, falls from a
    height, and sports-related incidents.
    Important dynamic changes are occurring in the
    prevalent types of injuries and the affected populations.

    2011 American Academy of Orthopaedic Surgeons

    Injury Assessment Strategies and Clearance


    Clinicians treating trauma patients must effectively assess and predict the structural integrity of the entire
    spine, and especially the cervical spine because of its
    exposed position. Spine assessment and clearance are
    best accomplished with a systematic clinical evaluation
    and appropriate imaging studies. Knowledge of the injury mechanism, the patients preinjury functional status,
    and injury-related changes in neurologic function are important in a spine injury assessment. Posterior neck tenderness, ecchymosis, and interspinous crepitus or gapping are key examination findings. A formal neurologic
    evaluation, including mental status and extremity assessment, using the American Spinal Injury Association (ASIA) template (http://www.asia-spinalinjury.org/
    publications/2006_Classif_worksheet.pdf) should be
    part of a routine examination. It is very important to formally document these neurologic assessments in an ongoing fashion to provide a timeline of neurologic status.
    Chapter 44 provides specific information on neurologic
    status assessment.
    The greatest impact on outcome is prevention of secondary neurologic deterioration in a patient who is initially neurologically intact. It is important to optimize
    the chances for recovery in a patient with an established spinal cord injury. The risk of secondary neurologic injury and long-term patient morbidity is largely
    correlated with the presence of a spine injury that was
    overlooked because of inadequate imaging studies.
    Therefore, an effective spine clearance algorithm and

    Orthopaedic Knowledge Update 10

    5: Spine

    Dr. Chapman or an immediate family member serves as


    a board member, owner, officer, or committee member
    of the North American Spine Society, AO Spine International, AO Spine North America, and the Cervical Spine
    Research Society; is a member of a speakers bureau or
    has made paid presentations on behalf of Medtronic Sofamor Danek and Synthes USA; serves as a paid consultant to Synthes USA; serves as an unpaid consultant to
    DePuy (a Johnson & Johnson Company), Stryker, Alseres
    Pharmaceuticals, and Paradigm Spine; has received research or institutional support from DePuy (a Johnson &
    Johnson Company), Medtronic Sofamor Danek, Synthes,
    Stryker, HansJoerg and the Wyss Foundation; and has received nonincome support (such as equipment or services), commercially derived honoraria, or other nonresearchrelated funding (such as paid travel) from
    Synthes, Stryker, and Medtronic Sofamor Danek. Dr.
    Bransford or an immediate family member is a member
    of a speakers bureau or has made paid presentations
    on behalf of AO and Synthes; serves as a paid consultant
    to Synthes; and has received research or institutional
    support from AO, Biomet, Pfizer, Wright Medical Technology, DePuy (a Johnson & Johnson Company), Spinevision, Stryker, and Synthes.

    Historically, the focus of cervical spine trauma care has


    been on highkinetic energy injuries affecting relatively
    young and healthy individuals. Decreasing rates of cervical spine trauma have been reported in this demographic group, along with increasing rates of survival.
    The cause may be improvements in automobile safety
    features, such as airbags. However, in patients older
    than 65 years, injuries resulting from low-energy mechanisms or preexisting spine or systemic comorbidities
    are of increasing concern because of the risk of morbidity and mortality. More than 20% of all cervical spine
    trauma is estimated to occur in patients older than 65
    years. The population older than 85 years is projected
    to double by 2025.2 Unstable injuries, such as odontoid
    fractures, are the most common injury variant in patients older than 65 years.3

    623

    Section 5: Spine

    Figure 1

    Coronal CT reformat of a 24-year-old man with


    type III occipital condyle fracture in the setting
    of a highly unstable occipitocervical dissociation
    with occiput-C1 widening and C1-C2 widening
    (arrow).

    5: Spine

    implementation of spinal column protection are integral to the overall trauma care pathway.
    Triage of patients who may need spine imaging and
    immobilization can follow several suggested pathways.
    The widely accepted, relatively simple National Emergency X-Radiology Utilization Study (NEXUS) criteria
    for clinical cervical spine clearance includes five points:
    the patient (1) is cognitively unimpaired; (2) does not
    have neck pain; (3) has a nonfocal neurologic examination; (4) does not have tenderness, swelling, ecchymosis, or major lacerations in the head-neck area; and (5)
    has a pain-free neck range of motion. Patients who
    meet these criteria do not need further cervical spine
    imaging.4 Spine injury is suspected in any patient who
    has been involved in a traumatic event and does not
    meet all of these criteria. A formal, methodical clinical
    evaluation is required, including documentation of the
    injury history, neck inspection and palpation, and a
    neurologic assessment using the ASIA standards. The
    role of routine cervical screening radiographs has been
    reevaluated based on several large-scale studies, and the
    increasingly common availability of rapid-acquisition
    CT technology in emergency departments has made CT
    the preferred imaging modality.5 The inherent limitations of conventional radiographs include limited visualization of the transition zones, especially in the craniocervical and cervicothoracic region. Helical cervical
    spine CT increasingly is being validated as the preferred
    diagnostic modality for at-risk patients. More specifically, routine screening CT of the cervical spine has
    been recommended for patients with craniofacial, long
    bone, or pelvic trauma; impaired cognitive status; focal
    neurologic findings on examination; a history of an ankylosing spine disorder; a history of high-energy
    trauma (such as a fall of 10 feet or a motor vehicle
    crash at a speed of 30 miles per hour); or if there was
    an associated death at the scene of the traumatic
    624

    Orthopaedic Knowledge Update 10

    event.4-6 The disadvantage of this imaging approach is


    the considerable radiation dose to the thyroid and
    other soft tissues. Neck clearance continues to be challenging in patients with a persistent severe cognitive impairment, although recent studies suggest that these patients can be cleared of a clinically unstable injury if CT
    reveals no abnormality.4 Most centers use a three-phase
    protocol for spine clearance for at-risk patients. In the
    first phase, a helical CT of the entire cervical spine,
    with sagittal and coronal reformatted views, is reviewed and presumably cleared. The second phase involves a secondary review of all spine imaging studies
    after an attempt at clinical reevaluation. If the absence
    of any radiographic sign of injury is confirmed, the
    third phase is initiated, in which upright lateral spine
    radiographs are used to assess for the presence of newonset deformity. Another approach is the use of MRI as
    a screening tool for these patients in the third phase.
    The considerable cost and logistic factors related to
    MRI use have continued to limit its popularity.
    For patients with questionable ligamentous instability, a traction test can be helpful in demonstrating relevant disruption. This test is done under fluoroscopy by
    an experienced examiner (preferably a surgeon) and
    uses low in-line weight application of no more than
    10 lb. Flexion-extension radiographs remain a mainstay of cervical spine instability evaluation for awake
    patients without known neurologic or major musculoskeletal injury but not for patients with severe head injury. For now, plain CT with a secondary review protocol remains a reasonable clearance system for patients
    with a protracted lack of interactive cognitive skills.
    Routine MRI has been recommended for any patient
    with cervical spinal cord injury and for screening a patient with an ankylosing disorder or a possible occult
    spine injury.7 In addition to revealing acute hemorrhage
    and cord signal changes, some imaging sequences, such
    as T2-weighted fat suppression views, also can show
    acute ligament injuries of the cervical spine. There is a
    strong relationship between mechanism of injury, cord
    signal changes, and severity of spinal cord injury as
    seen on MRI.

    Injury Classification

    Upper Cervical Spine


    Occipital condyle fractures have received increased attention as detection rates have increased with the routine use of CT in trauma applications. The simple
    Anderson-Montesano three-part system has remained
    largely unchallenged and provides helpful guidance for
    management.8
    This system differentiates impaction injuries (type I)
    from shear injuries that extend into the skull base (type
    II). Both of these injury types usually are inherently stable, but little is known about their long-term clinical
    outcomes. A type III injury is an avulsion injury of the
    alar ligaments, and it has the potential to be a highly
    unstable craniocervical disruption (Figure 1).

    2011 American Academy of Orthopaedic Surgeons

    Chapter 48: Cervical Spine Trauma

    2011 American Academy of Orthopaedic Surgeons

    juries into bony avulsion injury (type I) or ligamentous


    injury (type II) has been suggested because of the inherently different likelihood of healing with nonsurgical
    care.12 Purely ligamentous TAL disruption has almost
    no chance of healing, but most bony avulsion injuries
    can be expected to heal with appropriate nonsurgical
    management.
    Odontoid fractures are represented by the wellknown Anderson-dAlonzo spine injury classification.14
    Although simple and intuitively clear, this system includes an exceedingly rare injury in its type I category,
    and it does not differentiate type II injuries by the
    severity-related factors that distinguish their prognosis
    or treatment. Some subtypes of type II fractures are
    useful for avoiding management pitfalls, but they are
    not part of a systematic, integrated odontoid classification system.15
    Fractures of the axis have been divided into the
    broad categories of vertebral body fractures and hangmans fractures. The four-tiered classification of hangmans fracture separates type II fractures into type II
    and type IIA.16 Type II fractures are intrinsically more
    stable from a discoligamentous standpoint; they can
    usually be managed in traction and converted to external immobilization. Type IIA fractures feature flexiondistraction through the C2-3 disk with posterior ligamentous disruption. An additional subtype, the
    Eismont-Starr atypical hangman variant, is associated
    with a much higher neurologic injury rate (Figure 2).
    The Francis fracture severity scale is a relatively simple
    and reproducible means of describing angulation and
    translational displacement. In general, the upper cervical spine injury classifications are highly specific and
    very detailed, but a systematic regional classification
    has proved elusive.11
    It is important to remember that a specific injury entity must be seen in the context of its possible association with other upper cervical spine injuries. For instance, an odontoid fracture may be associated with a
    TAL disruption, and this injury is dramatically less
    likely to heal nonsurgically. Similarly, an isolated atlantoaxial rotatory subluxation may be eminently treatable with nonsurgical means. However, this injury may
    be associated with a contralateral atlantoaxial joint disruption that renders the entire upper cervical spine unstable in the form of a craniocervical disruption. These
    combination injuries are not uncommon in the upper
    cervical spine. A detailed assessment of the entire functional unit is required, with subsequent comprehensive
    treatment to optimize the result.

    5: Spine

    The Traynelis classification of atlanto-occipital dissociations depends on the direction of displacement.9


    This system is limited by absence of a severity component and is likely to disproportionately show anterior
    cranial displacement relative to the cervical spine because of the size of the head. As with a true ligamentous disruption of any joint in the body, an injury description using the direction of displacement can be
    somewhat misleading if the two adjoining bony ends
    can be manipulated in any direction.
    The Harborview craniocervical injury classification
    attempts to identify the severity of the traumatic disruption in a three-tier system analogous to that of basic
    ligamentous extremity injury.10 Type I injuries are isolated and can be treated nonsurgically; these include
    stable, unilateral type III occipital condyle injuries or
    isolated alar ligament tears. A type III injury is an obvious complete disruption of all interconnecting ligaments; patients are subclassified on the basis of
    whether they survive to reach the emergency department. The limitation of this system lies in the ambiguous definition of a type II injury, which is a craniocervical disruption with borderline radiographic screening
    values. These injuries are inherently unstable but may
    be missed on cursory evaluation. This injury category
    points out the potential for incomplete and occult craniocervical disruption, which remains a challenge to
    timely recognition. Studies have suggested at least a
    30% delay in diagnosis with potential for serious secondary neurologic deterioration in patients with these
    potentially life-threatening injuries.10 The advent of a
    systematic head-and-neck CT protocol and increased
    awareness of this injury has reduced the incidence of
    missed craniocervical injuries.
    There have been few concerted efforts to revise the
    existing classification systems for atlas fractures.11 The
    basic questions pertain to stability prediction and the
    fate of displaced intra-articular fractures. The Levine
    classification differentiates problematic fractures from
    injuries with an anticipated uncomplicated course.12
    The less concerning fractures include posterior arch
    fractures, transverse process injuries, and some lateral
    mass fractures. Segmental anterior arch fractures and
    displaced intra-articular injuries, as well as comminuted three- or four-part bursting injuries, are of concern because of their instability and complex management course. One of the key factors in determining the
    stability of atlas fractures is the integrity of the transverse atlantal ligament (TAL), which is not specifically
    addressed in the Levine classification system. Previously
    it was believed that a combined overhang of the C1 lateral masses by more than 6.9 mm, as measured on
    open-mouth odontoid radiographs, was indicative of a
    TAL disruption. However, this long-held belief was
    challenged by study of advanced imaging modalities,
    which found that only 39% of atlas fractures with a
    disrupted TAL were detected if radiographs alone were
    used.13 The 7-mm overhang criterion for determining a
    TAL disruption is no longer believed to be relevant as a
    screening tool; scrutiny of relevant CT and MRI is recommended instead. A simple categorization of TAL in-

    Lower Cervical Spine and


    Cervicothoracic Junction
    Classifications of lower cervical spine injuries have
    been formulated around anatomic, biomechanical, or
    combined concepts and features. A lack of basic characteristics such as simplicity and interobserverintraobserver reliability, as well as a lack of relevance
    to treatment and outcomes, has limited the general acceptance of lower cervical spine classification systems.17

    Orthopaedic Knowledge Update 10

    625

    Section 5: Spine

    Figure 2

    A, Preoperative axial CT scan of an atypical hangmans fracture in a 73-year-old woman with a history of C4-C6 fusion presenting with ASIA D spinal cord injury. B, Postoperative lateral radiograph after C2-C3 anterior cervical diskectomy and instrumented fusion.

    5: Spine

    Conceptually, the AO-ASIF system accepted by the Orthopaedic Trauma Association has the merit of combining widely accepted injury types with some correlation
    to treatment algorithms. The three basic injury categories consist of a simple type A injury, including inherently stable fractures that usually result from an axial
    loading mechanism; a type B injury, including bending
    injuries such as a unilateral or bilateral dislocation with
    or without fractures; and a type C injury, including circumferentially destabilized fracture-dislocations. Unfortunately, a tiered system of subcategories has greatly increased the complexity of this system at the cost of
    reproducibility. This system has limited relevance for
    management. The most detailed system that incorporates an injury severity gradient is the mechanistic
    Allen-Ferguson model.18 This system is based on the assumption of a unidirectional force of varying grades of
    energy applied in a highly predictable manner. However, this system is hampered by a lack of discrete differentiators and insufficient interobserver reliability; it
    has had limited use for research purposes.
    Recently, attempts to simplify pleomorphic lower
    cervical spine injuries into the simple injury categories
    typical of conventional classification systems have been
    expanded by the concept of severity scores, which attempt to quantify injuries by attaching a numeric score
    to key elements of the cervical spinal column. The Cervical Spine Injury Severity Scale (CSISS) measures displacement of injury in the anterior, posterior, and two
    lateral columns and assigns a total score.19 The alternative Spine Trauma Study Group system is referred to as
    the subaxial injury classification. This system derives
    626

    Orthopaedic Knowledge Update 10

    an injury score from a combination of three components: injury morphology, integrity of the diskoligamentous complex, and neurologic injury.20 Neurologic
    injury status, as determined from the physical examination, is incorporated into the overall injury description.
    There is general agreement that neither severity scale
    will serve as the sole tool for stability assessment or
    treatment decision making. However, by providing a
    checklist of the important components of cervical spine
    stability, these classifications help clinicians create a
    more reproducible decision-making process and invite
    researchers to compare treatment results based on injury severity calculations. The intraobserver and interobserver evaluations have been encouraging.
    No single system or concept has emerged as clearly
    preferable to the other systems. However, recent studies
    have found that the interobserver and intraobserver reliability of both severity scales is better than that of the
    more traditional classification systems. These severity
    scales have the potential to improve understanding of
    injuries by providing a checklist for complete evaluation, and they may improve understanding of treatment
    outcomes relative to injury severity.

    Management

    Emergency Management in the Field


    The emergency management of patients with a spine
    trauma is important for limiting the potential of further
    injury to a destabilized spinal column and for minimizing further bleeding and pain. The basic concepts of

    2011 American Academy of Orthopaedic Surgeons

    Chapter 48: Cervical Spine Trauma

    first responder care include avoidance of neck and back


    manipulation. Supine immobilization on a rigid backboard is used with full spine precautions and a rigid
    neck collar. The resuscitation phase consists of maintaining normal or near-normal blood pressures to maximize cord perfusion while seeking to normalize tissue
    oxygenation and striving for a hematocrit level above
    30%. Manual inline traction, awake, fiberoptic intubation, and transnasal intubation are recommended as
    adjuvant techniques to establish formal airway access
    for patients with a potential cervical spine injury while
    minimizing the potential for secondary injury displacement.21

    Reduction

    2011 American Academy of Orthopaedic Surgeons

    5: Spine

    Traction-induced realignment is a very important emergent intervention option for a displaced cervical spine
    injury, with the potential to achieve indirect neural canal decompression. The timing and technique of reduction of a cervical spine fracture-dislocation remains
    controversial, however, with respect to neuroimaging.22
    Secondary neurologic deterioration may occur as a result of disk or bone fragments being dislodged into the
    spinal canal during a reduction maneuver. The additional diagnostic insight afforded by MRI must be balanced against the potential for damage from leaving a
    cervical spine fracture-dislocation unreduced and the
    need to subject a patient with a dislocated neck to additional transfers. Even in an efficient and wellequipped trauma center, MRI is time consuming. The
    actual incidence of clinically threatening mass effects in
    patients with a subaxial fracture-dislocation was found
    to be much lower than originally feared, however.23
    Prospective studies found that it is safe for an awake,
    alert, examinable patient with spinal cord injury to undergo closed reduction with sequential skeletal traction
    and avoidance of neck manipulation before MRI is performed.24 Early reduction of cervical fracturedislocations may improve the prospects for neural injury recovery, although the incidence and specific
    circumstances leading to improvement remain unclear.
    The current general recommendation is that patients
    with a confirmed spinal cord injury should receive an
    attempt at formal closed reduction with skeletal cranial
    traction aided by serial neurologic checks and followed
    by a postreduction neuroimaging study to assess for
    ongoing cord compression.22 If the patient has ongoing
    cord compression, emergent surgical intervention with
    removal of impinging structures and stabilization is encouraged. For a patient who is neurologically intact,
    closed reduction before MRI remains an option if MRI
    is not immediately available. Closed reduction of a dislocated cervical spine in an unresponsive or otherwise
    unexaminable patient usually is discouraged until neuroimaging has been obtained and has confirmed the absence of ongoing cord compression from a disk or bone
    fragment. As the use of open anterior or posterior cervical spine decompression and instrumentation techniques has increased, there has been a recent trend toward bypassing closed reduction and taking patients

    directly to the operating room for definitive surgical decompression and instrumentation (Figure 3).
    Any form of neck traction is generally contraindicated in the presence of distraction trauma in the cervical spine because of the danger of increasing neural
    trauma and compromising arterial flow to the brain
    and spinal cord. The application of cranial tongs may
    be contraindicated in some types of skull fractures for
    fear of causing a fracture propagation and secondary
    brain injury. Therefore, application of skull tongs in the
    presence of fractures is not advisable unless approved
    by a surgeon familiar with neurotrauma.
    Closed reduction of a dislocated lower cervical spine
    should be performed in a controlled setting. The principles include patient monitoring (cardiovascular, respiratory, and neurologic), incrementally increased skeletal traction using fluoroscopy or serial radiographs,
    intravenous analgesia, and muscle relaxation. As traction is applied to the cervical spine, periodic radiographs assess for overdistraction in any of its segments.
    Manual reduction attempts are generally discouraged
    because they can exert uncontrollable forces on the
    neck and may cause a disk or bone fragment to shear
    off into the canal. Cervical reduction efforts should be
    abandoned and an urgent MRI should be obtained if
    the patients neurologic status deteriorates during reduction efforts. Reduction also is usually abandoned if
    realignment fails with traction weight amounting to
    two thirds of the patients body weight. This weight
    recommendation is not absolute, however, and it depends on individual clamp specifications. For most
    graphite-based tongs, a fixed limitation of 80 lb has
    been suggested because of the risk of clamp deformation at higher loads, with subsequent clamp pullout. In
    patients with a persistent impinging spinal cord lesion,
    emergency surgical intervention aimed at neural element decompression and stabilization of the affected
    injury segment may have to be considered (Figure 3).

    Acute Steroid Administration


    This topic is discussed in greater detail in chapter 44.
    The pharmacologic care options for patients with a suspected spinal cord injury generally are limited to intravenous administration of methylprednisolone. Blood
    pressure and cardiac output support are provided
    through intravenous administration of vasopressors to
    patients with neurogenic shock.21 The popularity of aggressive steroid management has tapered off considerably because of the absence of a demonstrable major
    clinical impact on cord recovery since completion of
    the North American Spinal Cord Injury (NASCIS) studies.25 There have been persistent questions about the
    methodology used in these studies, however. The general recommendation is that intravenous steroid administration is only a treatment option and not a recommendation or a standard of care. Steroid use has not
    been formally studied in patients with a nerve root injury or gunshot injury and, therefore, is not recommended for these indications.

    Orthopaedic Knowledge Update 10

    627

    Section 5: Spine

    Figure 3

    Algorithm for management of cervical spine dislocations.

    Nonsurgical Care

    5: Spine

    Sound decision making for treatment of any spine


    trauma is based on a comprehensive multifactorial assessment that defies the use of a simple binary algorithm. The scientific literature does not provide decisive
    guidance on preferred treatments. There is a prevalence
    of type III and IV evidence based on small patient cohorts and personal observations. Treatment preferences
    strongly differ based on the clinicians training background, type of practice, and practice location.26 In addition to the considerations for the thoracolumbar
    spine, the neck has complexities related to its exposed
    location and delicate bony structures in close proximity
    to vital arteries, neural elements, and pharyngeal structures. Craniocervical injuries and penetrating trauma
    can pose an immediate vital threat from airway compromise and anoxia. Usually decisive emergency surgical intervention is required. Vertebral artery injuries
    may considerably alter the usual diagnostic and treatment algorithm for trauma patients. For instance, anterior neck procedures, although they are less invasive
    than thoracolumbar procedures, have difficulties related to biomechanical limitations and potential postoperative aspiration and dysphagia, especially in patients older than 65 years. The important decisionmaking factors include the presence of neurologic
    injury, structural damage to key supporting structures,
    differentiation of osseous and ligamentous trauma, and
    specific injury mechanisms.19,20 Other patient factors
    also heavily influence treatment decision making, in628

    Orthopaedic Knowledge Update 10

    cluding patient age and size, quality of bone structure,


    preoperative alignment, presence of ankylosing spine
    disorders, overall injury load, and other preexistent comorbidities. General factors that favor a successful outcome of nonsurgical care include an absence of neurologic injury, predominantly bony injuries with intact
    key supporting ligaments, preservation of a satisfactory
    alignment, and a single-system injury. The choices of
    nonsurgical care range from activity restriction for a
    patient with an inherently stable injury to external immobilization with a brace or halo vest or prolonged
    recumbent skeletal traction for a patient with a very
    unstable injury. Soft collars have no inherent biomechanical stabilizing effects on the lower cervical spine
    and usually are reserved for symptom reduction in patients with neck muscle sprains. Rigid neck collars are
    suitable for external immobilization after surgery and
    can be considered for patients with a minimally deformed compression fracture or an apophyseal injury.
    However, conventional neck collars offer little stabilization to the transition zones, such as the cervicothoracic
    region. Some additional stability can be provided by
    thoracic and cranial attachments to a rigid neck collar.
    Nevertheless, injuries treated with such combination
    devices need to have some inherent stability because in
    actual use there often is a fair amount of subaxial motion.
    Halo vests continue to provide the most rigid form
    of cervical spine external immobilization. However, a
    halo vest assembly cannot fully immobilize the midcer-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 48: Cervical Spine Trauma

    vical spine. In a phenomenon known as snaking, focal


    kyphosis in the midcervical spine can be seen on a recumbent lateral radiograph, but an upright lateral radiograph shows maintained lordosis. For this reason a
    halo vest assembly is primarily used in patients with an
    upper cervical spine injury. In general, halo vest treatment is unsuitable for patients who have extreme obesity, polytrauma, or chest deformity or injury. Halo
    vests also are unsuitable for patients who are frail and
    elderly, primarily because the pulmonary constraint increases the risk of aspiration. Halo ring applications
    usually are contraindicated for patients with a skull
    fracture or another cranial defect. Several studies described the limitations of these devices and emphasized
    the high complication rates from infection, pin site
    loosening, or failure of stabilization.27,28 Complications
    occurred in as many as 35% of patients. Most of the
    complications were minor, however, and 84% of patients had satisfactory healing without surgery.27 Properly applied halo vest immobilization remains the most
    useful nonsurgical treatment for a select group of
    mainly osseous cervical spine injuries.

    Surgical Principles: Timing and


    General Concepts

    2011 American Academy of Orthopaedic Surgeons

    5: Spine

    The timing of surgical intervention for cervical spine


    trauma is somewhat controversial, in part because of
    the vague nature of definitions regarding emergent
    care. The most commonly used timeline to differentiate
    early and late surgery in spine trauma is 72 hours, although 48 and 24 hours also have been suggested. Interventions taking place after 24 hours are not considered acute in many other specialties, however. A
    feasibility study found that surgical intervention within
    8 hours was possible for no more than 10% of patients.29 Important considerations in the timing of surgery for spine injury include the overall injury burden
    (injury severity) and the presence of comorbidities, ankylosis of the spinal column, vertebral artery injury,
    ability to reduce dislocations, persistent cord compression, or neurologic injury. The five basic categories of
    neurologic injury are applicable to the cervical spine:
    neurologically intact status, incomplete spinal cord injury, complete spinal cord injury, root injury, and status
    unknown because of persistent cognitive impairment.
    The presence of neurologic injury, especially with persistent cord compression, is commonly regarded as an
    indication for emergent decompression. Early surgical
    spine intervention for trauma has been overwhelmingly
    described as safe in studies mostly of patients with thoracolumbar injury.30 In general, early surgical intervention for spine trauma results in reduced overall length
    of stay and decreased intensive care stay as well as pulmonary deterioration. Treatment at a trauma center decreases the likelihood of paralysis by 33%, compared
    with treatment at a nontrauma center.31 A more aggressive approach toward spinal column trauma management and more effective integrated care were identified
    as possible causes for this finding, which was based on
    the study of large administrative databases. If early sur-

    gical intervention for cervical spine trauma is chosen,


    adherence to trauma management principles is recommended, such as maintenance of spine immobilization, physiologic blood pressure (mean arterial pressure
    > 85 mm Hg), hematocrit level (> 30), and oxygenation
    as well as atraumatic airway management. Maintenance of physiologic blood pressure has been increasingly emphasized to avoid a second-shock trauma to
    the neural elements. Secondary postresuscitation hypotension is particularly damaging in patients with central nervous system injuries and should be avoided if
    possible. If available, electrophysiologic neuromonitoring may be useful in acute surgical spine trauma management.
    Despite absence of specific pertinent studies, the important factors in recommending early surgical care for
    patients with a confirmed complete spinal cord injury
    are expedited mobilization, improved skin care, simplified chemical deep venous thrombosispulmonary embolism prophylaxis, and early rehabilitation care. There
    are no clear guidelines as to the timing of surgery for
    patients with a cervical spine fracture and concurrent
    neurologic injury. Despite animal studies with findings
    favoring early surgical intervention,32-36 this practice
    has not been fully validated in clinical studies. Emerging studies have found neurologic improvement with
    early decompression and stabilization, however. The
    unpublished Surgical Treatment for Acute Spinal Cord
    Injury Study, which retrospectively assessed the timing
    of intervention in more than 200 patients with incomplete spinal cord injury, found an improved motor
    score and ASIA status for patients treated early.
    The goals of surgical treatment of cervical spine injuries are to restore physiologic alignment, protect and
    decompress the compromised neural elements, and provide effective stabilization to incapacitated segments.
    Ideally, these goals are achieved by using the least invasive and atraumatic technique possible and involving
    the fewest possible motion segments in any arthrodesis
    construct. Most spine trauma can be treated from either an anterior or posterior approach, with combined
    anterior-posterior procedures reserved for the most
    complex injuries or for patients with preexisting concurrent multifocal stenosis or deformity. Insights gained
    from advanced neuroimaging and refinements in surgical implants for the cervical spine are expanding the
    treatment options. Ultimately, cervical spine surgery
    will allow rapid mobilization of a patient with minimal
    reliance on external immobilization devices.

    Craniocervical Injuries
    Recognition of potentially unstable craniocervical dissociation can be lifesaving in some patients, and it represents the most important step in preventing further
    damage to patients with a nondisrupted spinal cord. An
    injury affecting any component of the upper cervical
    spine should be scrutinized for a more complex injury
    because the upper cervical spine forms an integrated
    anatomic and functional unit.10 Occasionally, a surgeon
    may need to differentiate a truly unstable injury from a

    Orthopaedic Knowledge Update 10

    629

    Section 5: Spine

    Figure 4

    A, Parasagittal CT reformat in a 23-year-old man


    involved in a high-speed motor vehicle collision
    with obvious occiput C1 distraction and
    occipital-cervical dissociation (arrow). B, Postoperative lateral radiograph demonstrating occiput to C2 posterior instrumented fusion with
    structural iliac crest allograft and morcellized
    autograft and bone graft extenders.

    5: Spine

    partially disrupted injury by using a traction test if


    there is still uncertainty after a dedicated CT and MRI
    of the craniocervical junction. Traction is generally undesirable for craniocervical dissociations because it can
    subject the upper cervical spinal cord to undue tension
    and aggravate any underlying neurologic injury. Even a
    halo ring and vest offer only marginal immobilization
    of a truly unstable craniocervical dissociation, while
    tending to distract the head from the neck. Temporary
    immobilization using sandbags around the head and
    crossover tape may afford better immobilization to the
    injured region until definitive surgery is performed. Surgical stabilization should be done as early as is medically safe. Preoperative baseline electrophysiologic assessment with motor- and somatosensory-evoked
    potentials can aid in safely positioning a patient with
    an unstable injury. The preferred surgical management
    consists of an occipitocervical arthrodesis to C2 or C3,
    using rigid segmental fixation and posterior decompression as necessary (Figure 4). More limited fixation, as
    from the occiput to the C1 ring, does not treat the more
    global instability of a disrupted craniocervical junction.

    Atlas and Transverse Atlantal Ligament Injury


    In general, most atlas fractures can be treated nonsurgically with suitable immobilization. The subtypes with
    a high likelihood of unsatisfactory nonsurgical outcome
    include disruption of the TAL or a displaced fracture of
    the lateral mass such as a sagittal split injury.37 Atlantoaxial instability with eventual cord compression, a
    630

    Orthopaedic Knowledge Update 10

    painful cock-robin position of the head, and suboccipital headache can be the result of lack of congruous
    healing of the C1 lateral masses between the occipital
    condyles and the C2 superior articular processes. An
    atlantal fracture malunion or nonunion usually requires
    a challenging late craniocervical reconstruction. In contrast, early recognition of an unstable atlantal fracture
    may allow atlantoaxial motion-preserving C1 primary
    internal fixation with posterior lateral mass screws and
    direct internal reduction without fusion.
    Most patients with a confirmed TAL disruption require atlantoaxial instrumented arthrodesis. This procedure is most commonly done through posterior surgery with rigid segmental fixation, although anterior
    techniques have been used. Cable or wire fixation of
    C1 and C2 has a secondary role of securing bone graft
    because of its inherent biomechanical limitations. The
    segmental fixation options include C1-C2 transarticular screws, C1 lateral mass screws, and C2 fixation
    achieved with pedicle, pars, or translaminar screws.38
    These instrumentation options offer an unprecedented
    ability to adapt to the patients individual anatomic and
    biomechanical needs, with reliable fracture healing.

    Odontoid Injuries
    Most odontoid fractures are amenable to successful
    nonsurgical management. Type I injury is rare and requires close evaluation for a potential craniocervical
    dissociation. Similarly, most type III fractures, in which
    the typical fracture pattern reaches into the cancellous
    body of the axis, can be expected to heal well with appropriate nonsurgical realignment and immobilizations. Type II odontoid fractures continue to be the
    subject of considerable debate and uncertainty. For
    well-selected patients, nonsurgical treatment is likely to
    lead to union. The prognostically favorable factors include minimal fracture translation, angulation, and absence of comminution. Patient-related factors, including good general health, no nicotine use, and no other
    cervical spine abnormalities, are another key to successful treatment. For a patient with good bone quality
    who has an unstable odontoid fracture of a suitable
    pattern, anterior odontoid screws placed by an experienced surgeon in atraumatic fashion offer the potential
    for primary fracture healing with preservation of some
    atlantoaxial motion15 (Figure 5). Typically, a single
    well-placed screw offers sufficient biomechanical fracture fixation, with healing rates similar to those of dual
    screws.
    There remains significant controversy as to the preferred management of type II odontoid fractures, which
    are encountered with increasing frequency in geriatric
    patients.39 The treatment recommendations range from
    surgery with an attempt at anterior odontoid screw fixation or primary posterior arthrodesis and fixation to
    palliative soft neck collar placement, which can be expected to result in nonunion. Posterior atlantoaxial segmental arthrodesis offers the advantage of immediate
    stability and mobilization, with minimal reliance on external immobilization. Regardless of the treatment,

    2011 American Academy of Orthopaedic Surgeons

    Chapter 48: Cervical Spine Trauma

    Figure 5

    A, Preoperative lateral radiograph of a 24-year-old man initially managed in a halo vest but with increasing subluxation of his type II dens fracture (arrow). B, Postoperative lateral radiograph after placement of two cannulated
    odontoid screws. C, Postoperative open-mouth radiograph of two cannulated odontoid screws.

    Hangmans Fracture
    Most type I and most type II hangmans fractures can
    be treated nonsurgically with immobilization. However,
    a type IIA fracture, with a typical C2-3 disk disruption
    and accompanying kyphosis and translation, can be
    treated with more predictable results using surgical stabilization. Either posterior C1-C3 posterior instrumented fusion or anterior C2-C3 cervical decompression and instrumented fusion can be used. Despite the
    biomechanical advantages of posterior instrumentation, the necessary incorporation of the C1 segment
    limits its appeal, unless direct pars fracture with internal fixation screws is feasible. Anterior C2-C3 fixation
    offers preservation of atlantoaxial motion, but it is less
    than straightforward because of the approach and several technical challenges.
    In a type III injury, there is a bilateral pars fracture
    and subluxation of the C2 facet joint on C3. It is difficult to achieve closed reduction of the dislocation and

    2011 American Academy of Orthopaedic Surgeons

    common concurrent spinal cord injury, and closed reduction may be impossible because the C2 posterior
    pars and lamina are dissociated from both the proximal
    and caudal spine elements. Early open reduction followed by C1-C3 or C2-C3 instrumented fusion using
    segmental fixation is recommended.

    Lower Cervical Spine Injuries


    With the advent of modern rigid fixation systems, surgeons frequently are able to reliably achieve stability
    using anterior or posterior fixation only. Posterior instrumentation offers better biomechanical fixation stiffness in flexion, the ability to reduce dislocated facet
    joints directly, the ability to perform stable multilevel
    fixation extending into the transition zones, higher
    union rates with segmental fixation, and the opportunity to perform a multilevel neural element decompression of cord and individual roots. However, anterior
    neck surgery performed in a simple supine position is
    less painful and prone to complications than posterior
    surgery. The potential for a more meaningful neurologic recovery is afforded by decompression of the anterolateral corticospinal tracts, with better biomechanics in extension loading. In a prospective comparison of
    anterior-posterior cervical surgery, 70% of patients
    treated with anterior surgery improved at least one
    Frankel grade, compared with 57% of patients treated
    with posterior surgery.40 Posterior cervical spine surgery has been associated with increased bleeding, more
    wound-healing complications, and prolonged myofascial incisional pain. This constellation has led to a trend
    toward anterior neck surgery for most types of unstable
    lower cervical spine trauma.
    As a general strategy, the approach to an injured
    lower cervical spine should be chosen based on the lo-

    Orthopaedic Knowledge Update 10

    5: Spine

    there is a high risk of swallowing difficulty or aspiration. The 1-year mortality rate is as high as 40% for
    these patients.39
    Because of disagreement as to the treatment algorithm for unstable type II odontoid fractures, its management depends on the surgeons preference and the
    perceived patient needs. In general, posterior atlantoaxial arthrodesis using segmental fixation offers the greatest likelihood of successful healing of an unstable type
    II odontoid injury, with the least reliance on external
    mobilization. Treatment recommendations for an impaired elderly patient remain to be clarified. Palliative
    management using a soft neck collar is acceptable for a
    medically compromised elderly patient with a short expected life span.

    631

    Section 5: Spine

    Figure 6

    A, Trauma lateral radiograph showing C4-C5 bilateral jumped facets (arrow) in a 52-year-old man after a 20-foot
    fall. Postoperative lateral (B) and AP (C) radiographs after closed reduction in a fluoroscopy suite and then surgical
    fixation with lateral mass screws into C4 and C5.

    5: Spine

    cation of the most severe structural damage. This principle implies, for example, that burst fractures should
    be treated via an anterior approach, and facet dislocations, with or without fracture, should be treated via a
    posterior approach. Similarly, depressed lamina fractures are treated through a posterior approach. As in
    any trauma surgery, a neural decompression should be
    accompanied by rigid internal fixation and arthrodesis
    to maintain lasting physiologic alignment.
    The posterior implant options primarily consist of
    rod-and-screw systems, with lateral mass screw placement being the standard of care for the C3 through C6
    segments (Figure 6). Over the past decade, these techniques have been established as safe and effective for
    posterior cervical stabilization. In contrast, pedicle
    screw fixation of the C3 through C6 segments has been
    used only for stabilization of certain degenerative conditions and has not become a primary form of posterior
    cervical spine fixation. Because of the absence of suitable lateral masses at the axis and in the cervicothoracic junction, pedicle screw fixation has emerged as
    the posterior fixation technique of choice for instrumentation of the C2, C7, and upper thoracic segments.
    Common trauma indications for anterior subaxial
    cervical spine surgery include unstable burst fracture
    in a metabolically healthy patient or a patient with a
    previously reduced lower cervical spine fracturedislocation. The limitations of anterior subaxial trauma
    surgery, compared to posterior neck procedures, include
    the usual exposure restriction to two or three motion
    segments, poor access to the cervical transition zones,
    and increased exposure-related morbidity such as dysphagia. Anterior cervical plating offers less stiffness in
    632

    Orthopaedic Knowledge Update 10

    flexion, torsion, and axial loading than segmental posterior stabilization techniques. Higher rates of nonunion and hardware failure are reported than with posterior procedures in patients who undergo multilevel
    anterior arthrodesis and in patients with osteopenia.
    Anterior subaxial neck procedures can be divided
    into three phases: decompression, anterior column reconstruction, and anterior stabilization. Several treatment variables apply to each phase. Depending on the
    indication, anterior cervical decompression surgery can
    be accomplished with either diskectomy or corpectomy.
    In an acute trauma setting, multilevel anterior corpectomies are rarely if ever indicated. A corpectomy has a
    significantly more destabilizing effect on the neck than
    a diskectomy. Thus, a patients need for decompression
    must be weighed against the patients biomechanical
    needs and physiologic circumstances. If supplemental
    posterior surgery is not needed, anterior stabilization
    can be achieved with a low-profile plate and unicortical
    vertebral body screws that are rigidly locked into the
    plate. Although bicortical fixation has been recommended to increase biomechanical stability in the presence of trauma, this factor must be weighed against the
    risk of dural or neurologic injury. Rigid anterior plate
    fixation has minimized the need for supplemental external immobilization with a halo vest, and it improves
    the ability to maintain physiologic neck alignment until
    bony healing has been achieved. Dynamic locking
    plates have been introduced with the goal of improving
    graft healing by load sharing in patients with degenerative indications. However, these devices have little or
    no place in the treatment of a traumatically disrupted
    spinal column. The results of anterior surgery in pa-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 48: Cervical Spine Trauma

    Figure 7

    A, Preoperative sagittal CT scan in a 17-year-old boy who jumped over a fence and landed on his head, sustaining
    a C3 axial load, burst-type injury with ASIA type A spinal cord injury. B, Preoperative T2 sagittal MRI scan demonstrating high signal in the patients spinal cord. C, Postoperative lateral radiograph after a C3 corpectomy and reconstruction with a titanium cage and anterior plating.

    BurstAxial Load Injuries


    High-grade burst fractures are most commonly treated
    with a corpectomy, anterior strut grafting, and rigid an-

    2011 American Academy of Orthopaedic Surgeons

    terior plate fixation (Figure 7). Supplemental posterior


    fixation may be considered if the patient is osteopenic
    or if there are other concerns about stability.42 Reconstruction of an anterior column defect can be achieved
    with a tricortical structural iliac crest graft, structural
    fibular allograft, or a structural cage with autologous
    local bone graft core. Anterior column reconstruction
    options have emerged from concerns about morbidity
    associated with autologous iliac crest bone graft. No
    major study has compared the healing rates of patients
    who received autologous iliac crest graft for a traumatic injury and those who underwent anterior column
    corpectomy reconstruction using fibula allograft or a titanium cage.

    5: Spine

    tients with subaxial spine trauma in general have been


    favorable, even in patients with a flexion-type injury
    and despite the inherently more limited biomechanical
    stiffness of these constructs compared with posterior
    devices.41
    Combined anterior-posterior surgery for patients
    with subaxial trauma has been superseded by thirdgeneration anterior-posterior instrumentation systems,
    which offer rigid fixation options. The exception is in
    patients with an unusually severe fracture-dislocation,
    fracture malunion, displaced fracture-dislocation in
    conjunction with an ankylosing disorder or other deformity, or severe multilevel posttraumatic myelopathy
    combined with cervical stenosis. For some of these patients, staging procedures on separate days can achieve
    the treatment goals while lessening the physiologic impact of a same-day combined procedure. The specific
    approach is chosen largely on the basis of the individual patients injury and comorbidities. For instance, an
    initial posterior approach is more effective for reduction and stabilization in most patients with a fracturedislocation or ankylosing spine disease. A supplemental
    anterior approach can be used at a later date. In contrast, patients with kyphotic fracture malunion or a severe burst fracture first usually require an anterior approach, followed by a secondary posterior stabilization
    and decompression of neural elements, as needed.

    Unilateral Facet Fracture-Dislocations


    Unilateral facet fracture-dislocations are relatively uncommon and have been reported in less than 6% of cervical spine fractures.43,44 These injuries are believed to
    occur as a result of flexion and rotatory forces acting
    on the spine during the injury sequence. The typical radiographic features include modest kyphosis and translation of as much as 25% of vertebral body width. The
    reported incidence of traumatic disk herniations is
    23%.14 The fracture may involve the superior or inferior articular processes or a comminuted lateral mass.
    A floating lateral mass is a separation from the vertebral body with a varying amount of facet joint disruption. There have been several attempts to classify unilateral facet fracture-dislocation, but the great injury
    variability has precluded any widely accepted standard

    Orthopaedic Knowledge Update 10

    633

    Section 5: Spine

    5: Spine

    interpretation. A recent categorization consists of three


    types with three subcategories each.45 Type A injuries
    have a facet fracture, type B injuries have a dislocation
    without fracture, and type C injuries feature a combination. This classification system has not yet undergone
    validation studies.
    Patients with these injuries usually are treated with
    closed reduction and postreduction neuroimaging to assess for neural element compression. Nerve root injury
    is the prevalent form of neurologic injury in these patients, usually on the side of the dislocation. Nonsurgical treatment has been suggested for patients with normal or near-normal alignment and minimal or
    improving neurologic symptoms. This treatment usually consists of closed reduction for a period of time,
    followed by external immobilization with a cervicothoracic brace or halo vest. Follow-up radiographs are reviewed for maintenance of alignment. The surgical options include anterior diskectomy and bone grafting
    with locking-plate fixation, posterior foraminotomy
    and arthrodesis using bone graft, and segmental stabilization with a screw-and-rod construct. Posterior fixation usually necessitates sacrificing an additional motion segment because of compromised fixation on the
    side with the fractured lateral mass. Other factors to be
    considered include the need for a foraminotomy, which
    is best accomplished from the posterior approach; and
    the quality of bone, with posterior segmental instrumentation offering better fixation than anterior surgery.
    In a study of 90 patients with isolated facet injuries,
    surgical care was associated with better outcomes in
    terms of pain and functional scores than nonsurgical
    care, although the length of stay was nearly twice as
    long in the surgically treated patients.45 Persistent instability and further settling in the injury zone were possible causes.

    Bilateral Facet Fracture-Dislocations


    Bilateral facet fracture-dislocation from a bending
    mechanism is a serious injury because of its potential
    impact on the spinal cord. Although the incidence of
    traumatic disk herniation in bilateral facet fracturedislocation is as low as 13%, its propensity to induce
    potential secondary neurologic deterioration after
    closed reduction is a cause for concern. Closed reduction under controlled circumstances, followed by neuroimaging, is a well-supported treatment for a communicative patient or a patient with severe spinal cord
    injury. Definitive segmental surgical stabilization and
    decompression, as needed, have been widely recommended. These goals can be accomplished with posterior segmental fixation using a screw-based system or
    with anterior stabilization in a patient with good bone
    quality. The posterior technique is preferred if the patient has poor bone quality or if posterior decompression of displaced laminar and facet fragments is necessary (Figure 6).

    634

    Orthopaedic Knowledge Update 10

    Flexion-Teardrop Injuries
    A flexion-teardrop injury occurs when there is a combined loss of anterior column integrity in flexion and
    tensile failure of the posterior ligamentous complex. A
    teardrop-shaped triangular fragment typically is
    avulsed from the inferior edge of the rostral vertebral
    body while the vertebral body is pushed back into the
    spinal canal. The presence of neurologic injury is variable. The treatment recommendations range from nonsurgical care to anterior, posterior, or combined
    anterior-posterior surgery. A comparison of treatment
    with a halo vest to surgical care with anterior corpectomy, strut grafting, and plating found that the surgical
    procedure had superior radiographic and health-related
    quality-of-life outcomes.40 Although this study reported
    no complications of surgical treatment and found that
    outcomes were correlated with an absence of kyphosis,
    other studies reported complications after anterior-only
    fixation in the presence of osteopenia, incomplete reduction, or major disengagement of facet joints. Overall, anterior treatment alone appears to offer a reasonably good outcome under the correct circumstances. A
    combination of anterior decompression and strut grafting with posterior instrumentation remains an option
    for patients with impaired bone quality.

    Extension Injuries
    Hyperextension fractures are commonly associated
    with an ankylosing spine condition such as disseminated idiopathic skeletal hyperostosis or ankylosing
    spondylitis. In patients with a pretraumatic spinal column kyphosis, fractures in an ankylosing spine often
    appear as a hyperextension injury. The frequently irregular fracture planes typically indicate the presence of a
    fracture-dislocation with inherent structural compromise.7 Closed reduction should be attempted with the
    greatest of care in a patient with this type of injury because secondary spinal cord injury can occur with uncontrolled neck manipulation. If medically feasible,
    early surgical intervention is frequently desirable because closed reduction is difficult if not impossible to
    maintain, and epidural hematoma formation can further compromise the spinal cord. Typically, definitive
    care consists of a multilevel posterior segmental stabilization in association with posterior spinal canal decompression (Figure 8). In patients with an anterior column
    gap, secondary anterior stabilization can be achieved
    with a structural bone graft and plate fixation. Given
    the long lever arms of the spinal column and the presence of vertebral osteopenia in patients with an ankylosing spine disorder, fixation failure is somewhat likely
    after isolated anterior fracture stabilization.7

    Fracture-Dislocations
    Fracture-dislocation is commonly associated with spinal cord injury. Patients with cervical fracturedislocation often have significant translational displacement, and they may need to be evaluated for a potential
    vertebral artery injury if the transverse foramina have
    fracture involvement. Closed reduction can be difficult

    2011 American Academy of Orthopaedic Surgeons

    Chapter 48: Cervical Spine Trauma

    Figure 8

    A, Preoperative sagittal CT scan of a 67-year-old man with a history of laryngeal carcinoma and diffuse idiopathic
    skeletal hyperostosis (DISH) who sustained a ground-level fall and a C6-C7 hyperextension injury (arrow). B and C,
    Postoperative AP and lateral radiographs after C4-T2 posterior segmental instrumentation and fusion.

    Cervicothoracic Junction Injuries


    Injuries to the cervicothoracic junction (C7-T2) are
    only sporadically reported, but they may amount to as
    high as 9% of all blunt neck trauma. 46 The high rate of
    missed or delayed diagnosis probably results from the
    difficulty of imaging in this region. The increasing use
    of CT with reformatting as a primary screening tool
    may decrease the incidence of missed injuries. The most
    common cervicothoracic junction injuries are of the
    flexion type. These injuries are difficult to reduce
    closed because of the steep inclination angle of the facet
    joints of C7 and T1 and the other upper thoracic segments. In nonsurgical treatment, there is an inability to
    compensate for the bending forces typically exerted on
    the cervicothoracic junction. Posterior segmental instrumented fusion generally is the primary treatment
    for an unstable cervicothoracic injury. Anterior treatment is not preferred in this transition zone because of
    limited access, approach-related morbidity, and poor
    biomechanical fixation strength in the vertebral bodies
    of the upper thoracic spine.

    2011 American Academy of Orthopaedic Surgeons

    Special Circumstances

    Ankylosing Spine Conditions


    The incidence of fractures in patients with ankylosing
    spondylitis, disseminated idiopathic skeletal hyperostosis, and end-stage spondylosis appears to be increasing.
    Injuries in an ankylosing spine may be the result of a
    highkinetic energy impact mechanism or a low-impact
    event such as a ground-level fall. Patients with an ankylosing spine condition require an increased index of
    suspicion; the onus is on the clinician to prove the absence rather than the presence of a fracture. Even the
    slightest crack may indicate an unstable injury. Radiographic identification may be difficult because of the
    presence of other radiographic abnormalities. Other
    medical comorbidities are frequently encountered and
    may demand urgent medical attention, thus distracting
    from the spine care needs. Preinjury spine deformities
    are common, and frequently they pose serious immobilization and transfer problems. Most injuries in patients
    with an ankylosing spine condition are of the extension
    type and are around C5-C7, although injuries such as
    an odontoid fracture also can occur. The possibility of
    noncontiguous injuries in more than 10% of patients is
    a reason to perform advanced neuroimaging of the entire spinal column for detection. Other management
    concerns revolve around impaired bone quality from
    the underlying musculoskeletal disease, the potential
    for epidural hematoma formation in hyperemic inflammatory tissues disrupted by trauma, and the possibility

    Orthopaedic Knowledge Update 10

    5: Spine

    to maintain because of loss of key structural elements


    such as facet joints and soft-tissue attachments. After
    the best possible closed reduction is achieved and neuroimaging is performed, the early surgical care usually
    involves posterior multilevel segmental instrumentation
    and arthrodesis. Secondary anterior column reconstruction may be necessary, depending on whether the anterior column is restored through indirect posterior reduction.

    635

    Section 5: Spine

    of occult esophageal or aortic injuries. For all but nondisplaced injuries, the preferred management usually is
    multisegmental posterior instrumentation and neural
    element decompression, as clinically indicated (Figure 8). Anterior surgery has a supplemental role because of the inherent biomechanical limitations and
    limited surgical access. Positioning of the patient for
    prone surgery can be daunting. A neurologically intact
    patient with a kyphotic deformity in the presence of an
    ankylosing spine disorder is in danger of secondary
    neurologic deterioration during any transfer or unguided realignment attempt. Realignment can be undertaken under certain conditions, but usually the spinal
    column is left close to its normal preinjury position to
    minimize the chance of uncontrolled displacement of
    the spinal canal. Intraoperative imaging can be difficult, and posterior bony landmarks may be severely
    distorted from the underlying inflammatory disease
    process and multilevel autofusions. Despite comprehensive multispecialty care, the survival rates in patients
    older than 80 years have been poor.7

    Spine Injuries in Elderly Patients

    5: Spine

    The prevalence of cervical spine fractures is 2.4% to


    4.7% in elderly patients, generally categorized as those
    older than 65 years.47,48 The injury is caused by a
    ground-level fall in 62% of these patients. A spine fracture in elderly patients generally is more difficult to diagnose than in younger individuals because baseline,
    widespread spondylosis and deformity are often present. Like a fracture in a patient with an ankylosing
    spine condition, a fracture in these patients may be
    overlooked because of the low-impact injury mechanism, such as a ground-level fall, and the paucity of focal
    examination findings. Unstable type II odontoid fractures pose a particular treatment dilemma in this population.
    Certain types of short-segment fixation that are suitable for a similar injury in younger patients are far
    more likely to fail in patients with age-related osteopenia and loss of physiologic mobility of the spinal column. There are greater perioperative risks such as aspiration, intolerance of external immobilization devices,
    and a need for anticoagulation for concurrent comorbidities. Much work remains to be done to identify optimal integrated treatment pathways for the elderly patient with cervical spine fracture.49

    ments in overall outcomes with screening or treatment


    programs.51 Transcranial Doppler screening may help
    identify clinically relevant flow disruption. Long-term
    follow-up studies have revealed persistent vertebral artery occlusion beyond 26 months following an initial
    injury.52,53 A confirmed vertebral artery injury may considerably affect surgical planning because of the need to
    provide antiembolic coverage and ensure preservation
    of the artery during surgery. The management options
    consist of endovascular stenting or embolization and
    expedient surgical instrumentation of the injured segments. As with extremity injuries and concurrent arterial injuries, early decisive surgical stabilization usually
    is preferable to prolonged recumbence in traction. Any
    surgery must minimize the risk of perioperative injury
    to the remaining intact vertebral artery.

    Emerging Concepts
    With the availability of advanced spine imaging on an
    unprecedented scale, the increasing implementation of
    proven trauma recovery and resuscitation algorithms,
    and sophisticated and safe instrumentation systems,
    several advances are overdue related to relatively
    straightforward issues in cervical spine trauma care.
    The assessment and treatment of cervical spine fractures remains highly variable and inconsistent, despite
    many areas of improvement. There is a lack of implementation of a universal systematic evaluation and
    classification system for cervical spine trauma, despite
    their increasingly well-proven efficacy. The ongoing
    state of diversity and personal preferences has been detrimental to education and has diminished attempts at
    scientific comparison. Despite an absence of absolute
    scientific proof of intervention variables such as timing
    to neural decompression, the implementation of certain
    standardized treatment algorithms appears to be desirable and preferable to individualized care. Emerging
    data on the care of patients with severe spine injury in
    tertiary care centers may underscore the advantages of
    systematic care for this at-risk population.

    Annotated References
    1.

    Irwin ZN, Arthur M, Mullins RJ, Hart RA: Variations


    in injury patterns, treatment, and outcome for spinal
    fracture and paralysis in adult versus geriatric patients.
    Spine (Phila Pa 1976) 2004;29(7):796-802.

    2.

    US Census Bureau: Population Projections of the United


    States by Age, Sex, Race, and Hispanic Origin: 19952050. Washington, DC, US Department of Commerce
    (Publication No P25-1130), 1995.

    3.

    Sokolowski MJ, Jackson AP, Haak MH, Meyer PR Jr,


    Szewczyk Sokolowski M: Acute outcomes of cervical
    spine injuries in the elderly: Atlantaxial vs subaxial injuries. J Spinal Cord Med 2007;30(3):238-242.

    Vertebral Artery Injuries


    Approximately 11% of patients with a significant cervical spine injury such as an unstable burst fracture or
    fracture-dislocation have disruption of physiologic vertebral artery flow.50 If imaging reveals a displaced fracture involving the foramen transversarium, further assessment with CT angiography or magnetic resonance
    angiography is recommended. When aggressive screening and an individualized treatment protocol are used
    for blunt vertebral artery injuries, potentially preventable stroke or death is rare. No high-quality comparative studies have convincingly demonstrated improve636

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 48: Cervical Spine Trauma

    This retrospective database review of 193 consecutive


    patients older than 65 years over a 12-year period concluded that surgical treatment of subaxial injuries was
    associated with an improved survival rate versus nonsurgical management.
    4.

    5.

    6.

    7.

    Harris TJ, Blackmore CC, Mirza SK, Jurkovich GJ:


    Clearing the cervical spine in obtunded patients. Spine
    (Phila Pa 1976) 2008;33(14):1547-1553.
    A retrospective cohort study of 367 obtunded trauma
    patients showed that initial CT imaging identified all
    unstable cervical spine injuries, and subsequent upright
    radiographs did not identify any additional injuries but
    significantly delayed spine clearance.
    Blackmore CC, Mann FA, Wilson AJ: Helical CT in the
    primary trauma evaluation of the cervical spine: An
    evidence-based approach. Skeletal Radiol 2000;29(11):
    632-639.
    Bailitz J, Starr F, Beecroft M, et al: CT should replace
    three-view radiographs as the initial screening test in patients at high, moderate, and low risk for blunt cervical
    spine injury: A prospective comparison. J Trauma 2009;
    66(6):1605-1609.
    This prospective study of 1,583 consecutive patients
    comparing cervical spine radiographs to CT concluded
    that CT should replace plain radiographs for the initial
    evaluation of blunt cervical spine injury in patients at
    any risk for injury.

    8.

    Anderson PA, Montesano PX. Morphology and treatment of occipital condyle fractures. Spine (Phila Pa
    1976). 1988;13(7):731-736.

    9.

    Traynelis VC, Marano GD, Dunker RO, et al. Traumatic atlanto-occipital dislocation: Case report. J Neurosurg 1986;65:863-870.

    10.

    Bellabarba C, Mirza SK, West GA, et al: Diagnosis and


    treatment of craniocervical dislocation in a series of 17
    consecutive survivors during an 8-year period. J Neurosurg Spine 2006;4(6):429-440.

    11.

    Bono CM, Vaccaro AR, Fehlings M, et al; Spine Trauma


    Study Group: Measurement techniques for upper cervical spine injuries: Consensus statement of the Spine
    Trauma Study Group. Spine (Phila Pa 1976) 2007;
    32(5):593-600.
    This review article from the Spine Trauma Study Group
    discusses the various imaging measurements available
    and how these measurements are documented.

    2011 American Academy of Orthopaedic Surgeons

    Levine AM, Edwards CC: Traumatic lesions of the occipitoatlantoaxial complex. Clin Orthop Relat Res
    1989;239:53-68.

    13.

    Dickman CA, Greene KA, Sonntag VK: Injuries involving the transverse atlantal ligament: Classification and
    treatment guidelines based upon experience with 39 injuries. Neurosurgery 1996;38(1):44-50.

    14.

    Anderson LD, DAlonzo RT: Fractures of the odontoid


    process of the axis. J Bone Joint Surg Am 1974;56(8):
    1663-1674.

    15.

    Levine AM, Edwards CC: The management of traumatic spondylolisthesis of the axis. J Bone Joint Surg
    Am 1985;67(2):217-226.

    16.

    Maak TG, Grauer JN: The contemporary treatment of


    odontoid injuries. Spine (Phila Pa 1976) 2006;31(11,
    suppl):S53-S60, discussion S61.

    17.

    Kwon BK, Vaccaro AR, Grauer JN, Fisher CG, Dvorak


    MF: Subaxial cervical spine trauma. J Am Acad Orthop
    Surg 2006;14(2):78-89.

    18.

    Allen BL Jr, Ferguson RL, Lehmann TR, OBrien RP. A


    mechanistic classification of closed, indirect fractures
    and dislocations of the lower cervical spine. Spine (Phila
    Pa 1976) 1982;7(1):1-27.

    19.

    Moore TA, Vaccaro AR, Anderson PA: Classification of


    lower cervical spine injuries. Spine (Phila Pa 1976)
    2006;31(11, suppl):S37-S43, discussion S61.

    20.

    Vaccaro AR, Hulbert RJ, Patel AA, et al; Spine Trauma


    Study Group: The subaxial cervical spine injury classification system: A novel approach to recognize the importance of morphology, neurology, and integrity of the
    disco-ligamentous complex. Spine (Phila Pa 1976)
    2007;32(21):2365-2374.
    The authors compared the subaxial cervical spine injury
    classification system (SLIC) to the Harris and Ferguson
    and Allen systems by 20 spine surgeons to 11 cervical
    trauma cases. They concluded that the SLIC provides a
    comprehensive classification system for subaxial cervical
    trauma.

    21.

    Baptiste DC, Fehlings MG: Update on the treatment of


    spinal cord injury. Prog Brain Res 2007;161:217-233.
    The authors present an overview of the pathobiology of
    spinal cord injury and current treatment choices before
    focusing the rest of the discussion on the variety of
    promising neuroprotective and cell-based approaches
    that have recently moved or are very close to clinical
    testing.

    22.

    Grauer JN, Vaccaro AR, Lee JY, et al: The timing and
    influence of MRI on the management of patients with
    cervical facet dislocations remains highly variable: A
    survey of members of the Spine Trauma Study Group.
    J Spinal Disord Tech 2009;22(2):96-99.
    In this questionnaire study sent to 25 fellowship-trained
    spine surgeons, the authors conclude that the timing and

    Orthopaedic Knowledge Update 10

    5: Spine

    Caron T, Bransford R, Nguyen Q, Agel J, Chapman J,


    Bellabarba C: Spine fractures in patients with ankylosing spinal disorders. Spine (Phila Pa 1976) 2010;35(11):
    E458-E464.
    This retrospective review of 122 spine fractures in 112
    patients with ankylosing spinal disorders concludes that
    these patients are at high risk for complications and
    death and should be counseled accordingly. Multilevel
    posterior segmental instrumentation allows effective
    fracture healing.

    12.

    637

    Section 5: Spine

    The authors studied 4,121 patients diagnosed with traumatic spinal cord injuries and concluded that trauma
    center care is associated with reduced paralysis. National guidelines to triage all such patients to trauma
    centers are followed little more than half the time.

    utilization of MRI for patients with traumatic cervical


    facet dislocations remain variable.
    23.

    Grant GA, Mirza SK, Chapman JR, et al: Risk of early


    closed reduction in cervical spine subluxation injuries.
    J Neurosurg 1999;90(1, suppl)13-18.

    24.

    Vaccaro AR, Falatyn SP, Flanders AE, et al: Magnetic


    resonance evaluation of the intervertebral disc, spinal
    ligaments, and spinal cord before and after closed traction reduction of cervical spine dislocations. Spine
    1999;24(12):1210-1217.

    25.

    26.

    5: Spine

    27.

    Grauer JN, Vaccaro AR, Beiner JM, et al: Similarities


    and differences in the treatment of spine trauma between surgical specialties and location of practice. Spine
    (Phila Pa 1976) 2004;29(6):685-696.
    Bransford RJ, Stevens DW, Uyeji S, Bellabarba C,
    Chapman JR: Halo vest treatment of cervical spine injuries: A success and survivorship analysis. Spine (Phila
    Pa 1976) 2009;34(15):1561-1566.
    This retrospective review of 342 patients with cervical
    spine fractures treated with halo vest immobilization
    found treatment was successful in 85% of patients, and
    74% of survivors completed their intended treatment
    period. Complications, though common, were mostly
    not severe.

    Carlson GD, Gordon CD, Oliff HS, Pillai JJ, LaManna


    JC: Sustained spinal cord compression. J Bone Joint
    Surg Am 2003;85:86-94.

    33.

    Dimar JR, Glassman SD, Raque GH, Zhang YP, Shields


    CB: The influence of spinal canal narrowing and timing
    of decompression on neurologic recovery after spinal
    cord contusion in a rat model. Spine 1999;24:16231633.

    34.

    Fehlings MG, Sekhon LH, Tator C: The role and timing


    of decompression in acute spinal cord injury. Spine
    2001;26:s101-s110.

    35.

    Fehlings MG, Tator CH: An evidence-based review of


    decompressive surgery in acute spinal cord injury: Rationale, indications, and timing based on experimental
    and clinical studies. J Neurosurg Spine 1999;91:1-11.

    36.

    Shields CB, Zhang YP, Shields LB, Han Y, Burke DA,


    Mayer NW: The therapeutic window for spinal cord decompression in a rat spinal cord injury model. J Neurosurg Spine 2005;3:302-307.

    37.

    Bransford RJ, Falicov A, Nguyen QT, Chapman JR:


    The C1 lateral mass sagittal split fracture: An unstable
    Jefferson fracture variant. J Neurosurg Spine 2009;
    10(5):466-473.
    In this retrospective review of all C1 ring fractures, the
    authors review three surviving patients with C1 unilateral sagittal splits treated nonsurgically who went on to
    develop cock-robin deformities and eventually required
    occiput to C2 fusions.

    28.

    Glaser JA, Whitehall R, Stamp WG, et al: Complications associated with the halo-vest: A review of 245
    cases. J Neurosurg 1986;65(6):762-769.

    38.

    Wright NM: Posterior C2 fixation using bilateral, crossing C2 laminar screws: Case series and technical note.
    J Spinal Disord Tech 2004;17(2):158-162.

    29.

    Levi AD, Hurlbert RJ, Anderson P, et al: Neurologic deterioration secondary to unrecognized spinal instability
    following trauma: A multicenter study. Spine (Phila Pa
    1976) 2006;31(4):451-458.

    39.

    30.

    Bellabarba C, Fisher C, Chapman JR, Dettori JR, Norvell DC: Does early fracture fixation of thoracolumbar
    spine fractures decrease morbidity or mortality? Spine
    (Phila Pa 1976) 2010;35(9, suppl):S138-S145.
    In this systematic review of articles between January
    1990 and December 2008, 68 articles were screened and
    9 met criteria. The authors conclude that patients with
    unstable thoracic fractures should undergo early (< 72
    hours) stabilization of their injury to reduce morbidity
    and, possibly, mortality.

    Smith HE, Kerr SM, Fehlings MG, et al: Trends in epidemiology and management of type II odontoid fractures: 20-Year experience at a model system spine injury
    tertiary referral center. J Spinal Disord Tech 2010; October. Epub ahead of print.
    The authors retrospectively reviewed 263 consecutive
    type II odontoid fractures and found a statistically significant increase in the rate of presentation of type II
    odontoid fractures with time.

    40.

    Brodke DS, Anderson PA, Newell DW, Grady MS,


    Chapman JR: Comparison of anterior and posterior approaches in cervical spinal cord injuries. J Spinal Disord
    Tech 2003;16(3):229-235.

    41.

    Fisher CG, Dvorak MF, Leith J, Wing PC: Comparison


    of outcomes for unstable lower cervical flexion teardrop
    fractures managed with halo thoracic vest versus anterior corpectomy and plating. Spine (Phila Pa 1976)
    2002;27(2):160-166.

    31.

    638

    Suberviola B, Gonzlez-Castro A, Llorca J, Ortiz-Meln


    F, Miambres E: Early complications of high-dose
    methylprednisolone in acute spinal cord injury patients.
    Injury 2008;39(7):748-752.
    This retrospective review of 82 patients with acute spinal cord injuries concludes that the use of methylprednisolone is not associated with an improvement in neurologic function and is associated with an increased risk of
    infectious and metabolic complications.

    32.

    Macias CA, Rosengart MR, Puyana JC, et al: The effects of trauma center care, admission volume, and surgical volume on paralysis after traumatic spinal cord injury. Ann Surg 2009;249(1):10-17.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 48: Cervical Spine Trauma

    42.

    Johnson MG, Fisher CG, Boyd M, Pitzen T, Oxland


    TR, Dvorak MF: The radiographic failure of single segment anterior cervical plate fixation in traumatic cervical flexion distraction injuries. Spine (Phila Pa 1976)
    2004;29(24):2815-2820.

    43.

    Lowery DW, Wald MM, Browne BJ, et al: Epidemiology of cervical spine injury victims. Ann Emerg Med
    2001;38:12-16.

    44.

    Hadley MN, Fitzpatrick BC, Sonntag VK, et al: Facet


    fracture-dislocation injuries of the cervical spine. Neurosurgery 1992;30:661-666.

    45.

    Dvorak MF, Fisher CG, Aarabi B, et al: Clinical outcomes of 90 isolated unilateral facet fractures, subluxations, and dislocations treated surgically and nonoperatively. Spine (Phila Pa 1976) 2007;32(26):3007-3013.
    This retrospective outcomes study looked at 90 isolated
    unilateral facet fractures, subluxations, and dislocations
    and concluded that nonsurgically treated patients report
    worse outcomes than surgically treated patients, particularly at longer follow-up.
    Nichols CG, Young DH, Schiller WR: Evaluation of cervicothoracic junction injury. Ann Emerg Med 1987;16:
    640-642.

    47.

    Ngo B, Hoffman JR, Mower WR: Cervical spine injury


    in the very elderly. Emerg Radiol 2000;7:287-291.

    48.

    Schrag SP, Toedter LJ, McQuay N Jr: Cervical spine


    fractures in geriatric blunt trauma patients with lowenergy mechanism: Are clinical predictors adequate?
    Am J Surg 2008;195(2):170-173.
    This retrospective case-control study of 99 patients examined clinical predictors in geriatric patients with
    blunt trauma and concluded that predictors are inade-

    2011 American Academy of Orthopaedic Surgeons

    49.

    Sokolowski MJ, Jackson AP, Haak MH, Meyer PR Jr,


    Sokolowski MS: Acute mortality and complications of
    cervical spine injuries in the elderly at a single tertiary
    care center. J Spinal Disord Tech 2007;20(5):352-356.
    The authors carried out a retrospective database review
    of 979 patients older than 65 years with cervical spine
    injuries and concluded that statistically comparable survival rates were achieved in both surgically treated and
    nonsurgically treated patient populations.

    50.

    Anonymous: Management of vertebral artery injuries


    after nonpenetrating cervical trauma. Neurosurgery
    2002;50(3, suppl):S173-S178.

    51.

    Fassett DR, Dailey AT, Vaccaro AR: Vertebral artery injuries associated with cervical spine injuries: A review of
    the literature. J Spinal Disord Tech 2008;21(4):252258.
    A literature review was performed assessing vertebral
    artery injuries associated with cervical spine injuries and
    concluded that screening for and treatment of asymptomatic vertebral artery injuries may be considered, but it
    is unclear based on the current literature whether these
    strategies improve outcomes.

    52.

    Biffl WL, Ray CE Jr, Moore EE, et al: Treatment-related


    outcomes from blunt cerebrovascular injuries: The importance of routine follow-up arteriography. Ann Surg
    2002;235:699-707.

    53.

    Miller PR, Fabian TC, Croce MA, et al: Prospective


    screening for blunt cerebrovascular injuries: Analysis of
    diagnostic modalities and outcomes. Ann Surg 2002;
    236:386-395.

    Orthopaedic Knowledge Update 10

    5: Spine

    46.

    quate for the evaluation of the cervical spine in geriatric


    trauma patients with a low-energy injury mechanism.

    639

    Chapter 49

    Thoracolumbar Trauma
    Normal Chutkan, MD

    Jonathan Tuttle, MD

    Introduction
    Traumatic spinal fractures occur in approximately
    150,000 patients in North America annually.1 The thoracolumbar region is one of the most commonly affected areas and can result in significant disability.
    There is a bimodal distribution that tends to differ by
    age and mechanism. In the younger patient population,
    high-energy mechanisms such as a fall from a height or
    a high-speed motor vehicle collision predominate. In elderly patients, a fall from standing height can be significant enough to cause an osteoporotic compression
    fracture. The management of these two types of fracture mechanisms may differ significantly. Controversy
    exists with regard to the best management approach
    because both surgical and nonsurgical treatment have
    been reported to be successful in the literature. This is
    confounded by the heterogeneous nature of trauma patients and the many variables that need to be considered such as body habitus, presence or absence of
    closed head injury, polytrauma, osteoporosis, spondyloarthropathy, and medical comorbidities.

    The thoracolumbar junction is defined as T11L2. In


    this region the relatively rigid thoracic spine transitions
    into a more mobile lumbar spine. A change in the facet
    orientation also affects motion when transitioning from
    the thoracic into the lumbar spine. The thoracic facets
    have a more coronal orientation that resists flexion and
    extension while allowing more torsional and lateral
    bending movements. The lumbar facets have a more
    sagittal orientation to allow for significant flexion and

    Initial Assessment

    Dr. Chutkan or an immediate family member serves as a


    board member, owner, officer, or committee member of
    Walton Rehabilitation Hospital, Medical College of
    Georgia, and AO North America; has received royalties
    from Globus Medical; serves as a paid consultant to or is
    an employee of Globus Medical; and has received research or institutional support from Synthes. Dr. Tuttle
    or an immediate family member is a member of a
    speakers bureau or has made paid presentations on behalf of AO and has received research or institutional
    support from Synthes.

    Initial treatment of thoracolumbar injuries begins in the


    field with adherence to the Basic Life Support and Advanced Trauma Life Support guidelines and attention
    to airway, breathing, and circulation. Hypotension
    with bradycardia may be caused by loss of central sympathetic regulation after a spinal cord injury at or
    above T6, which is termed spinal or neurogenic shock.
    Precautionary cervical spine immobilization and use of
    a rigid backboard are essential. Information on the
    mechanism of injury, gross neurologic status, and associated injuries is helpful in initiating appropriate treatment. Transportation to the nearest facility with the resources to manage acute trauma is warranted.

    2011 American Academy of Orthopaedic Surgeons

    5: Spine

    Anatomy

    extension. The thoracic spine is additionally stabilized


    by the rib cage and costovertebral articulations. In the
    sagittal plane the thoracic spine normally has an average of 35 of kyphosis (range, 20 to 50) whereas the
    lumbar spine averages 40 of lordosis (range, 30 to
    50).
    The posterior ligamentous complex (PLC) is an important component when determining the stability of a
    fracture. The PLC is composed of the facet capsules,
    ligamentum flavum, and interspinous and supraspinous
    ligaments and is sometimes referred to as the posterior
    tension band. The PLC makes up one of the three categories in the most recently devised fracture classification system.
    The normal adult spinal cord terminates in the conus
    medullaris at the L1 level, which means the spinal cord
    is at risk for injury throughout much of the thoracolumbar junction. The spinal canal diameter in the
    thoracic spine is relatively narrow and therefore not
    able to tolerate significant canal intrusion. The blood
    supply to the spinal cord is via a single anterior spinal
    artery and two posterior spinal arteries. Both the anterior and posterior spinal arteries are perfused in a segmental fashion from radicular arteries arising from the
    posterior intercostal arteries. The artery of Adamkiewicz is thought to be a dominant anterior radicular artery originating from a left intercostal vessel between
    T8-L2 and is seen in 10% to 16% of patients. In these
    patients it may provide a major portion of the blood
    supply to the anterior thoracolumbar spinal cord.

    Assessment

    Orthopaedic Knowledge Update 10

    641

    Section 5: Spine

    rapid screening with helical CT of the head, thorax, abdomen, and pelvis is often a routine part of the trauma
    evaluation.5
    CT allows axial images as well as sagittal and coronal reformats that are superior to plain films when
    evaluating fractures or dislocations. Both plain radiographs and CT show spinal alignment and bony morphology; however, CT shows greater detail and helps
    prevent missing smaller fractures or underestimating
    fracture severity. CT can be particularly helpful in
    obese patients in whom fine detail may be lost on plain
    films and for visualization of transition zones except
    when the patient weighs too much for the CT table.
    Another issue with CT in patients with spine trauma is
    the amount of radiation exposure.

    Figure 1

    Increased interpedicular distance from an L1


    burst fracture (arrow).

    Physical Examination

    5: Spine

    A detailed examination is necessary and should include


    major muscle groups, light touch and pinprick sensation, deep tendon and bulbocavernosus reflexes, rectal
    tone, and perianal sensation. The sensory examination
    may be more useful for determining the level of injury,
    especially in the thoracic spine. The umbilicus is innervated by T10, whereas T12 innervates the lower abdomen. The first lumbar nerve root innervates the inguinal region. Voluntary anal sphincter tone and perianal
    sensation may signify an incomplete spinal cord injury.
    Useful scales to guide evaluation of the patient with
    spinal injury are the American Spinal Injury Association form and the Frankel Impairment Scale.2,3
    Physical examination should include a thorough
    evaluation of the entire spine. Careful log rolling will
    allow for inspection and palpation of the back. Any
    wounds, palpable step-offs, or areas of tenderness are
    to be noted. Because there is an 8% to 11% chance of
    cervical injury associated with thoracolumbar trauma,
    radiographic evaluation of the entire spine is indicated.

    Imaging
    Initial imaging of the trauma patient includes either
    plain radiographs, CT, or both.4 Traditionally AP and
    lateral plain radiographs were used to screen patients at
    risk for fracture based on mechanism of injury or clinical suspicion of fracture, and advanced imaging modalities such as CT and MRI were reserved for more
    detailed evaluation once an injury had been identified.
    There is now literature to support a move from plain
    radiographs to CT for initial fracture evaluation as
    642

    Orthopaedic Knowledge Update 10

    Plain Radiographs
    Plain radiographs can still provide useful information.
    The lateral view allows for evaluation of the sagittal
    alignment and measurement of any kyphotic deformity.
    Screening lateral films are usually taken in the supine
    position. Alignment may worsen on weight bearing,
    alerting the clinician to the possibility of a more serious
    injury and/or disruption of the PLC. Upright conventional radiography continues to allow unequaled insight into postural alignment and segmental stability.
    Vertebral body height can also be evaluated; a loss of
    height of more than 50% may be indicative of a posterior ligamentous injury. The AP view is helpful in evaluating coronal alignment. Malalignment of the spinous
    processes is suggestive of a rotational injury, whereas
    widening of the interpedicular distance (Figure 1) may
    indicate a burst fracture. An increase in the interspinous distance may indicate a flexion injury. Focal scoliosis may be present in lateral compressive injuries.
    Computed Tomography
    CT is becoming the screening tool of choice at many institutions. Although reformatted sagittal and coronal
    images can be obtained, the quality of the reformatted
    images is dependent on the slice thickness of the screening studies. Once an injury is detected, if there is any
    question as to the quality of the screening studies, it is
    recommended that a more detailed thin-cut (2-mm)
    study be obtained at that level. CT is considered the
    gold standard for evaluating the osseous structures and
    is particularly helpful in assessing canal encroachment.
    Facet fractures and dislocations are easily evaluated
    with CT, and any asymmetry or malalignment should
    be noted. The naked or empty facet sign may signify a subluxation or dislocation (Figure 2). Careful
    evaluation of combined axial and reformatted images
    can help delineate osseous injury morphology and often
    leads to an appreciation of possible concomitant ligamentous or soft-tissue injuries.
    Magnetic Resonance Imaging
    MRI is helpful in evaluating nonosseous structures, the
    neural elements, and the PLC.6-8 Disk herniations, epidural hematomas, occult injuries, and other possible

    2011 American Academy of Orthopaedic Surgeons

    Chapter 49: Thoracolumbar Trauma

    Figure 2

    Naked or empty facet sign from a facet dislocation (arrow).

    Figure 3

    Increased signal within the spinal cord on a T2weighted MRI after a fracture-dislocation injury
    (arrow).

    5: Spine

    hemorrhage and/or edema and is a poor prognostic


    sign. T2-weighted MRI or short tau inversion recovery
    MRI is also useful to identify occult fractures that may
    be missed on plain films and CT. MRI can be particularly helpful in patients with multiple osteoporotic
    compression fractures with acute fractures showing increased T2 signal compared to normal signal in chronic
    fractures.

    Spinal Stability

    Figure 4

    Ligamentum flavum, interspinous, and supraspinous ligament injury after facet dislocation.

    soft-tissue neural compressive lesions are best demonstrated with MRI. The sensitivity for detecting PLC injury on physical examination alone is relatively low.
    T2-weighted and fat-suppressed T2-weighted images
    are helpful in evaluating the PLC. Increased signal is indicative of edema or frank disruption and may signal a
    more severe or unstable injury. The anulus fibrosus, anterior longitudinal ligament, posterior longitudinal ligament, and spinal cord will also show increased signal
    on T2-weighted MRI when injured (Figures 3 and 4).
    Increased signal within the spinal cord is seen with

    2011 American Academy of Orthopaedic Surgeons

    Instability has been defined as the loss of the ability of


    the spine under physiologic loads to maintain its pattern of displacement so that there is no initial or additional neurologic deficit, no major deformity, and no
    incapacitating pain.9 A scoring system was developed
    to aid in determining stability; however, many of these
    data were based on in vitro data, and a true objective
    clinical definition remains elusive.

    Fracture Classification
    The goal of any fracture classification system includes
    ease of application, ability to guide treatment, and excellent interobserver and intraobserver reliability. An
    initial thoracolumbar classification described the fracture by anatomic deformation and mechanism of injury.10 This work was later revised; one concept that
    was added was the integrity of the PLC and its importance in stability. A later classification system used a

    Orthopaedic Knowledge Update 10

    643

    Section 5: Spine

    Table 1

    Thoracolumbar Injury Classification Scale


    Category

    Points

    Injury morphology
    Compression
    Burst

    1
    +1

    Translational/rotational

    Distraction

    Neurologic status
    Intact

    Nerve root

    Cord, conus medullaris


    Incomplete

    Complete

    Cauda equina

    PLC
    Intact

    Injury suspected/indeterminate

    Injured

    (Adapted with permission from Vaccaro AR, Lehman RA Jr, Hurlbert RJ, et al: A
    new classification of thoracolumbar injuries: The importance of injury morphology,
    the integrity of the posterior ligamentous complex, and neurologic status. Spine
    (Phila Pa 1976) 2005;30:2325-2333.)

    5: Spine

    two-column model.11 Yet another fracture morphology


    classification system separated degrees of instability in
    an effort to devise a treatment strategy.12 A middle column was added to the two-column model. The loadsharing classification system warned of the dangers of
    short-segment posterior fixation for highly comminuted, kyphotic, and poorly apposed burst-type fractures due to the likelihood of construct failure.13
    The AO Spine classification system was much more
    comprehensive and categorized fractures into three
    main types (A, B, and C), which were then further subclassified into three subtypes that were also broken into
    three subgroups.14 Type A fractures were caused by
    compression injuries. Type B fractures resulted from
    distraction, and type C injuries were rotational. One
    drawback to this system, like the Denis system, is the
    further into the classification subtypes an observer reported, the less reliable the results. However, the interobserver and intraobserver reliability are on par or
    slightly better than the Denis system.15
    The Spine Study Trauma Group devised a thoracolumbar injury classification system based on expert
    opinion from multiple level I trauma centers.16-18 The
    system was first published containing a mechanistic injury model called the Thoracolumbar Injury Severity
    Score (TLISS) and was later revised to a fracture morphology system. The fracture morphology version was
    referred to as the Thoracolumbar Injury Classification
    System (TLICS) and it defined three main areas to eval644

    Orthopaedic Knowledge Update 10

    uate: fracture morphology, PLC injury, and neurologic


    status (Table 1).
    Fracture morphology was divided into four main
    categories that are progressively more severe: compression, burst, translation/rotational, and distraction.
    Compression fractures are the least severe and are characterized by loss of vertebral body height without retropulsion of bone into the spinal canal. Burst fractures
    are defined by a portion of the fractured vertebral body
    retropulsed into the spinal canal and may be an axial,
    lateral, or flexion type. When combined with rotation
    or translation, a burst fracture is classified as the more
    severe translation or rotational fracture morphology,
    which also includes unilateral or bilateral facet dislocations and translation/rotational fractures not associated
    with a compression or burst fracture. The final category is distraction and includes both flexion-distraction
    and extension-distraction injuries; flexion-distraction
    injuries are more common. A Chance fracture can be
    considered a flexion-distraction injury where the anterior and posterior elements all fail in tension. The
    Chance fracture can be entirely within osseous structures or can be a combination of osseous and ligamentous tissues. A true bony Chance fracture can be
    treated with extension bracing or a cast, whereas an osteoligamentous Chance fracture usually requires surgical stabilization.
    The goal of the TLICS was to guide treatment with
    reliability and reproducibility. Evaluation has shown
    improved reliability compared to previously published
    data from the AO or Denis classification systems and
    among different spine specialties. The interobserver and
    intraobserver reliability showed slightly better kappa
    values than published results for the Denis and the
    AO Spine classification systems, indicating better
    reliability.19-22 Another study indicated there was moderate reliability when comparing a set of cases between
    fellowship-trained orthopaedic spine surgeons and neurosurgeons.23

    Treatment Options
    The treatment options for managing thoracolumbar
    fractures are based on stability. Determining stability is
    sometimes more difficult than would initially be expected, and controversy exists in the literature as to the
    most effective treatment.24-29 Conservative treatment
    such as bracing with activity modification, pain medication, and serial imaging is adequate for less severe
    fractures and avoids the potential complications of surgery. With more severe fractures, such as a fracturedislocation with translation or rotation, surgical intervention is frequently warranted. A classification system
    may be useful to help the clinician determine the relative stability of the spine. It is also important to design
    an instrumentation construct that is unlikely to fail,
    and the load-sharing classification of thoracolumbar
    fractures may be helpful.30-32
    Surgical stabilization may be more advantageous
    when it occurs early after trauma and for factors other

    2011 American Academy of Orthopaedic Surgeons

    Chapter 49: Thoracolumbar Trauma

    Figure 5

    A, Initial standing film showing a TLSO after lumbar pincer-type fracture. B, Failed nonsurgical treatment resulted in
    increased kyphosis and increasing back pain 3 months after injury and treatment in TLSO. C, Radiograph 1 year
    after anterior approach for corpectomy and posterior approach for short-segment pedicle screw instrumentation.

    2011 American Academy of Orthopaedic Surgeons

    pain, fewer complications, and lower cost when compared with surgical management in neurologically intact patients with stable burst fractures. A recent study
    of interim results found AO type A3 fractures to have
    similar outcomes when treated with a custom TLSO
    compared to no orthosis.36 Failure of nonsurgical management may be manifested by patient inability to tolerate brace or cast immobilization, incapacitating pain,
    progressive deformity, or progressive neurologic impairment.
    Surgery is often warranted in patients with unstable
    spine injuries. These patients frequently have a major
    spine injury causing mechanical instability, neurologic
    instability, or both, according to the Denis classification. When the AO classification or TLICS is applied,
    these patients tend to have type B or C injuries or a
    TLICS greater than 4, respectively. Decompression in
    addition to spinal stabilization may be required if a
    neurologic injury is present, particularly if the injury is
    incomplete.
    Surgical intervention may be needed for the patient
    in whom nonsurgical treatment has failed (Figure 5).
    Early standing films may show significantly increased
    segmental kyphosis and increasing neurologic deficit;
    continued pain or failure of immobilization may occur
    later. After 3 to 4 weeks, a reconstructive procedure
    may be necessary and can be much more involved than
    surgical intervention immediately after injury. The patient discussed in Figure 5 required anterior corpectomy with release of the anterior longitudinal ligament
    and posterior osteotomies to correct sagittal malalignment because of a 3-month delay in surgical treatment
    after initial injury.

    Orthopaedic Knowledge Update 10

    5: Spine

    than neurologic deficit.33-35 Data from retrospective


    studies suggest that patients with thoracolumbar
    trauma may have fewer days in intensive care and on a
    ventilator, a shorter hospital stay, and fewer respiratory
    infections when surgery is completed within 3 days of
    hospitalization. Large prospective studies would be
    helpful to delineate the effect on outcome related to the
    timing of stabilization. One difficulty encountered
    when trying to devise a study related to trauma patients
    is the lack of patient uniformity (patients may or may
    not have single or multisystem injuries, traumatic brain
    injury, spinal-related neurologic deficit, and underlying
    ankylosing disorder, or may be thin or obese).
    Conservative treatment is used for neurologically intact patients with stable fractures such as compression
    fractures, one-column and minor injuries using the Denis classification, type A injuries using the AO system,
    and TLICS scores lower than 4. Pain medication, bracing or casting in extension, activity modification, and
    serial imaging are usually effective. A removable thoracolumbosacral orthosis (TLSO) is the most commonly
    used form of immobilization; however, hyperextension
    casting with a Risser-type body cast may also be used
    but is less well tolerated by patients. Immobilization
    has been recommended for a minimum of 10 to 12
    weeks; however, new data suggest stable AO type A3
    fractures may not need bracing in certain patient populations.25 Serial imaging and follow-up are necessary
    to detect any evidence of progressive spinal deformity
    and to monitor fracture healing. Progressive improvement in pain and return to function can be expected for
    most patients. Nonsurgical management has been associated with equivalent functional outcomes with less

    645

    Section 5: Spine

    Table 2

    TLICS Surgical Approach Algorithm


    Posterior Ligamentous Complex
    Neurologic Status

    Intact

    Disrupted

    Intact

    Posterior approach

    Posterior approach

    Root injury

    Posterior approach

    Posterior approach

    Posterior (anterior) approach

    Posterior (combined) approach

    Incomplete spinal cord or cauda equina injury


    Complete spinal cord or cauda equina injury

    Combined approach

    5: Spine

    (Adapted with permission from Vaccaro AR, Lehman RA Jr, Hurlbert RJ, et al: A new classification of thoracolumbar injuries: The importance of injury morphology, the
    integrity of the posterior ligamentous complex, and neurologic status. Spine (Phila Pa 1976) 2005;30:2325-2333.)

    Figure 6

    Radiograph showing an anterior-only construct.

    Surgical intervention can be anterior, posterior, or


    circumferential. The TLICS system suggested a surgical
    approach based on the neurologic status of the patient
    and the integrity of the PLC. A posterior approach
    alone was recommended for patients with intact neurologic status or root injury, whereas an anterior approach alone was recommended for an incomplete spinal cord injury with an intact PLC. Patients presenting
    with a cauda equina syndrome may be treated with an
    anterior, posterior, or combined approach depending
    upon where decompression and stabilization are
    needed. Complete spinal cord injury patients are
    treated in a manner similar to cauda equina patients,
    646

    Orthopaedic Knowledge Update 10

    with a preference for the posterior approach. One


    study noted that many institutions would consider decompression of the spinal cord or cauda equina with
    associated PLC injury to maintain cerebrospinal fluid
    dynamics and prevent the formation of syringomyelia,16
    despite the patient having a complete spinal cord injury.
    (Table 2). Combined or circumferential approaches are
    usually reserved for patients who require anterior column decompression and/or reconstruction following
    posterior realignment and stabilization.
    Anterior surgery is frequently indicated for an incomplete spinal cord injury or cauda equina syndrome
    resulting from retropulsed bone due to a burst-type
    fracture. A subtotal corpectomy with removal of retropulsed bone is often required to decompress the canal.
    A structural cadaver allograft or a cage may be used to
    reconstruct the anterior column and maintain alignment following decompression. In two studies reviewing neurologic improvement, the Frankel grade was
    noted to improve by one grade; in one study, the average kyphosis was improved from 22.7 to 7.4 with
    loss of sagittal alignment averaging 2.1 after treatment. For most patients with an intact PLC, the use of
    anterior instrumentation allows for an anterior-only
    construct (Figure 6). In patients with evidence of PLC
    disruption (AO type B), the use of anterior-only constructs is controversial. Although there are limited reports of successful use of this technique in the literature, it should be considered with caution. Anterior
    surgery is also an option for pincer-type fractures due
    to the high risk of nonunion and persistent pain. In stable burst fractures there is often the option of anterior
    or posterior procedures. One study showed better outcomes among patients treated with anterior-only surgery compared with posterior-only surgery.29
    Posterior surgery can be useful for direct and indirect decompression and stabilization. Direct decompression can be achieved by removing the facet/lamina/
    pedicle ipsilateral to the retropulsed bone within the
    spinal canal and removing the fracture fragment or tapping it anterior. This procedure is particularly useful in
    patients with an incomplete neurologic injury and canal
    encroachment from retropulsed bone. In neurologically
    intact patients, decompression may not be necessary

    2011 American Academy of Orthopaedic Surgeons

    Chapter 49: Thoracolumbar Trauma

    Osteoporotic Vertebral Compression Fractures


    With an aging baby boomer generation, the incidence
    of osteoporotic vertebral compression fracture (VCF) is
    likely to increase. Currently, approximately 700,000
    VCFs occur per year in the United States. VCF is the
    most common osteoporotic fracture, occurring twice as
    often as hip fractures.37 The literature suggests approximately 20% to 25% of patients older than 70 years
    will experience a VCF; this percentage increases to
    about 50% for patients older than 80 years. 37 Other
    studies have found that a patient with one VCF is five
    times as likely to experience a second VCF within 1
    year. Two VCFs result in an even higher risk of the occurrence of a third VCF.37
    VCFs may be treated nonsurgically or surgically.
    Most patients respond to nonsurgical treatment, which

    2011 American Academy of Orthopaedic Surgeons

    Figure 7

    AP (A) and lateral (B) radiographs of a patient


    who underwent short-segment pedicle screw
    fixation for a burst fracture.

    involves medical management of the underlying osteoporosis, pain medication, bracing, and activity modification. Surgical treatment includes percutaneous options such as vertebroplasty or kyphoplasty, or open
    surgery. Open surgical treatment may be indicated for
    patients with a neurologic deficit from a significant kyphotic deformity or retropulsed bone, or for reconstruction of significant spinal malalignment as a salvage
    procedure. When open surgery is necessary, serious
    consideration should be given to long constructs with
    multiple fixation points and/or combined anteriorposterior procedures to reduce the risk of hardware
    failure because of osteoporotic bone.
    Most patients with VCFs do not have a neurologic
    deficit; the primary indication for surgical intervention
    tends to be intractable pain. These patients often have
    significant medical comorbidities that may limit surgical options. Minimally invasive techniques have been
    developed that allow surgical treatment of painful
    VCFs with minimal surgical morbidity. Percutaneous
    vertebroplasty and kyphoplasty involve injection of
    polymethylmethacrylate cement into the fractured
    body. In contrast to vertebroplasty, cavity creation in
    kyphoplasty is with a balloon tamp with injection of a
    more viscous cement. Both procedures result in significant pain reduction in the immediate postoperative period (60% to 100%); however, kyphoplasty reportedly
    has less chance of cement extravasation. Kyphoplasty
    also is advantageous because it can partially restore
    vertebral body height and correct kyphosis, although
    the clinical significance of this benefit remains controversial. To date there are no long-term studies showing

    Orthopaedic Knowledge Update 10

    5: Spine

    because it further destabilizes the spine and may increase the possibility of dural tear or neural injury. The
    spinal canal has the potential to remodel as it heals
    with increased spinal canal diameter over time.
    Indirect decompression can be achieved in a patient
    with an intact posterior longitudinal ligament using
    posterior instrumentation. Postural reduction and distraction in the sagittal plane allows for fracture reduction via ligamentotaxis. The most popular way to provide stabilization is via pedicle screws and rods (Figure
    7), although a hook-and-rod construct may be used.
    Pedicle screw constructs spanning at least two levels
    above and two levels below the fracture have been
    found to decrease the occurrence of progressive kyphosis and hardware failure. Progressive kyphosis without
    hardware failure is not necessarily a clinical problem
    but should be monitored with radiographs. Short segment instrumentation (one level above to one level below) is usually sufficient for Chance-type fractures,
    compression fractures, and some burst fractures but
    has been associated with increased hardware failure
    and progressive kyphosis, especially when the anterior
    column is incompetent and unable to provide stability.
    One study showed that increased vertebral body comminution, poor bony fragment apposition, and increased kyphosis can help predict short segment instrumentation failure.13 Rotational injuries and fracturedislocations are usually best managed by a posterior
    approach, which allows for realignment and multilevel
    fixation.
    Combined anterior-posterior procedures are generally reserved for severe injuries with significant posterior column disruption and loss of anterior column integrity. These injuries usually are treated with initial
    stabilization and realignment via a posterior approach
    followed by anterior column reconstruction either at
    the same setting or as a staged procedure. A disadvantage of the combined procedure is the added morbidity
    of both an anterior and posterior approach. Another
    indication for combined procedures is in the setting of
    significant osteoporosis, where a combined approach
    may reduce the risk of hardware failure.

    647

    Section 5: Spine

    a clinical benefit of kyphoplasty over vertebroplasty.


    However, kyphoplasty is more expensive than vertebroplasty. One randomized controlled study found that
    pain related outcomes were similar when comparing
    patients treated with kyphoplasty and those treated
    nonsurgically at the 1-year follow-up visit.38 The study
    also noted at the 1-year follow-up that the kyphoplasty
    patients were more likely to require less activity restriction and narcotic use than control subjects treated nonsurgically. The kyphoplasty results are in contrast to a
    recently published study where the role of vertebroplasty was called into question when compared to a
    sham surgery.39 This study had methodological errors
    that made it difficult to compare its results to those of
    other kyphoplasty studies or to studies retrospectively
    comparing vertebroplasty to routine nonsurgical treatment.

    Emerging Concepts

    5: Spine

    Minimally invasive surgery is gaining ground in the


    treatment of thoracolumbar trauma. Most of the literature is from case series and retrospective studies, and
    these techniques have not been accepted as the standard of care for treating trauma patients. A 2008 study
    documented the treatment of AO A2- and A3-type
    fractures in 18 patients with combined short-segment
    minimally invasive pedicle screw instrumentation and
    kyphoplasty using calcium phosphate cement in the
    fractured vertebral body.40 The patients did not have
    progressive kyphosis beyond 1 to 5, and no additional compression fractures were noted during the average 22-month follow-up period.
    Another review of currently available technology
    discussed anterior endoscopic approaches as well as
    percutaneous pedicle screw placement.1 The authors
    noted that technology is still evolving for these approaches and that there is a learning curve associated
    more with anterior endoscopic approaches than posterior percutaneous pedicle screw placement. With improved three-dimensional imaging and navigation systems, the role of minimally invasive surgery may
    continue to increase in popularity.

    injuries of the spine with paraplegia and tetraplegia: I.


    Paraplegia 1969;7(3):179-192.
    4.

    Dai LY, Wang XY, Jiang LS, Jiang SD, Xu HZ: Plain radiography versus computed tomography scans in the diagnosis and management of thoracolumbar burst fractures. Spine (Phila Pa 1976) 2008;33(16):E548-E552.
    This study reviewed the difference between compression
    and burst fractures based on plain radiography diagnosis compared with CT diagnosis. The authors found that
    vertebral body comminution was often underestimated
    with plain radiographs, which was not the case when
    evaluating fractures with CT. They concluded treatment
    is better directed from CT than plain radiography.

    5.

    Hauser CJ, Visvikis G, Hinrichs C, et al: Prospective


    validation of computed tomographic screening of the
    thoracolumbar spine in trauma. J Trauma 2003;55:228235.

    6.

    Lee HM, Kim HS, Kim DJ, Suk KS, Park JO, Kim NH:
    Reliability of magnetic resonance imaging in detecting
    posterior ligament complex injury in thoracolumbar spinal fractures. Spine (Phila Pa 1976) 2000;25(16):20792084.

    7.

    Dai LY, Ding WG, Wang XY, Jiang LS, Jiang SD, Xu
    HZ: Assessment of ligamentous injury in patients with
    thoracolumbar burst fractures using MRI. J Trauma
    2009;66(6):1610-1615.
    A retrospective study validating the use of MRI as an
    imaging modality to determine PLC injury is presented.
    The authors noted that the PLC injury did not correlate
    with neurologic injury or fracture severity.

    8.

    Oner FC, van Gils AP, Faber JA, Dhert WJ, Verbout AJ:
    Some complications of common treatment schemes of
    thoracolumbar spine fractures can be predicted with
    magnetic resonance imaging: Prospective study of 53
    patients with 71 fractures. Spine (Phila Pa 1976) 2002;
    27(6):629-636.

    9.

    White A, Panjabi M: The problem of clinical instability


    in the human spine: A systematic approach, in Clinical
    Biomechanics of the Spine, ed 2. Philadelphia, PA, JB
    Lippincott, 1990, pp 277-378.

    10.

    Sethi MK, Schoenfeld AJ, Bono CM, Harris MB: The


    evolution of thoracolumbar injury classification systems. Spine J 2009;9(9):780-788.
    The authors document the challenges and evolution of
    the thoracolumbar classification systems.

    11.

    Holdsworth FW: Fractures, dislocations, and fracturedislocations of the spine. J Bone Joint Surg Am 1970;
    52(8):1534-1551.

    12.

    Denis F: The three column spine and its significance in


    the classification of acute thoracolumbar spinal injuries.
    Spine (Phila Pa 1976) 1983;8(8):817-831.

    13.

    McCormack T, Karaikovic E, Gaines RW: The load


    sharing classification of spine fractures. Spine (Phila Pa
    1976) 1994;19(15):1741-1744.

    Annotated References
    1.

    648

    Rampersaud YR, Annand N, Dekutoski MB: Use of


    minimally invasive surgical techniques in the management of thoracolumbar trauma: Current concepts. Spine
    (Phila Pa 1976) 2006;31(11, suppl):S96-S102, discussion S104.

    2.

    Maynard FM Jr, Bracken MB, Creasey G, et al; American Spinal Injury Association: International standards
    for neurological and functional classification of spinal
    cord injury. Spinal Cord 1997;35(5):266-274.

    3.

    Frankel HL, Hancock DO, Hyslop G, et al: The value of


    postural reduction in the initial management of closed

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 49: Thoracolumbar Trauma

    14.

    Magerl F, Aebi M, Gertzbein SD, Harms J, Nazarian S:


    A comprehensive classification of thoracic and lumbar
    injuries. Eur Spine J 1994;3(4):184-201.

    15.

    Wood KB, Khanna G, Vaccaro AR, Arnold PM, Harris


    MB, Mehbod AA: Assessment of two thoracolumbar
    fracture classification systems as used by multiple surgeons. J Bone Joint Surg Am 2005;87(7):1423-1429.

    16.

    Vaccaro AR, Lehman RA Jr, Hurlbert RJ, et al: A new


    classification of thoracolumbar injuries: The importance
    of injury morphology, the integrity of the posterior ligamentous complex, and neurologic status. Spine (Phila
    Pa 1976) 2005;30(20):2325-2333.

    17.

    Vaccaro AR, Zeiller SC, Hulbert RJ, et al: The thoracolumbar injury severity score: A proposed treatment
    algorithm. J Spinal Disord Tech 2005;18(3):209-215.

    18.

    Patel AA, Dailey A, Brodke DS, et al; Spine Trauma


    Study Group: Thoracolumbar spine trauma classification: The Thoracolumbar Injury Classification and Severity Score system and case examples. J Neurosurg
    Spine 2009;10(3):201-206.
    A description of the TLICS scheme and its application
    to three clinical case vignettes are discussed.

    19.

    Patel AA, Vaccaro AR, Albert TJ, et al: The adoption of


    a new classification system: Time-dependent variation in
    interobserver reliability of the thoracolumbar injury severity score classification system. Spine (Phila Pa 1976)
    2007;32(3):E105-E110.

    20.

    Harrop JS, Vaccaro AR, Hurlbert RJ, et al; Spine


    Trauma Study Group: Intrarater and interrater reliability and validity in the assessment of the mechanism of
    injury and integrity of the posterior ligamentous complex: A novel injury severity scoring system for thoracolumbar injuries. Invited submission from the Joint
    Section Meeting On Disorders of the Spine and Peripheral Nerves, March 2005. J Neurosurg Spine 2006;4(2):
    118-122.

    Raja Rampersaud Y, Fisher C, Wilsey J, et al: Agreement between orthopedic surgeons and neurosurgeons
    regarding a new algorithm for the treatment of thoracolumbar injuries: A multicenter reliability study. J Spinal Disord Tech 2006;19:477-482.

    24.

    Wood K, Buttermann G, Mehbod A, et al: Operative


    compared with nonoperative treatment of a thoracolumbar burst fracture without neurological deficit: A
    prospective, randomized study. J Bone Joint Surg Am
    2003;85(5):773-781.

    25.

    Bailey CS, Dvorak MF, Thomas KC, et al: Comparison


    of thoracolumbosacral orthosis and no orthosis for the
    treatment of thoracolumbar burst fractures: Interim
    analysis of a multicenter randomized clinical equivalence trial. J Neurosurg Spine 2009;11(3):295-303.
    This study is ongoing but interim results show comparable outcomes in treating AO type A3 burst fractures
    with or without a custom TLSO. Participants could not
    have greater than 35 of kyphosis or a neurologic deficit. No statistically significant outcome has been identified between the two groups.

    26.

    Shen WJ, Shen YS: Nonsurgical treatment of threecolumn thoracolumbar junction burst fractures without
    neurologic deficit. Spine (Phila Pa 1976) 1999;24(4):
    412-415.

    27.

    Siebenga J, Leferink VJ, Segers MJ, et al: Treatment of


    traumatic thoracolumbar spine fractures: A multicenter
    prospective randomized study of operative versus nonsurgical treatment. Spine (Phila Pa 1976) 2006;31(25):
    2881-2890.

    28.

    Thomas KC, Bailey CS, Dvorak MF, Kwon B, Fisher C:


    Comparison of operative and nonoperative treatment
    for thoracolumbar burst fractures in patients without
    neurological deficit: A systematic review. J Neurosurg
    Spine 2006;4(5):351-358.

    29.

    Wood KB, Bohn D, Mehbod A: Anterior versus posterior treatment of stable thoracolumbar burst fractures
    without neurologic deficit: A prospective, randomized
    study. J Spinal Disord Tech 2005;18(suppl, Suppl)S15S23.

    30.

    Wang XY, Dai LY, Xu HZ, Chi YL: The load-sharing


    classification of thoracolumbar fractures: An in vitro
    biomechanical validation. Spine (Phila Pa 1976) 2007;
    32(11):1214-1219.
    This study used previously established in vitro biomechanical approaches and concluded that the loadsharing classification system was valid for determining
    stability.

    21.

    Vaccaro AR, Baron EM, Sanfilippo J, et al: Reliability


    of a novel classification system for thoracolumbar injuries: The Thoracolumbar Injury Severity Score. Spine
    (Phila Pa 1976) 2006;31(11, Suppl)S62-S69, discussion
    S104.

    22.

    Whang PG, Vaccaro AR, Poelstra KA, et al: The influence of fracture mechanism and morphology on the reliability and validity of two novel thoracolumbar injury
    classification systems. Spine (Phila Pa 1976) 2007;
    32(7):791-795.

    31.

    Dai LY, Jin WJ: Interobserver and intraobserver reliability in the load sharing classification of the assessment of
    thoracolumbar burst fractures. Spine (Phila Pa 1976)
    2005;30(3):354-358.

    The interrater reliability of the TLICS is on par or better


    than that of the AO or the Denis classification systems.

    32.

    Dai LY, Jiang LS, Jiang SD: Conservative treatment of


    thoracolumbar burst fractures: A long-term follow-up

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    5: Spine

    A review of the interobserver reliability when using the


    mechanistic TLISS classification system, the precursor to
    the TLICS, is presented. This study reviewed the TLISS
    system and showed how it compared favorably to prior
    thoracolumbar classification systems, such as the AO
    and Denis classifications.

    23.

    649

    Section 5: Spine

    results with special reference to the load sharing classification. Spine (Phila Pa 1976) 2008;33(23):2536-2544.
    A retrospective review of 127 patients treated conservatively and followed for a minimum of 3 years concluded
    that the load-sharing classification system can help predict failure of conservative management. This study is
    unique because it included patients with neurologic deficit as well as those without deficit. Thirty-seven patients included in the study had refused surgical intervention and underwent nonsurgical treatment.
    33.

    McHenry TP, Mirza SK, Wang J, et al: Risk factors for


    respiratory failure following operative stabilization of
    thoracic and lumbar spine fractures. J Bone Joint Surg
    Am 2006;88(5):997-1005.

    34.

    Croce MA, Bee TK, Pritchard E, Miller PR, Fabian TC:


    Does optimal timing for spine fracture fixation exist?
    Ann Surg 2001;233(6):851-858.

    35.

    36.

    5: Spine

    37.

    650

    The authors present a population-based cohort study


    that followed 2,680 white women for up to 15 years to
    evaluate their risk of developing an osteoporotic compression fracture based on the presence of vertebral
    compression fractures and bone mineral density.
    38.

    This randomized study compared patients undergoing


    kyphoplasty for an osteoporotic compression fracture
    with conservative management. The patients treated
    with kyphoplasty required less narcotic and had increased activity in comparison with the nonsurgically
    treated patients.
    39.

    Kerwin AJ, Frykberg ER, Schinco MA, Griffen MM,


    Murphy T, Tepas JJ: The effect of early spine fixation
    on non-neurologic outcome. J Trauma 2005;58(1):
    15-21.
    Bailey CS, Dvorak MF, Thomas KC, et al: Comparison
    of thoracolumbosacral orthosis and no orthosis for the
    treatment of thoracolumbar burst fractures: Interim
    analysis of a multicenter randomized clinical equivalence trial. J Neurosurg Spine 2009;11:295-303.
    The authors found equivalence between treatment with
    a TLSO and no orthosis for thoracolumbar burst fractures. No significant difference was found between
    treatment groups.

    Wardlaw D, Cummings SR, Van Meirhaeghe J, et al: Efficacy and safety of balloon kyphoplasty compared with
    non-surgical care for vertebral compression fracture
    (FREE): A randomised controlled trial. Lancet 2009;
    373(9668):1016-1024.

    Kallmes DF, Comstock BA, Heagerty PJ, et al: A randomized trial of vertebroplasty for osteoporotic spinal
    fractures. N Engl J Med 2009;361(6):569-579.
    A randomized controlled study comparing sham surgery
    to vertebroplasty found similar outcomes at 1 month after the procedure.

    40.

    Korovessis P, Hadjipavlou A, Repantis T: Minimal invasive short posterior instrumentation plus balloon kyphoplasty with calcium phosphate for burst and severe
    compression lumbar fractures. Spine (Phila Pa 1976)
    2008;33(6):658-667.
    A case series review is presented of 18 patients treated
    with balloon kyphoplasty and short-segment percutaneous pedicle screw instrumentation for L1-L4 compression or burst-type fractures.

    Cauley JA, Hochberg MC, Lui LY, et al: Long-term risk


    of incident vertebral fractures. JAMA 2007;298(23):
    2761-2767.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 50

    Lumbar Spondylolisthesis
    Toshinori Sakai, MD, PhD

    Koichi Sairyo, MD, PhD

    Introduction
    Spondylolisthesis is the displacement of one vertebra
    over the subjacent vertebra. This slippage, which can
    occur at anytime from infancy through adulthood, has
    several different causes. Based on the underlying cause
    of the slippage, spondylolisthesis is subdivided into five
    types: isthmic, degenerative, dysplastic, congenital
    (pathologic), and traumatic (Table 1). Although the radiographic translation seen in a spondylolisthesis is independent of the underlying cause, it is important to
    identify the cause because the natural history, symptoms, and treatment of the disorder differ based on the
    etiology.

    Epidemiology

    Dr. Sairyo or an immediate family member has received


    royalties from Japan MDM; is a member of a speakers
    bureau or has made paid presentations on behalf of Japan MCM; serves as an unpaid consultant to Japan Kyphoon; and has received research or institutional support from Alphatec Spine, Medtronic Sofamor Danek,
    Senko, and Stryker. Dr. Bhatia or an immediate family
    member has received royalties from Alphatec Spine; is a
    member of a speakers bureau or has made paid presentations on behalf of Biomet, Stryker, Alphatec Spine,
    Seaspine, and Globus Medical; serves as a paid consultant to Alphatec Spine, Biomet, and Seaspine; and has
    received research or institutional support from Alphatec
    Spine, Biomet, Arthrex, National Institutes of Health
    (NIAMS & NICHD), and Spinewave. Neither Dr. Sakai nor
    any immediate family member has received anything of
    value from or owns stock in a commercial company or
    institution related directly or indirectly to the subject of
    this chapter.

    2011 American Academy of Orthopaedic Surgeons

    cidence varies considerably among different ethnic


    groups. The incidence of lumbar spondylolysis is 6.4%
    in Caucasian males, 2.8% in African-American males,
    2.3% in Caucasian females, and 1.1% in AfricanAmerican females.1 The highest incidence reported is
    54% in native residents of Greenland.2 These results
    suggest that a genetic or hereditary factor may play a
    role in the development of spondylolysis.
    The incidence of spondylolysis and isthmic spondylolisthesis varies depending on the method of analysis. Studies using plain radiographs have shown a 4.6%
    incidence of spondylolysis, whereas studies using CT
    have shown rates between 5.7% and 5.9%.3,4 The fifth
    lumbar vertebra (L5) accounts for approximately 90%
    of spondylolysis cases, and unilateral spondylolysis is
    found in approximately 22% of cases. Multiple-level
    spondylolysis is rare and seen in less than 0.5% of
    cases.
    Degenerative spondylolisthesis has a 3:1 prevalence
    in women, with African-American women affected
    three times more frequently than Caucasian women.
    The most commonly involved level is L4-L5, followed
    by L3-L4. Unlike isthmic spondylolisthesis, the L5-S1
    level is rarely affected by degenerative spondylolisthesis. As the name implies, degenerative spondylolisthesis
    is caused by degenerative changes in the disk and facet
    complex, which lead to instability at the affected level.
    Because this type of spondylolisthesis is a degenerative

    5: Spine

    The various types of spondylolisthesis have different


    fundamental causes. Isthmic spondylolisthesis is caused
    by a defect in the pars interarticularis, which is called a
    spondylolysis, pars defect, or pars fracture (Figure 1).
    Along with the degenerative type, the isthmic type is
    one of the two most common forms of spondylolisthesis. Lumbar spondylolysis and isthmic spondylolisthesis
    occur in approximately 6% of the general population,
    and occur most commonly at the L5-S1 level. This in-

    Nitin N. Bhatia, MD

    Table 1

    Wiltse Classification of Spondylolisthesis


    Type

    Description

    Dysplastic: congenital abnormality of the upper


    sacrum or the arch of L5

    II

    Isthmic: lesion in the pars interarticularis


    A. Lytic: fatigue fracture of the pars
    B. Elongated but intact pars
    C. Acute fracture

    III

    Degenerative: resulting from long-standing


    intersegmental disease

    IV

    Traumatic: fracture in region other than the pars

    Pathologic: generalized or local bone disease

    (Reproduced from Jones TR, Rao RD: Adult isthmic spondylolisthesis. J Am Acad
    Orthop Surg 2009;17(10):609-617.)

    Orthopaedic Knowledge Update 10

    651

    Section 5: Spine

    crum. This lesion is caused by high-energy trauma and


    is rarely isolated. Most instances of traumatic spondylolisthesis are accompanied by multiple traumatic injuries and visceral, vascular, and neurologic symptoms.
    Because many patients die soon after the initial traumatic event, many cases of traumatic spondylolisthesis
    are not identified. A review of the literature reported
    approximately 30 cases of traumatic lumbosacral dislocation;8 however, it is likely that this number underrepresents the actual incidence of this type of injury.

    Pathogenesis

    Figure 1

    Axial CT image of L5 spondylolysis (also known


    as a pars fracture or pars defect). (Reproduced
    with permission from Cavalier R, Herman MY,
    Cheung EV, Pizzutillo PD: Spondylolysis and
    Spondylolisthesis in children and adolescents: I.
    Diagnosis, natural history, and nonsurgical
    mamagement. J Bone Joint Surg Am
    2006;14:417-424.)

    5: Spine

    condition, it most commonly occurs in older patients.


    The records and radiographs of 949 women and 120
    men age 50 years and older who had been treated by a
    spinal surgeon for low back pain were reviewed.5
    Women who had borne children had a significantly
    higher incidence of degenerative spondylolisthesis than
    nulliparous women (28% versus 16.7%, respectively).
    The incidence of degenerative spondylolisthesis was
    7.5% in the men, which was significantly less than in
    the women (P = 0.031).
    In congenital and dysplastic spondylolisthesis, the
    pars interarticularis is intact but the L5-S1 facet joints
    are abnormally developed. This deficiency in the facet
    joints leads to instability and the resultant anterior
    translation of the L5 vertebral body. Because the posterior arch is not fractured, as in isthmic spondylolisthesis, the L5 lamina translates anteriorly with the vertebral body and can cause central spinal canal stenosis,
    with symptoms of stenosis occurring with slippages of
    more than 35% (Figure 2). The exact incidences of
    these types of spondylolisthesis are unknown, but an
    incidence of 14% to 21% has been reported in relatively large series of patients treated for spondylolithesis.6,7
    Traumatic spondylolisthesis is characterized by a
    dislocated or subluxated lumbar spine, which has
    moved anterior to the sacrum because of bilateral dislocations or fractures of the L5-S1 facet joints, pedicles,
    pars interarticularis, or a fracture line crossing the sa652

    Orthopaedic Knowledge Update 10

    Various theories have been put forth regarding the possible cause of lumbar spondylolysis. Many authors believe that lumbar spondylolysis is a stress fracture of
    the pars interarticularis because spondylolysis frequently occurs in athletes in sports requiring repetitive
    trunk movements, especially extension;9-12 it frequently
    occurs in athetoid palsy patients with involuntary trunk
    movements.13 Spondylolysis has not been reported in
    fetuses, infants, or nonambulatory patients.14,15 The radiologic course is similar to that of a stress fracture of a
    long bone. The pars defects can heal with nonsurgical
    management.16-18
    The pathogenesis of isthmic spondylolisthesis following spondylolysis also has been extensively studied.
    By definition, isthmic spondylolisthesis is slippage associated with a spondylolysis of the cephalad involved
    vertebra; however, spondylolysis does not develop in all
    patients with this type of anterior slippage. In a study
    describing the natural history of spondylolysis and isthmic spondylolisthesis in 30 patients, the greatest slip
    progression occurred early in life.19 During the first decade of follow-up evaluation, the average slip progression was 7% for those that progressed. Progression in
    the second and third decades averaged 4%. In the
    fourth decade of follow-up, the average progression
    was only 2%. Therefore, the progression of isthmic
    spondylolisthesis occurs in younger patients; this type
    of spondylolisthesis may gradually stabilize as the patient ages.
    Degenerative spondylolisthesis is a disorder that affects older patients. Chronic degenerative changes that
    occur in the facet joint and disk space result in the loss
    of normal segmental stability. Certain anatomic variants, including hyperlordosis, sagittal orientation of the
    facet joints, and sacralization of the L5 vertebral body
    can predispose a patient to the development of degenerative spondylolisthesis. Chronic, low-level instability
    leads to further degenerative changes, including facet
    joint subluxation with capsular laxity, osteophyte formation, and disk-space narrowing. These changes lead
    to compression of the traversing nerve root of the involved level. In the most common expressions of L4-L5
    degenerative spondylolisthesis, the L5 nerve root is often symptomatic, with resultant lower lateral leg radiculopathy and possible foot and toe dorsiflexion weakness. The amount of displacement in degenerative
    spondylolisthesis tends to be limited to less than 40%

    2011 American Academy of Orthopaedic Surgeons

    Chapter 50: Lumbar Spondylolisthesis

    5: Spine

    Figure 2

    A, Photograph of a 9-year-old girl with grade IV dysplastic (Wiltse type I) spondylolisthesis of L5-S1. Note the position of flexion of her hips and knees. B, Popliteal angle measurement of 55 secondary to contracture of hamstring muscles. C, Standing lateral radiograph of the lumbosacral spine of the same patient, illustrating high-grade
    spondylolisthesis with lumbosacral kyphosis (arrows). (Reproduced with permission from Cavalier R, Herman MY,
    Cheung EV, Pizzutillo PD: Spondylolysis and Spondylolisthesis in children and adolescents: I. Diagnosis, natural history, and nonsurgical mamagement. J Bone Joint Surg Am 2006;14:417-424.)

    because of the eventual contact between the superior


    articular facet of the inferior level and the pars interarticularis of the superior level. Central spinal stenosis
    can occur as a result of facet joint hypertrophy, ligamentum flavum redundancy, and disk-space bulging.
    In congenital and dysplastic spondylolisthesis, abnormalities of the vertebral arch or facet joints lead to
    spondylolisthesis at the lumbosacral junction. Abnormalities include failure of formation of the facet joint
    or sagittal alignment of the L5-S1 facet complex. Spon-

    2011 American Academy of Orthopaedic Surgeons

    dylolysis, by definition, does not occur with dysplastic


    or congenital spondylolisthesis; therefore, the intact L5
    lamina may translate anteriorly with the vertebral body
    and can cause severe central spinal stenosis. This disorder usually becomes symptomatic in early adolescence,
    and it affects females approximately twice as frequently
    as males.
    Traumatic spondylolisthesis involves a bony or ligamentous injury that results in acute instability of the involved level. This type of injury can include high-

    Orthopaedic Knowledge Update 10

    653

    Section 5: Spine

    energy trauma resulting in ligamentous rupture, facet


    complex fracture, and possible facet subluxation and
    dislocation. Acute pars fractures secondary to highenergy fractures also can be classified as traumatic injuries. Although the traumatic pars fracture is seemingly similar to the spondylolytic pars fracture seen in
    isthmic spondylolisthesis, the traumatic pars fracture
    occurs when the pars fails under abnormal and excessive stress, whereas the spondylolytic defect occurs under normal physiologic stress.

    Clinical Presentation

    5: Spine

    Chronic isthmic spondylolisthesis frequently causes low


    back pain in adult patients. Radiculopathy may eventually develop in the lower extremities because of the fibrocartilaginous proliferation around the pars defect.
    This radiculopathy involves the exiting nerve root,
    which is the L5 nerve root in the most common type of
    L5 spondylolysis. The typical symptoms of chronic
    isthmic spondylolisthesis are low back pain caused by
    spinal instability and radiating leg pain caused by compression of the exiting nerve root.
    In degenerative spondylolisthesis, lateral recess and
    foraminal stenosis result in radiculopathy caused by
    compression of the traversing nerve root. Hypertrophy
    and subluxation of the involved facet complex, combined with the common degenerative changes of disk
    bulging and ligamentum flavum redundancy, cause
    compression on the exiting nerve root at that level.
    Central stenosis can occur in more advanced cases. Because the L4-L5 level is most commonly affected by degenerative spondylolisthesis, L5 radiculopathy from
    compression of the traversing L5 nerve root is the most
    common neural finding in these patients.
    The clinical presentations of congenital, dysplastic,
    and traumatic spondylolisthesis were discussed previously in this chapter.

    Treatment

    important in attaining bony healing of the pars. Based


    on a retrospective review of CT of 239 pars defects in
    134 young patients treated nonsurgically, an early stage
    of the defects at first presentation was an important
    prognostic indicator in attaining osseous healing with
    nonsurgical treatment.17 Nonsurgical treatments include nonsteroidal anti-inflammatory drugs, brace therapy, sports activity restrictions, and, occasionally,
    short-term bed rest. Regardless of whether the pars defect heals, most symptoms resolve over time with conservative treatment.
    It is likely that an adult patient with a long-standing
    lumbar spondylolysis and isthmic spondylolisthesis
    would also benefit from a nonsurgical treatment protocol. Physical therapy, home-based strengthening programs, weight reduction, activity modification, and
    possible injection therapy, including epidural injections,
    facet blocks, and pars injections, may be beneficial in
    certain patients. The associated degenerative changes
    that occur in the adult patient with a chronic lumbar
    isthmic spondylolisthesis, however, may require surgical decompression of the compressed nerve root or stabilization of the degenerative motion segment.
    Direct Repair of Spondylolysis
    Various techniques to directly repair a pars defect have
    been described. These techniques include bone grafting
    with the placement of wires, screws, or hook-screw
    constructs to stabilize the fractured pars. Minimally invasive repair techniques also have been described (Figure 3). The goal of these procedures is to restore the
    normal anatomy and save a spinal motion segment to
    retain the associated spinal mobility. For these procedures to be successful, the pain source must be the pars
    defect itself. The pain generator can be preoperatively
    verified by injecting the defect with a local anesthetic.
    In patients who do not respond to the local anesthetic
    injection, direct repair of the pars defect is not recommended; other causes of low back pain should be evaluated. If significant displacement has occurred at the
    site of the spondylolysis, direct repair of the defect may
    not be highly successful because of difficulty in achieving solid bony healing.

    Isthmic Spondylolisthesis and Spondylolysis


    Nonsurgical Treatment
    Spondylolysis is relatively common in children and adolescents. A prospective study reported a diagnosis of
    spondylolysis, with or without spondylolisthesis, in 9
    of 73 pediatric patients (12.3%) with a chief report of
    low back pain.20 Most adolescents with isthmic spondylolisthesis or spondylolysis can be successfully managed with nonsurgical treatment. In one recent metaanalysis study, 83.9% of adolescent patients who were
    nonsurgically treated for lumbar spondylolysis had a
    successful clinical outcome after at least 1 year, and
    bracing did not influence this outcome.21
    Bony union of the pars defect can be achieved in adolescents if they refrain from participation in sports activities and wear a trunk brace, although fracture healing is variable. Early diagnosis may be extremely
    654

    Orthopaedic Knowledge Update 10

    Decompression of Lumbar Nerve Roots


    Affected by Spondylolysis
    Radiculopathy can develop in an adult patient with
    spondylolysis as the condition becomes more chronic.
    The radiculopathy affects the exiting nerve root associated with the cephalad vertebra of the involved spinal
    segment because this nerve root is compressed by scar
    formation around the spondylolysis site. In the most
    common L5 spondylolysis with an L5-S1 spondylolisthesis, the L5 nerve root is involved. Decompressive
    laminectomy (the Gill procedure) has been described
    for patients with lumbar spondylolysis and associated
    radiculopathy. Subsequently, some authors reported
    that the Gill procedure can result in further vertebral
    slippage postoperatively and recommended spinal fusion in addition to laminectomy.22,23

    2011 American Academy of Orthopaedic Surgeons

    Chapter 50: Lumbar Spondylolisthesis

    Figure 3

    Minimally invasive technique for the direct repair of a pars defect. A, AP radiograph showing instrumentation placement. B, Postoperative photograph demonstrating incision size and location. C, Lateral radiograph showing instrumentation construct. (Reproduced with permission from Sairyo K, Sakai T, Yasui N: Minimally invasive technique for
    direct repair of the pars defects in young adults using a percutaneous pedicle screw and hook-rod system: A technical note. J Neurosurg Spine 2009;10:492-495.)

    Low-Grade Isthmic Spondylolisthesis


    Noninstrumented Fusion
    Because of the risk of increased spondylolisthesis following posterior decompression alone, spinal stabilization in addition to decompression has been recommended in adult patients with symptomatic isthmic
    spondylolisthesis.25 In one prospective randomized
    study comparing instrumented and noninstrumented
    lumbar posterolateral fusion for adult isthmic spondylolisthesis, posterolateral fusion performed without
    instrumentation relieved pain and improved function;
    the use of supplementary transpedicular instrumentation did not improve the fusion rate or the clinical outcomes.25
    The authors of a recent study retrospectively reviewed the long-term follow-up (mean, 19.7 years) outcomes of uninstrumented posterolateral spinal arthrodesis in adolescents with low-grade (grade I or II)
    lumbar isthmic spondylolisthesis.26 The outcome of spinal fusion was good, with 43 of 49 patients (87.7%) attaining solid fusion; 6 patients (12.3%) had a pseudarthrosis. The satisfactory results obtained in 94% of
    patients were closely associated with the rate of successful fusion.

    2011 American Academy of Orthopaedic Surgeons

    Instrumented Fusion
    Numerous surgical procedures have been described for
    isthmic spondylolisthesis, including decompression
    with or without posterolateral lumbar fusion and (possibly) with instrumentation and the addition of an interbody fusion. In a systematic review of the radiographic and clinical outcomes of adult patients who
    were surgically treated for low-grade isthmic spondylolisthesis, the authors concluded that a combined
    anterior and posterior procedure most reliably achieves
    fusion and a successful clinical outcome.27 However, a
    recent study reported that circumferential fusion
    achieved significantly better results than posterolateral
    fusion at 6 months and 1 year, although the difference
    diminished with time and was not significant at 2 years
    postoperatively.28
    In a prospective study to compare the outcomes of
    posterior lumbar interbody fusion and posterolateral
    fusion in patients with adult isthmic spondylolisthesis,
    the type of fusion did not affect the 2-year outcome.29
    In another prospective study, 164 adult patients with
    isthmic spondylolisthesis were evaluated to determine
    predicative factors for outcomes of spinal fusion.30 Patients who worked prior to surgery, males, and those
    who exercised regularly had better outcomes after fusion. The results of a systematic review of 29 selected
    high-quality studies on lumbar fusion showed no difference in outcomes between different fusion techniques.31
    Overall, the optimal type of surgery for low-grade
    adult isthmic spondylolisthesis remains controversial.

    5: Spine

    Less invasive techniques to decompress the involved


    nerve root in patients with spondylolysis have been developed.24 These decompression-only procedures are indicated in patients older than 40 years and in those
    with radiculopathy without low back pain and no evidence of spinal instability on dynamic radiographs.
    Good clinical outcomes with a mean follow-up period
    of 11.7 months have been reported. The advantage of
    these minimally invasive techniques is the feasibility
    of excising the edge of the spondylolysis site and associated scar tissue, with possibly less damage to the
    posterior elements, paravertebral muscles, and posterior ligamentous structures. Patients treated with a
    decompression-only procedure for spondylolysis should
    be counseled that their instability may continue to
    progress and that further surgery, including surgical fusion, may ultimately be necessary.

    High-Grade Spondylolisthesis
    Although high-grade isthmic spondylolisthesis (grade III,
    IV, or V) accounts for a distinct minority of all patients
    with spondylolisthesis, the treatment of high-grade spondylolisthesis can be complex and difficult. The optimal
    treatment of this pathology remains controversial. The
    clinical indications for the surgical treatment of a highgrade spondylolisthesis include continued pain despite
    conservative treatments, the progression of spinal deformity, and the presence of neurologic symptoms.

    Orthopaedic Knowledge Update 10

    655

    Section 5: Spine

    Most patients with high-grade spondylolisthesis or


    spondyloptosis (complete subluxation of the cephalad
    vertebra off the lower vertebra; grade V spondylolisthesis) become symptomatic during adolescence. A recent
    literature review evaluated the surgical treatment of
    high-grade spondylolisthesis in the pediatric population.32 The authors concluded that it was impossible to
    formulate clear guidelines for treating high-grade spondylolisthesis based on the best evidence available in the
    published literature because of the paucity of high-level
    studies on the topic. Various surgical techniques have
    been described, each with advantages and disadvantages.33-40 A study evaluating the long-term results of anterior, posterior, and circumferential in situ
    fusion for high-grade isthmic spondylolisthesis reported
    the superiority of circumferential fusion over the other
    methods studied.41

    Degenerative Spondylolisthesis

    5: Spine

    Nonsurgical Treatment
    As in many spinal disorders, the preferred initial treatment of patients with degenerative spondylolisthesis is
    nonsurgical. Nonsurgical treatment includes antiinflammatory medications, physical therapy, activity
    modification, and home-based exercise programs. Exercise programs frequently focus on core strengthening
    and aerobic conditioning, although no prospective randomized trials have been performed to identify the optimal nonsurgical modality. Other techniques used in
    conjunction with physical therapy include electrical
    stimulation, massage, heat packs, cold packs, ultrasound, and acupuncture; however, there are few high
    quality data supporting the use of these modalities.
    Epidural steroid injections are often used in the
    treatment of degenerative spinal conditions, including
    spinal stenosis and spondylolisthesis. The theoretic benefit of an epidural corticosteroid is its potent local antiinflammatory effect, which decreases the radicular and
    local pain caused by the degenerative joint changes and
    nerve compression. Although epidural steroid injections
    are frequently used and may temporarily improve
    symptoms, there have been no prospective randomized
    studies evaluating the efficacy of epidural injections for
    the long-term relief of symptoms in patients with degenerative spondylolisthesis. Two high-quality studies
    evaluating surgical treatment for symptomatic degenerative spondylolisthesis have shown that patients treated
    with conservative methods have inferior outcomes after
    at least 2 years of treatment compared with those
    treated surgically.42,43
    Surgical Treatment
    The primary surgical treatments for degenerative spondylolisthesis are decompression alone, decompression
    with noninstrumented fusion, and decompression with
    instrumented fusion. Surgical indications include back
    pain or leg symptoms that are recalcitrant to nonsurgical treatment, lead to a significant impairment in quality
    of life, and have associated significant or progressive
    neurologic deficits or neurogenic bowel or bladder symp656

    Orthopaedic Knowledge Update 10

    toms. The results of surgical treatments for radiculopathy and neurogenic claudication are believed to be better
    than results after surgical treatment for isolated axial
    back pain in patients with degenerative disease.
    Decompression Alone
    The goal of surgical decompression is the relief of
    symptomatic neurologic compression. The treatment of
    degenerative spondylolisthesis frequently includes central and lateral recess decompression because of the
    combined central spinal stenosis and facet joint changes
    that lead to lateral recess stenosis. Laminectomy is
    commonly performed in this setting. Several studies
    evaluated decompression alone in this patient
    population.44-46 The effectiveness of laminectomy alone
    has been described, with more than 80% of patients
    having good or excellent outcomes. Care must be
    taken, however, to prevent iatrogenic stability or
    worsen underlying instability. In one study, only 33%
    of patients treated with total facetectomy as part of the
    decompression procedure had good or excellent results
    versus 80% in those whose treatment included facet
    preservation.46 Most of these studies have limited value
    because of the small number of patients, retrospective
    analyses, and suboptimal follow-up periods. Overall,
    decompression alone can be used to treat selected patients with stable spondylolisthesis, but further instability may result and require additional surgical treatment.
    Decompression With Noninstrumented Fusion
    Because of the risk of worsening instability and vertebral body translation following decompression of a
    lumbar spondylolisthesis, a fusion has been advocated
    in conjunction with the decompressive procedure. Noninstrumented posterolateral lumbar fusion was among
    the first types of lumbar fusions advocated for this use.
    Several studies evaluated the success of noninstrumented fusion in patients with degenerative lumbar
    spondylolisthesis.46-48 In one study, 33% of the patients
    with degenerative spondylolisthesis had good or excellent results following laminectomy with total facetectomy, and 80% of the patients achieved good or excellent results following laminectomy with preservation of
    the facet joints.46 When a noninstrumented posterolateral fusion was added, the rate of good and excellent
    results increased to 90%, suggesting that the added stability provided by the fusion may improve results in
    this patient population.
    In a prospective, randomized study evaluating 50
    consecutive patients with degenerative lumbar spondylolisthesis,47 the patients were treated with either decompression alone or decompression with posterolateral fusion. The fusion group had significantly
    improved outcomes compared with the nonfusion
    group. These results were confirmed by other authors.48
    Decompression With Instrumented Fusion
    With the widespread acceptance of lumbar pedicle
    screws, instrumented lumbar fusions have become both

    2011 American Academy of Orthopaedic Surgeons

    Chapter 50: Lumbar Spondylolisthesis

    technically feasible and commonplace. The success


    rates of instrumented posterolateral lumbar fusions in
    association with decompression for degenerative spondylolisthesis have been evaluated. In a study comparing
    the results of decompression with instrumented fusion
    versus decompression with noninstrumented fusion for
    degenerative spondylolisthesis, the addition of instrumentation lead to a higher fusion rate (82% versus
    45%, P = 0.0015), but the clinical difference between
    patients treated with instrumented and noninstrumented fusion was not statistically significant at 2-year
    follow-up (P = 0.435).49 In a longer term study of this
    same patient group (evaluated at least 5 years postoperatively), the achievement of solid fusion resulted in
    better clinical outcomes than in instances when solid
    fusion was not accomplished.50 The authors suggested
    that because the addition of instrumentation led to
    higher fusion rates, which resulted in improved longterm clinical outcomes, instrumented fusion should be
    considered in the surgical treatment of lumbar degenerative spondylolisthesis.
    The most comprehensive prospective study evaluating the surgical treatments of degenerative spondylolisthesis was an arm of the Spine Patient Outcome Research Trial.43 At 4-year follow-up in randomized and
    observational cohorts, patients with degenerative spondylolisthesis who were treated surgically had greater
    pain relief and improvement in function throughout
    that time frame when compared with patients treated
    nonsurgically. Because various surgical treatments were
    used in the study, conclusions regarding the optimal
    surgical approach require further data analysis.

    Congenital and Dysplastic Spondylolisthesis

    Traumatic Spondylolisthesis
    Traumatic spondylolisthesis injuries are high-energy,
    unstable injuries that are frequently accompanied by
    other multisystem trauma. The initial treatment of
    these patients includes stabilization of the associated
    traumatic injuries and appropriate evaluation and diagnosis of the spondylolisthesis. Clinical and radiographic
    workups for possible bony or soft-tissue pelvic injuries
    and other noncontiguous spinal injuries should be included in the workup.
    The treatment of the traumatic spondylolisthesis requires stabilization of the subluxation or dislocation,
    usually with an instrumented fusion. Instrumentation
    to the pelvis or proximal to the involved motion segment may be needed to provide appropriate fixation.
    Pelvic fixation may be required if there is an associated

    2011 American Academy of Orthopaedic Surgeons

    Annotated References
    1.

    Roche MB, Rowe GG: The incidence of separate neural


    arch and coincident bone variations: A survey of 4,200
    skeletons. Anat Rec 1951;109(2):233-252.

    2.

    Simper LB: Spondylolysis in Eskimo skeletons. Acta Orthop Scand 1986;57(1):78-80.

    3.

    Sonne-Holm S, Jacobsen S, Rovsing HC, Monrad H,


    Gebuhr P: Lumbar spondylolysis: A life long dynamic
    condition? A cross sectional survey of 4,151 adults. Eur
    Spine J 2007;16(6):821-828.
    A survey of 4,151 individuals was used to identify the
    distribution and risk factors for lumbar spondylolysis.
    Men were significantly more at risk for L5 spondylolysis. In women, increased lumbar lordosis had a significant association with L5 spondylolysis. Increased pelvic
    inclination was associated with L5 spondylolysis in both
    men and women.

    4.

    Belfi LM, Ortiz AO, Katz DS: Computed tomography


    evaluation of spondylolysis and spondylolisthesis in
    asymptomatic patients. Spine (Phila Pa 1976) 2006;
    31(24):E907-E910.

    5.

    Sanderson PL, Fraser RD: The influence of pregnancy


    on the development of degenerative spondylolisthesis.
    J Bone Joint Surg Br 1996;78(6):951-954.

    6.

    Newman PH: Stenosis of the lumbar spine in spondylolisthesis. Clin Orthop Relat Res 1976;115(115):
    116-121.

    7.

    Boxall D, Bradford DS, Winter RB, Moe JH: Management of severe spondylolisthesis in children and adolescents. J Bone Joint Surg Am 1979;61(4):479-495.

    8.

    Vialle R, Wolff S, Pauthier F, et al: Traumatic lumbosacral dislocation: Four cases and review of literature.
    Clin Orthop Relat Res 2004;419(419):91-97.

    9.

    Jackson DW, Wiltse LL, Cirincoine RJ: Spondylolysis in


    the female gymnast. Clin Orthop Relat Res 1976;
    117(117):68-73.

    10.

    Seitsalo S, Antila H, Karrinaho T, et al: Spondylolysis in


    ballet dancers. J Dance Med Sci 1997;1:51-54.

    11.

    Soler T, Caldern C: The prevalence of spondylolysis in


    the Spanish elite athlete. Am J Sports Med 2000;28(1):
    57-62.

    12.

    Teitz CC: Sports medicine concerns in dance and gymnastics. Pediatr Clin North Am 1982;29(6):1399-1421.

    Orthopaedic Knowledge Update 10

    5: Spine

    Patients with congenital or dysplastic spondylolisthesis


    often become symptomatic in early adolescence as the
    slippage increases. Back pain, hamstring tightness, and
    spinal canal stenosis are caused by the intact posterior
    elements. After these symptoms develop, conservative
    treatment is rarely useful. Surgical treatment consists of
    stabilizing the motion segment with neural decompression if necessary. Various techniques have been used,
    but no high-quality studies comparing these techniques
    have been performed.

    pelvic fracture or ligamentous injury. Significant neurologic injury can occur because of the rapid neurologic
    compression that occurs with these injuries, and decompression of compressed nerve roots or the central
    canal may be required.

    657

    Section 5: Spine

    13.

    Sakai T, Yamada H, Nakamura T, et al: Lumbar spinal


    disorders in patients with athetoid cerebral palsy: A
    clinical and biomechanical study. Spine (Phila Pa 1976)
    2006;31(3):E66-E70.

    22.

    Osterman K, Lindholm TS, Laurent LE: Late results of


    removal of the loose posterior element (Gills operation)
    in the treatment of lytic lumbar spondylolisthesis. Clin
    Orthop Relat Res 1976;117(117):121-128.

    14.

    Rowe GG, Roche MB: The etiology of separate neural


    arch. J Bone Joint Surg Am 1953;35(1):102-110.

    23.

    15.

    Rosenberg NJ, Bargar WL, Friedman B: The incidence


    of spondylolysis and spondylolisthesis in nonambulatory patients. Spine (Phila Pa 1976) 1981;6(1):35-38.

    Sairyo K, Goel VK, Masuda A, et al: Biomechanical rationale of endoscopic decompression for lumbar spondylolysis as an effective minimally invasive procedure: A
    study based on the finite element analysis. Minim Invasive Neurosurg 2005;48(2):119-122.

    24.

    Sairyo K, Katoh S, Sakamaki T, Komatsubara S, Yasui


    N: A new endoscopic technique to decompress lumbar
    nerve roots affected by spondylolysis: Technical note.
    J Neurosurg 2003;98(3, suppl):290-293.

    25.

    Mller H, Hedlund R: Instrumented and noninstrumented posterolateral fusion in adult spondylolisthesis:


    A prospective randomized study. Part 2. Spine (Phila Pa
    1976) 2000;25(13):1716-1721.

    26.

    Girardo M, Bettini N, Dema E, Cervellati S: Uninstrumented posterolateral spinal arthrodesis: Is it the gold
    standard technique for I degrees and II degrees grade
    spondylolisthesis in adolescence? Eur Spine J 2009;
    18(Suppl 1):126-132.
    A retrospective review of the outcome of uninstrumented posterolateral spinal arthrodesis in adolescents
    with low-grade isthmic spondylolisthesis is presented.
    Good outcomes were reported, with 87.7% of patients
    attaining solid fusion. Pseudarthrosis was reported in
    12.3% of patients. The satisfactory results obtained in
    94% of patients were closely associated with the rate of
    successful fusion.

    27.

    Kwon BK, Hilibrand AS, Malloy K, et al: A critical


    analysis of the literature regarding surgical approach
    and outcome for adult low-grade isthmic spondylolisthesis. J Spinal Disord Tech 2005;18(suppl):S30-S40.

    28.

    Swan J, Hurwitz E, Malek F, et al: Surgical treatment


    for unstable low-grade isthmic spondylolisthesis in
    adults: A prospective controlled study of posterior instrumented fusion compared with combined anteriorposterior fusion. Spine J 2006;6(6):606-614.

    29.

    Ekman P, Mller H, Tullberg T, Neumann P, Hedlund


    R: Posterior lumbar interbody fusion versus posterolateral fusion in adult isthmic spondylolisthesis. Spine
    (Phila Pa 1976) 2007;32(20):2178-2183.
    The authors report on a prospective study to compare
    the outcome of posterior lumber interbody fusion and
    posterolateral fusion in patients with adult isthmic
    spondylolisthesis. The type of fusion did not affect the
    2-year outcomes. Despite the theoretic advantages of
    posterior lumber interbody fusion, no improvements in
    patient outcomes over posterolateral fusion were demonstrated.

    30.

    Ekman P, Mller H, Hedlund R: Predictive factors for


    the outcome of fusion in adult isthmic spondylolisthesis.
    Spine (Phila Pa 1976) 2009;34(11):1204-1210.
    The authors conducted a prospective study to determine
    predictive factors in the outcomes of 164 adult patients

    16.

    Morita T, Ikata T, Katoh S, Miyake R: Lumbar spondylolysis in children and adolescents. J Bone Joint Surg
    Br 1995;77(4):620-625.

    17.

    Fujii K, Katoh S, Sairyo K, Ikata T, Yasui N: Union of


    defects in the pars interarticularis of the lumbar spine in
    children and adolescents: The radiological outcome after conservative treatment. J Bone Joint Surg Br 2004;
    86(2):225-231.

    18.

    5: Spine

    19.

    20.

    21.

    658

    Sairyo K, Sakai T, Yasui N: Conservative treatment of


    lumbar spondylolysis in childhood and adolescence: The
    radiological signs which predict healing. J Bone Joint
    Surg Br 2009;91(2):206-209.
    The stage of the spondylolysis defect on CT and the
    presence or absence of high-signal change in the adjacent pedicle on T2-weighted MRI were evaluated to determine their relationship to bony healing in nonsurgically treated children. The authors reported that 87% of
    the early defects healed, 32% of progressive defects
    healed, and no terminal defects healed. In the defects
    with positive high-signal change, 77% healed after conservative treatment.
    Beutler WJ, Fredrickson BE, Murtland A, Sweeney CA,
    Grant WD, Baker D: The natural history of spondylolysis and spondylolisthesis: 45-year follow-up evaluation. Spine (Phila Pa 1976) 2003;28(10):1027-1035,
    discussion 1035.
    Bhatia NN, Chow G, Timon SJ, Watts HG: Diagnostic
    modalities for the evaluation of pediatric back pain: A
    prospective study. J Pediatr Orthop 2008;28(2):230233.
    A prospective study was performed to examine the diagnosis rate in pediatric patients with back pain. Of 73 patients presenting with back pain, no diagnosis was made
    in 57 patients (78.1%). These results suggest that pediatric back pain frequently does not carry a definitive diagnosis.
    Klein G, Mehlman CT, McCarty M: Nonoperative
    treatment of spondylolysis and grade I spondylolisthesis
    in children and young adults: A meta-analysis of observational studies. J Pediatr Orthop 2009;29(2):146-156.
    Meta-analysis suggested that 83.9% of patients with
    spondylolysis and grade I spondylolisthesis who were
    treated nonsurgically had a successful clinical outcome
    after at least 1 year. Bracing did not seem to influence
    outcomes. In contrast to the high rate of success with
    clinical parameters, most defects did not heal with nonsurgical treatment.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 50: Lumbar Spondylolisthesis

    dylolisthesis was evaluated. The slip was anatomically


    reduced by 100% in five patients and between 90% and
    95% in seven patients. Minimal loss of correction (5%)
    was observed in two patients. No neurologic complications were reported.

    with isthmic spondylolisthesis who were surgically


    treated with fusion. The results showed that patients
    working prior to surgery had more favorable outcomes.
    Male gender and participation in regular exercise also
    were indicators of a better outcome after fusion.
    31.

    Jacobs WC, Vreeling A, De Kleuver M: Fusion for lowgrade adult isthmic spondylolisthesis: A systematic review of the literature. Eur Spine J 2006;15(4):391-402.

    32.

    Transfeldt EE, Mehbod AA: Evidence-based medicine


    analysis of isthmic spondylolisthesis treatment including
    reduction versus fusion in situ for high-grade slips.
    Spine (Phila Pa 1976) 2007;32(19, suppl):S126-S129.
    The authors reviewed the available literature in an attempt to formulate evidence-based recommendations for
    the surgical treatment of high-grade spondylolisthesis in
    the pediatric population. Pseudarthrosis rates were decreased by performing an instrumented reduction with a
    fusion; however, there was no significant difference in
    clinical outcomes in patients treated with fusion in situ
    and reduction and fusion.

    33.

    Sasso RC, Shively KD, Reilly TM: Transvertebral Transsacral strut grafting for high-grade isthmic spondylolisthesis L5-S1 with fibular allograft. J Spinal Disord Tech
    2008;21(5):328-333.
    A retrospective study was conducted to evaluate the
    clinical and radiographic outcomes of 25 patients with
    high-grade isthmic spondylolisthesis treated with decompression and transvertebral, transsacral, strut grafting with a fibular allograft. Although there was no reduction in translational deformity, this technique
    offered excellent fusion results and good clinical outcomes, and it prevented the progression of sagittal
    translation and lumbosacral kyphosis.
    Smith MD, Bohlman HH: Spondylolisthesis treated by a
    single-stage operation combining decompression with in
    situ posterolateral and anterior fusion: An analysis of
    eleven patients who had long-term follow-up. J Bone
    Joint Surg Am 1990;72(3):415-421.

    35.

    Minamide A, Akamaru T, Yoon ST, Tamaki T, Rhee


    JM, Hutton WC: Transdiscal L5-S1 screws for the fixation of isthmic spondylolisthesis: A biomechanical evaluation. J Spinal Disord Tech 2003;16(2):144-149.

    36.

    Gaines RW: L5 vertebrectomy for the surgical treatment


    of spondyloptosis: Thirty cases in 25 years. Spine (Phila
    Pa 1976) 2005;30(6, suppl):S66-S70.

    37.

    Hu SS, Bradford DS, Transfeldt EE, Cohen M: Reduction of high-grade spondylolisthesis using Edwards instrumentation. Spine (Phila Pa 1976) 1996;21(3):367371.

    38.

    Floman Y, Millgram MA, Ashkenazi E, Smorgick Y,


    Rand N: Instrumented slip reduction and fusion for
    painful unstable isthmic spondylolisthesis in adults.
    J Spinal Disord Tech 2008;21(7):477-483.
    The safety and clinical outcomes of surgically instrumented slip reduction in 12 adults with isthmic spon-

    2011 American Academy of Orthopaedic Surgeons

    Goyal N, Wimberley DW, Hyatt A, et al: Radiographic


    and clinical outcomes after instrumented reduction and
    transforaminal lumbar interbody fusion of mid and
    high-grade isthmic spondylolisthesis. J Spinal Disord
    Tech 2009;22(5):321-327.
    The authors report on a retrospective cohort study of
    instrumented reduction and transforaminal lumbar interbody fusion in mid- and high-grade cases of adult
    isthmic spondylolisthesis. The average anterolisthesis
    was 51.0% preoperatively, 13.2% in the immediate
    postoperative period, and 17.0% at final follow-up.

    40.

    Doita M, Uno K, Maeno K, et al: Two-stage decompression, reduction, and interbody fusion for lumbosacral
    spondyloptosis through a posterior approach using
    Ilizarov external fixation. J Neurosurg Spine 2008;8(2):
    186-192.
    A 33-year-old woman with spondyloptosis was treated
    with a two-stage surgical procedure involving decompression, reduction, and posterior fusion using an
    Ilizarov external fixator and transpedicular fixation system. The spondylolisthesis was partially reduced without neurologic alterations and without complications.

    41.

    Helenius I, Lamberg T, Osterman K, et al: Posterolateral, anterior, or circumferential fusion in situ for highgrade spondylolisthesis in young patients: A long-term
    evaluation using the Scoliosis Research Society questionnaire. Spine (Phila Pa 1976) 2006;31(2):190-196.

    42.

    Anderson PA, Tribus CB, Kitchel SH: Treatment of neurogenic claudication by interspinous decompression:
    Application of the X STOP device in patients with lumbar degenerative spondylolisthesis. J Neurosurg Spine
    2006;4(6):463-471.

    43.

    Weinstein JN, Lurie JD, Tosteson TD, et al: Surgical versus nonsurgical treatment for lumbar degenerative spondylolisthesis. N Engl J Med 2007;356(22):2257-2270.
    In a comparison of surgical and nonsurgical treatment
    for lumbar degenerative spondylolisthesis, patients with
    degenerative spondylolisthesis and spinal stenosis who
    were treated surgically had substantially greater improvement in pain relief and function over a 2-year period than patients treated nonsurgically.

    44.

    Fitzgerald JA, Newman PH: Degenerative spondylolisthesis. J Bone Joint Surg Br 1976;58(2):184-192.

    45.

    Epstein NE: Decompression in the surgical management


    of degenerative spondylolisthesis: Advantages of a conservative approach in 290 patients. J Spinal Disord
    1998;11(2):116-122.

    46.

    Lombardi JS, Wiltse LL, Reynolds J, Widell EH, Spencer C III: Treatment of degenerative spondylolisthesis.
    Spine (Phila Pa 1976) 1985;10(9):821-827.

    Orthopaedic Knowledge Update 10

    5: Spine

    34.

    39.

    659

    Section 5: Spine

    Herkowitz HN, Kurz LT: Degenerative lumbar spondylolisthesis with spinal stenosis: A prospective study
    comparing decompression with decompression and intertransverse process arthrodesis. J Bone Joint Surg Am
    1991;73(6):802-808.

    48.

    Ghogawala Z, Benzel EC, Amin-Hanjani S, et al: Prospective outcomes evaluation after decompression with
    or without instrumented fusion for lumbar stenosis and
    degenerative Grade I spondylolisthesis. J Neurosurg
    Spine 2004;1(3):267-272.

    49.

    Fischgrund JS, Mackay M, Herkowitz HN, Brower R,


    Montgomery DM, Kurz LT: Degenerative lumbar spondylolisthesis with spinal stenosis: A prospective, randomized study comparing decompressive laminectomy
    and arthrodesis with and without spinal instrumentation. Spine (Phila Pa 1976) 1997;22(24):2807-2812.

    50.

    Kornblum MB, Fischgrund JS, Herkowitz HN, Abraham DA, Berkower DL, Ditkoff JS: Degenerative lumbar spondylolisthesis with spinal stenosis: A prospective
    long-term study comparing fusion and pseudarthrosis.
    Spine (Phila Pa 1976) 2004;29(7):726-733, discussion
    733-734.

    5: Spine

    47.

    660

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 51

    Thoracic Disk Herniation


    Mark B. Dekutoski, MD

    Incidence
    Thoracic disk herniation detected by MRI is present in
    20% to 40% of asymptomatic control subjects.1,2 Thoracic diskectomy for clinically symptomatic patients accounts for less than 1% of all diskectomies performed
    in North America.3,4

    Classification

    Etiology
    The thoracic spine includes mobile areas of transition
    at the junctions and areas of relative stiffness in flexion

    Dr. Dekutoski or an immediate family member serves as a


    board member, owner, officer, or committee member of
    AOSpine North America and AOSpine North America Education Committee; has received royalties from Medtronic Sofamor Danek; is a member of a speakers bureau or
    has made paid presentations on behalf of Medtronic Sofamor Danek; serves as a paid consultant to Medtronic
    Sofamor Danek; has received research or institutional
    support from Mayo Clinic Practice and Mayo Clinic Foundation; and has received nonincome support (such as
    equipment or services), commercially derived honoraria,
    or other nonresearch-related funding (such as paid travel) from Medtronic Sofamor Danek.

    2011 American Academy of Orthopaedic Surgeons

    Clinical Presentation
    Patients present with a spectrum of symptoms that can
    vary from thoracic pain, which is typically aggravated
    by rotation, to radicular complaints, to presentation of
    long track signs as evidence of myelopathy. Onset typically occurs during the fourth through sixth decades of
    life. Symptoms commonly occur in the cervical thoracic
    junction, usually marked by interscapular pain.
    Midthoracic pathology can cause pain with radicular
    or myelopathic features, and lower thoracic disk herniations can cause groin pain or even lower root symptoms because the thoracic disk can have a mass effect
    on the concomitant anatomic motor cells of the ventral
    cord. This condition manifests as a lower motor neuropathy. The typical motor neuron presentation may
    include bladder dysfunction and gait disturbance. The
    slow, insidious onset can make diagnosis more difficult.
    Delayed diagnosis is common because of the nonspecific nature of the symptoms. The differential diagnosis
    should include rare neurologic conditions that present
    with imbalance and/or central radicular features, including amyotrophic lateral sclerosis, multiple sclerosis,
    transverse myelitis, and more common syndromes such
    as those seen with shingles/herpes zoster, rib fractures,
    cholecystitis, kidney stones, pleuritic syndromes, and
    scapulothoracic bursal syndromes.

    Orthopaedic Knowledge Update 10

    5: Spine

    Disk herniations of the thoracic spine are classified


    based on their segmental level, canal location, size, imaging characteristics, and clinical presentation. Symptomatic thoracic disks tend to occur with greater prevalence in the junctional segments than in the rigid
    segments and are often classified as cervical and/or upper lumbar disk herniations. Central and large disks
    (greater than 40% of canal diameter) are associated
    with a greater incidence of myelopathy and worse functional outcomes.5 Calcific changes to the disk and dural
    interface noted on CT can predict a greater likelihood
    of cerebrospinal fluid complications with intervention.
    Classification based on clinical presentation is common
    and follows the spectrum of asymptomatic axial pain
    syndromes provoked by rotation to radicular syndromes and/or myelopathy.

    secondary to the ribs. Costovertebral articulations,


    however, allow the coupled motions of lateral bending
    and rotation. Annular disruption, disk and plate fissuring, and the cascade of disk repair and degeneration are
    associated with repetitive rotation. Although trauma
    has been documented to cause defects in the end plate
    (Schmorl nodes), disk herniation is generally associated
    with the apoptotic changes that occur with aging and
    stiffening of the spine. Thoracic disk herniation also occurs with the spectrum of conditions marked by diskopathy of the thoracic disks and is hallmarked by the
    condition of diffuse idiopathic skeletal hyperostosis and
    the enthesopathic condition of ankylosing spondylitis.
    Intradiskal calcification and calcification of the extruded thoracic disk occur more commonly in the thoracic spine.

    661

    Section 5: Spine

    Physical Examination
    The physical examination should evaluate for thoracic
    tenderness and pain with rotation. A detailed neurologic examination should assess the sensory dermatome
    level, long track signs, evidence of spasticity or hyperreflexia, gait disturbance, and sphincter tone. Clinical
    findings can present as radicular symptoms, incomplete
    cord syndrome, and/or more unilateral cord symptoms.

    Imaging
    MRI should follow the clinical history and the development of a differential diagnosis. Decisions regarding
    imaging require clinical validation because populationbased control studies have demonstrated image findings
    consistent with thoracic disk herniation in 37% of
    asymptomatic individuals.1,2 The differential diagnoses
    should include retroperitoneal neoplasm and other
    intra-abdominal and/or intrathoracic pathology. Syndromes that create intrinsic cord pathology, such as arteriovenous malformation, and demyelinating conditions such as amyotrophic lateral sclerosis, transverse
    myelitis, and cord tumors also should be considered.
    Concomitant CT is of value in assessing the calcific
    character of the disk and dural interface.

    Natural History

    5: Spine

    The natural history of thoracic disk injury has been


    studied in small case series.3,5-10 Most patients with intermittent mechanical and/or radicular pain have a period of inflammatory symptoms marked by back
    and/or chest wall pain that gradually subsides over 6 to
    18 months. This condition is typically commensurate
    with a reduction in rotational activities that aggravate
    symptoms such as shoveling, golf, or hitting a slap shot
    in hockey. Imaging studies of patients with symptomatic thoracic disk herniations have revealed associated symptom reduction with a reduction in the extruded disk volume on follow-up MRI studies.
    Nonsurgical treatments include analgesic support,
    core stabilization, and radicular anesthetic blocks. Immobilization with corsets and/or braces can be considered. There are few quality data to support these treatment methods.
    Surgical intervention is stratified by neurologic status. In patients with myelopathy and/or progression of
    neurologic deficit, cord decompression affords the potential to stabilize or improve symptoms. For patients
    with radicular symptoms, persistent, unremitting pain,
    and disability that is refractory to pain management
    and therapeutic injections, surgical decompression may
    be of significant benefit. Patients who are not neurologically compromised and have pain that interferes substantially with their quality of life after an active period
    (longer than 6 months) of nonsurgical management
    may be considered to have a limited indication for sur662

    Orthopaedic Knowledge Update 10

    gery. The patient with axial pain syndromes must be


    well informed about the significant surgical and neurologic risks and the limited functional benefit described
    in several large clinical series.
    MRI should be part of the preoperative evaluation
    and surgical planning, and can be supplemented with
    CT to assess calcification. The presence of calcification
    can predict the surgical finding of significant resorption
    and adherence of the dura to the disk and the potential
    need for dural reconstruction at the time of resection.
    Because disk herniations tend to be more chronic and
    more adherent to the dura, dural repair is commonly
    needed and should be planned for when calcification
    is present.

    Surgical Approach
    Thoracic disk herniations are more commonly located
    anteromedial rather than lateral to the dural contents.
    Traditional posterior laminectomy often requires medial retraction and manipulation of the cord, which can
    provoke neurologic defects. A spectrum of approaches
    and techniques, globally described as anterolateral or
    posterolateral techniques, have been used to effect decompression of the thoracic spinal cord (Figure 1). All
    approaches other than laminotomy destabilize the
    facet, costotransverse joint, and posterolateral disk
    complex. Several recent case series have highlighted
    and illustrated these techniques.11,12
    Anterior or anterolateral techniques comprise transthoracic and/or a variance of transpleural and retropleural techniques that involve resection of the rib
    head and a lateral approach to the vertebral body and
    foramen. During these procedures, the posterior portion of the disk and/or body is excised to access the
    midline and ventral disk herniation. Fusion is commonly necessary to avoid iatrogenic instability, further
    disk collapse, further segmental instability symptoms,
    and progression of the local inflammatory cascade
    and/or neural compression. Video-assisted thoracic
    techniques in noncalcified and smaller-volume compressive lesions have equivalent outcomes to thoracotomy when performed by experienced surgeons.
    Posterolateral procedures are variants of a costotransversectomy and transpedicular and oblique approaches
    to the anterolateral dura that limit cord retraction. These
    posterolateral techniques involve resection of the lateral
    lamina, facet, pedicle, and costovertebral joint to create
    an oblique window to access the anterolateral and lateral aspects of the spinal canal. These approaches have
    a more limited window, require significant bony resection, and are also associated with significant postlaminectomy and postfacetectomy instability unless they are
    combined with a posterolateral fusion.
    Most authors vary their approach based on the disk
    level and characteristics. For calcified disks, large disks,
    and those with a more midline location, an anterolateral approach provides the greatest access for dural repair with the least amount of neural retraction. Compressive lesions located in upper thoracic levels may

    2011 American Academy of Orthopaedic Surgeons

    Chapter 51: Thoracic Disk Herniation

    Figure 1

    Different surgical approaches for addressing thoracic disk pathology: transpedicular (A), lateral extracavitary (B),
    costotransversectomy (C), and transthoracic (D). (Reproduced with permission from Cybulski G: Thoracic disc herniation: Surgical technique. Contemp Neurosurg 1992;14:1-6.)

    Annotated References
    1.

    Wood KB, Garvey TA, Gundry C, Heithoff KB: Magnetic resonance imaging of the thoracic spine: Evalua-

    2011 American Academy of Orthopaedic Surgeons

    tion of asymptomatic individuals. J Bone Joint Surg Am


    1995;77(11):1631-1638.
    2.

    Wood KB, Blair JM, Aepple DM, et al: The natural history of asymptomatic thoracic disc herniations. Spine
    (Phila Pa 1976) 1997;22(5):525-529, discussion 529530.

    3.

    Brown CW, Deffer PA Jr, Akmakjian J, Donaldson DH,


    Brugman JL: The natural history of thoracic disc
    herniation. Spine (Phila Pa 1976) 1992;17(6, suppl):
    S97-S102.

    4.

    Regan JJ: Percutaneous endoscopic thoracic discectomy.


    Neurosurg Clin N Am 1996;7(1):87-98.

    5.

    Hott JS, Feiz-Erfan I, Kenny K, Dickman CA: Surgical


    management of giant herniated thoracic discs: Analysis
    of 20 cases. J Neurosurg Spine 2005;3(3):191-197.

    6.

    Bozzao A, Gallucci M, Masciocchi C, Aprile I, Barile A,


    Passariello R: Lumbar disk herniation: MR imaging assessment of natural history in patients treated without
    surgery. Radiology 1992;185(1):135-141.

    7.

    Delauche-Cavallier MC, Budet C, Laredo JD, et al:


    Lumbar disc herniation: Computed tomography scan
    changes after conservative treatment of nerve root compression. Spine (Phila Pa 1976) 1992;17(8):927-933.

    8.

    Ellenberg MR, Ross ML, Honet JC, Schwartz M,


    Chodoroff G, Enochs S: Prospective evaluation of the
    course of disc herniations in patients with proven radiculopathy. Arch Phys Med Rehabil 1993;74(1):3-8.

    Orthopaedic Knowledge Update 10

    5: Spine

    require sternotomy and/or use of the venacaval window


    to access the levels. Most posterolateral disks and upper thoraciclevel disks (T3 through T5) are readily accessed via posterolateral approaches. Midthoracic and
    posterolateral disks are accessible via either approach.
    Communication of the relative risks, approach-related
    complications, outcomes, and surgeon experience are
    part of the surgical choice of an informed patient.
    One of the greatest risks in performing a thoracic
    disk herniation is wrong-level surgery. It is important to
    have a direct comparison of the axial imaging and the
    intraoperative radiographic technique by counting ribs.
    The ability to accurately identify a level for thoracic
    disk herniation also can be supplemented by placing a
    percutaneous fiducial into the pedicle or posterior elements and confirming this in the preoperative setting
    with CT and fluoroscopic imaging.13
    Outcomes for procedures for thoracic disk herniations have been limited to several small series.14-16 There
    is no evidence other than case series to guide therapy,
    and the limited volume of these cases precludes randomization. In larger series from referral centers, large
    disk size, midline location, and the presence of a calcific disk-dural interface were associated with more
    complications and worse functional outcomes.

    663

    Section 5: Spine

    9.

    Maigne J-Y, Rime B, Deligne B: Computed tomographic


    follow-up study of forty-eight cases of nonoperatively
    treated lumbar intervertebral disc herniation. Spine
    (Phila Pa 1976) 1992;17(9):1071-1074.

    10.

    Saal JA, Saal JS, Herzog RJ: The natural history of lumbar intervertebral disc extrusions treated nonoperatively. Spine (Phila Pa 1976) 1990;15(7):683-686.

    11.

    Ayhan S, Nelson C, Gok B, et al: Transthoracic surgical


    treatment for centrally located thoracic disc herniations
    presenting with myelopathy: A 5-year institutional experience. J Spinal Disord Tech 2010;23(2):79-88.
    A well-illustrated, select case series is presented by a
    highly experienced, reputable, referral spine practice.
    Level of evidence: IV.
    Bransford R: Early experience treating thoracic disc herniations using a modified transfacet pedicle-sparing decompression and fusion. J Neurosurg Spine 2010;12(2):
    221-231.
    A well-illustrated and described surgical technique in a
    small case series is presented by an experienced, selfcritical, referral spine practice. Level of evidence: IV.

    Hsu W, Sciubba DM, Sasson AD, et al: Intraoperative


    localization of thoracic spine level with preoperative
    percutaneous placement of intravertebral polymethylmethacrylate. J Spinal Disord Tech 2008;21(1):72-75.
    This article is an important technical reference to help
    with level localization and avoid wrong-level surgery.
    Level of evidence: IV.

    14.

    Ohnishi K, Miyamoto K, Kanamori Y, Kodama H, Hosoe H, Shimizu K: Anterior decompression and fusion
    for multiple thoracic disc herniation. J Bone Joint Surg
    Br 2005;87(3):356-360.

    15.

    Sheikh H, Samartzis D, Perez-Cruet MJ: Techniques for


    the operative management of thoracic disc herniation:
    Minimally invasive thoracic microdiscectomy. Orthop
    Clin North Am 2007;38(3):351-361, abstract vi.
    A technique paper with case illustration is presented.
    Level of evidence: IV.

    16.

    Bartels RH, Peul WC: Mini-thoracotomy or thoracoscopic treatment for medially located thoracic herniated
    disc? Spine (Phila Pa 1976) 2007;32(20):E581-E584.
    A small case series with technical notes is presented.
    Level of evidence: IV.

    5: Spine

    12.

    13.

    664

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 52

    New Technologies in Spine Surgery


    Lauren M. Burke, MD, MPH
    Warren D. Yu, MD

    Joseph R. OBrien, MD, MPH

    Introduction
    New technologies in spine surgery are rapidly evolving,
    with the current focus on motion conservation and
    nonfusion options. Development of these technologies
    aims at reducing arthodesis-related morbidities, such as
    bone graft donor site pain, pseudarthrosis, approachrelated morbidity, and adjacent-level degeneration. Cervical disk replacement shows promise with new data
    becoming available, yet the role for lumbar disk replacement is yet to be fully defined. Prospective controlled studies are currently under way for dynamic stabilization and facet replacement. Conclusions about
    efficacy and safety should be withheld until these data
    are available. Early results of interspinous spacers are
    promising as a minimally invasive alternative to decompression and fusion, and indications may continue to
    expand. More recently, novel tissue engineering strategies are being explored as potential treatment of degenerative disk disease.

    Cervical disk arthroplasty (CDA) has the potential to be


    superior to anterior diskectomy and fusion (ACDF). As
    the gold standard, ACDF has remarkable success, with

    Dr. OBrien or an immediate family member serves as a


    board member, owner, officer, or committee member of
    Doctors Research Group; is a member of a speakers bureau or has made paid presentations on behalf of
    Stryker and DePuy, a Johnson & Johnson Company;
    serves as a paid consultant to DePuy, a Johnson & Johnson Company, and Stryker; has received research or institutional support from DePuy, a Johnson & Johnson Company and Stryker; and has stock or stock options in
    Doctors Research Group. Dr. Yu or an immediate family
    member serves as a paid consultant to Medtronic, Zimmer, Seaspine, and SpineFrontier and has received research or institutional support from Johnson & Johnson
    and Stryker. Neither of the following authors or any immediate family member has received anything of value
    from or owns stock in a commercial company or institution related directly or indirectly to the subject of this
    chapter: Dr. Burke and Dr. Benke.

    2011 American Academy of Orthopaedic Surgeons

    excellent long-term results reported above the 90th percentile. Fusion rates follow the same trend. The most
    compelling argument for a motion-preserving alternative to fusion is the incidence of symptomatic adjacentlevel disease, believed to be approximately 3% annually. Approximately 25% of these patients may require
    reoperation for symptomatic adjacent-segment degeneration at 10 years. Some authors hypothesize that stiffening the spine through fusion accelerates degeneration
    at the adjacent segments. Disk arthroplasty aims to decrease adjacent-segment degeneration through motion
    preservation.
    CDA is a motion-preserving procedure with limited
    indications, which currently include primarily radiculopathy caused by the compressive effect of a herniated
    cervical disk or osseous foraminal stenosis limited to
    one- and two-level disease (Figure 1). Treatment of myelopathy with CDA is still controversial, but is possible
    if the symptoms are mild and anterior compression is
    present. Although axial neck pain is currently not an
    indication for arthroplasty, it is being studied. Spondylolysis, deformity, instability, and subluxation are
    contraindications.1 Other relative contraindications include osteopenia, osteoporosis, autoimmune disorders
    including rheumatoid arthritis, prior infection, and
    congenital stenosis.
    One limitation of recent literature on CDA is the
    lack of long-term results. This is a fairly new procedure, still undergoing several Food and Drug Administration (FDA) Investigational Device Exemption (IDE)
    clinical trials; however, the early 2- and 3-year
    follow-up results are promising. The recent literature
    shows better clinical outcomes in the CDA groups compared to those receiving ACDF, although both treatment arms show statistically significant excellent outcomes when compared to preoperative scores. Some
    authors attribute patient enthusiasm for being selected
    for the disk replacement group as an etiology for improved outcomes in the CDA group as compared to the
    ACDF group.
    A group of authors reported their experience with the
    Bryan CDA (Medtronic Sofamor Danek, Memphis, TN)
    at 2-year follow-up in 2003.2 This study included 103
    single-level patients and 44 bilevel patients followed for
    1 to 2 years. Success rates for single-level CDA and bilevel CDA were 90% and 94%, respectively. Another
    study reported 93% success rates at 3-year follow-up in
    2007.1 Yet another study demonstrated success rates in

    Orthopaedic Knowledge Update 10

    5: Spine

    Disk Arthroplasty

    Michael T. Benke, MD

    665

    5: Spine

    Section 5: Spine

    Figure 1

    AP (A) and lateral (B) radiographs of single-level cervical disk arthroplasty.

    single-level and bilevel CDA of 90% and 96%, respectively.3 These success rates are comparable to those of
    ACDF. The literature also supports a complication rate
    equal to or less than that of ACDF.
    Although CDA holds promise, few long-term data
    are available and the long-term durability of these implants remains to be seen. Wear debris may be an issue.
    Like all surgical procedures, patients must be carefully
    chosen for the appropriate procedure.
    Comparison of CDA to lumbar replacement surgery
    is inevitable, but they are two highly different procedures. Lumbar disk arthroplasty has been used for the
    treatment of axial back pain; surgical treatment generally has lower clinical success rates. Axial back pain
    may be treated surgically if a 6- to 12-month course of
    nonsurgical treatment was unsuccessful. Preoperative
    disability should be significant and gauged with standardized outcome measures such as the Oswestry Disability Index (ODI). Most studies on surgery for axial
    back pain define success as improvement (but not elimination) of disability. Most patients will continue postoperative narcotic use, and only 10% on average return
    666

    Orthopaedic Knowledge Update 10

    to work. Additionally, isolation of a pain-generating


    segment is a crucial part of the algorithm for back pain
    surgery. Some authors advocate diskography or MRI
    for this purpose, but others think that facet blocks and
    localizing injections can help determine the pain generator. However the pain generator is identified, it is important to note that outcomes decline for multilevel
    procedures. For axial back pain surgery, one-level surgical outcomes are the best.
    Treatment of discogenic back pain may involve fusion or arthroplasty (Figure 2). Theoretically, lumbar
    arthroplasty should reduce or eliminate pain from a degenerated disk and restore or maintain normal motion
    at the index level, theoretically decreasing adjacentsegment disease. Indications for lumbar disk arthroplasty are similar to those of fusion. Patients should
    have intractable back pain due to discogenic disk disease. Accompanying radicular pain should be less prevalent than back pain. All patients should have at least 6
    months of unsuccessful nonsurgical treatment. Contraindications include previous laminectomy, pars defect, facet disease, deformity, and instability.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 52: New Technologies in Spine Surgery

    Figure 2

    AP (A) and lateral (B) radiographs of single-level lumbar disk arthroplasty. (Courtesy of Khaled Kebaish, MD.)

    2011 American Academy of Orthopaedic Surgeons

    Dynamic Stabilization
    Several pedicle-based dynamic stabilization systems
    have been developed and are in various stages of biomechanical and clinical evaluation. These systems stabilize a spinal segment without rigid arthrodesis to theoretically decrease the incidence of adjacent-level
    degeneration. These implants are pedicle based and
    control motion at the index level. Variation occurs at
    the interpedicular spacer. Graf Artificial Ligament System (SEM Co, Montrouge, France) and Dynesys Dynamic Stabilization System (Zimmer Spine, Minneapolis, MN) (Figure 3) are two with the longest clinical
    experience.
    Potential indications for dynamic stabilization are
    grade I spondylolisthesis, spinal stenosis with instability, recurring disk herniation, and degenerative disk disease with mechanical back pain. All patients undergoing dynamic stabilization should have had an
    unsuccessful course of nonsurgical treatment. Contraindications to this surgery are similar to those of other
    spine surgery with instrumentation, as these implants
    use pedicle screws. Poor bone stock, metabolic bone
    disease, and active infection, as well as scoliosis, severe
    spondylolisthesis, and postlaminectomy destabilization
    are all contraindications.
    The limited data available for dynamic stabilization
    are contradictory and inconclusive. Some report positive clinical outcomes at 10-year follow-up in patients
    with degenerative spondylolisthesis and flexion insta-

    Orthopaedic Knowledge Update 10

    5: Spine

    Variable results have been reported in the literature.


    A 2007 study reported a mean 13.2-year follow-up on
    106 patients treated with lumbar disk arthroplasty,
    with 82% good or excellent outcome at final followup. In addition, 7.5% of patients required additional
    surgery and posterior instrumentation for fusion and of
    those, 2.8% because of adjacent-level disease. Ninety
    percent of implants retained at least 4 of motion at 10
    years.4 More recent reported results are not as promising. A retrospective review compared one-level and
    two-level disk arthroplasty groups.5 There was no statistical significance between the two groups and no
    control group in the study. Overall satisfaction was
    70% at 2 years. An important issue addressed in a prospective study is the difference in results at particular
    levels.6 Most arthroplasty procedures are performed at
    L4-5 or L5-S1 levels, or are bilevel procedures. The reported results showed a decline in overall outcomes
    when the lumbosacral junction is included, as well as
    increased complication rates.6
    Lumbar disk arthroplasty is a relatively new procedure with variable evidence. Choosing the right patient
    for this surgery is most challenging, as the absence of
    improvement in back pain is common after surgery for
    discogenic disk disease. Revisions are exceedingly difficult, with injury to the great vessels sometimes an unforgiving complication. Future studies and long-term
    results are in progress.

    667

    Section 5: Spine

    Figure 4

    The Total Posterior Arthroplasty System (TOPS).


    A, Pedicle screw instrumentation. B, Posterior
    view. C, Anterior view.

    Facet Replacement

    Figure 3

    Model of a posterior Dynamic Stabilization


    System.

    5: Spine

    bility, but results are less favorable in this time period


    in patients with degenerative scoliosis.7 Prospective
    data reports vary on clinical outcomes. Results on
    single-level dynamic stabilization for spondylolisthesis
    suggest that clinical outcomes are favorable and remain
    that way for a minimum 4-year follow-up.8 According
    to one study, 21% of patients had evidence of screw
    loosening or breakage at 2-year follow-up; however, no
    reoperations occurred for this hardware failure.8 A reported 47% of patients in this study showed adjacentsegment degeneration, which was statistically significant. Another prospective study of microdecompression
    and the Dynesys system reported only 50% favorable
    outcome, with 30% of patients reporting persistent
    lumbar pain at 12-month follow-up.9 Reoperation rates
    reached 19% due to hardware complications.9 Current
    data suggest dynamic stabilization may be an acceptable alternative to fusion in selected cases of one- and
    two-level degenerative lumbar pathologies.
    The discussed implants are nonfusion devices. Other
    constructs are being developed that are hybrids, allowing fusion at one level and dynamic stabilization at the
    adjacent segment in hopes of slowing or preventing degeneration at levels adjacent to a fusion. Although
    some early clinical outcomes have been positive, published data remain limited. Further studies are imperative to establish efficacy and potential risks.
    668

    Orthopaedic Knowledge Update 10

    Facet arthroplasty is the newest form of posterior dynamic or nonfusion stabilization. The spinal unit is
    composed of the disk and two facet joints. Each of
    these three joints has the potential for degeneration and
    pain generation. Facet arthroplasty, following standard
    decompression of the neural elements, allows for the
    replacement of the diseased facets with preservation of
    motion as an alternative to traditional spinal fusion.
    Although several designs are in various stages of development, only two have published literature. The first is
    an anatomic reconstruction where each facet joint is replaced with unlinked articulating metal-on-metal components (Total Facet Arthroplasty System [TFAS], Archus Orthopedics, Redmond, WA). The second design
    is a nonanatomic reconstruction of the posterior articulating elements. Both facet joints are replaced with a
    single nonanatomic linked articulating core composed
    of polycarbonate urethane (Total Posterior Arthroplasty System [TOPS], Impliant, Ramat Poleg, Israel)
    (Figure 4).
    Potential indications for facet arthroplasty have focused on spinal stenosis patients with or without grade
    I spondylolisthesis. Facet removal allows for wide decompression whereas facet arthroplasty confers stability
    with motion and precludes the need for fusion. IDE trials are currently under way for both the anatomic design (TFAS) and the nonanatomic design (TOPS). Each
    randomized, controlled, prospective IDE trial is comparing the facet replacement device with instrumented
    fusion. To date, there are no published data from these
    trials.
    Recent biomechanical data are available for each of
    the facet arthroplasty designs. In a cadaver study, three-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 52: New Technologies in Spine Surgery

    Interspinous Spacer Technology


    Neurogenic claudication is a common spinal pathology
    that historically was treated nonsurgically with activity
    modification, nonsteroidal anti-inflammatory medications, and epidural steroid injections. Open surgical decompression is indicated in recalcitrant cases. The common reports of neurogenic claudication are pain with
    ambulation that is exacerbated by standing upright and
    lumbar extension, but symptomatic relief with lumbar
    flexion. The shopping cart sign is commonly seen in
    stenotic patients with neurogenic claudication. These
    patients have improved walking endurance when leaning forward on a shopping cart, which provides relative
    flexion in the lumbar spine, opens the canal, and
    stretches the redundant ligamentum flavum that causes

    2011 American Academy of Orthopaedic Surgeons

    neural compression. Nonsurgical treatment has limited


    effects, and symptoms may deteriorate over time.
    Interspinous spacer technology has been developed
    for treatment of mild to moderate intermittent neurogenic claudication. Implants are placed between the
    spinous processes through a small posterior incision, as
    far anterior as allowed, sacrificing the interspinous ligaments. They produce relative kyphosis at the index
    level without disrupting overall sagittal balance. Biomechanical studies showed an increase in canal area by
    18%, foraminal area by 25%, and foraminal width by
    41% with the X-STOP device (Medtronic, Minneapolis, MN)13 (Figure 5).
    Since 2005, when the FDA approved the first and
    only implant (X-STOP) for neurogenic claudication,
    other devices have been developed, with clinical trials
    under way for many. Based on a multicenter, prospective, randomized IDE trial, early clinical data for the
    X-STOP demonstrate good to excellent results at 2
    years compared to nonsurgical treatment. Outcomes
    were assessed using the Zurich Claudication Questionnaire, ODI and Medical Outcomes Study Short Form36, and all demonstrated statistically significant improvement in the X-STOP group at all time points
    relative to the control group.14 Patient satisfaction in
    the X-STOP group was 73% compared to 36% of control patients. In a smaller prospective study, 24 patients
    showed a 71% satisfaction rate at 1-year follow-up;
    however, 29% of this group required epidural steroid
    injections for recurrence of symptoms.15 A subsequent
    study of intermediate follow-up (average, 4.2 years)
    found that outcomes of X-STOP surgery are stable over
    time as measured by ODI.16
    Implantation of these devices is not without risk.
    Fracture of the spinous processes can occur intraoperatively or postoperatively. Depending on symptoms,
    fracture may necessitate surgical decompression and fusion. One case of bilateral posterior facet stress fractures after insertion of an interspinous implant has
    been reported in the literature.17
    With many of these devices in clinical trials, more
    data will become available on their efficacy and safety.
    Currently long-term data are limited; however, interspinous devices are an attractive option for elderly or
    medically frail patients with neurogenic claudication
    who may not be able to tolerate a more extensive procedure.

    5: Spine

    dimensional kinematics of TFAS-implanted spines were


    compared to those of intact spines and spines with posterior pedicle screw stabilization at the L4-5 level.
    Range of motion of the TFAS was 81% of the intact
    spine in flexion, 68% in extension, 88% in lateral
    bending, and 128% in axial rotation.10 A similar cadaver study was done comparing multidirectional mobility of the TOPS implanted spine to the intact spine at
    the L4-5 level. Range of motion was almost ideally restored in lateral bending and axial rotation, and allowed 85% of the intact range of motion in flexion and
    extension.11
    Authors of a 2007 study reported on 29 patients
    who underwent decompression and implantation of
    TOPS as part of a prospective, multicenter, pilot study
    performed outside the United States.12 All patients had
    spinal stenosis and/or spondylolisthesis at L3-4 or L4-5
    due to facet arthropathy. Visual analog score for leg
    pain improved from 88 to 12, ODI score dropped from
    57% to 16%, and the Zurich Claudication Questionnaire score decreased from 57% to 26% at 1-year
    follow-up. No cases of slip progression and no signs of
    screw loosening were found.
    Other potential indications for facet replacement
    may be for axial low back pain generated from facet arthropathy. This small subset of patients is difficult to
    define. Another possible indication for facet arthroplasty may be in conjunction with lumbar disk arthroplasty. In theory, this technology would replace all three
    degenerated joints of the functional spinal unit. Cost
    and implant failure may limit the combined use of these
    two technologies.
    The goal of facet replacement is to attain posterior
    stabilization without fusion while allowing wide posterior decompression. As in total disk replacement, motion segment wear is inherent to arthroplasty systems in
    general and may be problematic in facet replacements.
    Like posterior dynamic stabilization systems, current
    facet arthroplasty systems are pedicle based and subject
    to hardware loosening and failure. Further research is
    required before the widespread use of facet arthroplasty can be advocated and before conclusions can be
    made on efficacy and safety.

    Disk Regeneration
    A separate, more novel approach to the treatment of
    degenerative disk disease is through the regeneration of
    intervertebral disk tissue via tissue engineering strategies. Degeneration is characterized by the loss of water
    content from the nucleus pulposus, the loss of macromolecules such as aggrecan, the loss of blood supply
    from the capillary beds, and increased enzymatic activity such as that from the matrix metalloproteinase
    (MMP) family. Through the modulation of intervertebral disk biology with the administration of cells or

    Orthopaedic Knowledge Update 10

    669

    5: Spine

    Section 5: Spine

    Figure 5

    AP (A) and lateral (B) radiographs of the X-STOP interspinous spacer in a patient with neurogenic claudication.

    growth factors, many researchers are investigating


    methods to alter the biologic imbalance of catabolism
    and anabolism that leads to loss of disk height, annular
    tears, and disk herniation.
    Gene therapy represents one approach in this research
    arena. In recent studies, cells have been induced to produce factors such as transforming growth factor1; tissue inhibitors of metalloproteinases (TIMPs); and Lin11, Isl-1, Mec-3) mineralization protein (LMP-1).
    Significant in vitro work has been done to modulate the
    expression of these factors to potentially reverse the molecular processes that occur during disk degeneration.
    Both viral and nonviral vectors have been studied in the
    delivery of the transgenes to cells. Although many vectors have exhibited high transfection rates with minimal
    immunogenicity such as adeno-associated virus, significant safety precautions remain in the translation of gene
    therapy to humans. Nonviral delivery methods such as
    DNA liposomes and plasmid DNA accompanied by an
    ultrasonography contrast agent (microbubbles) have
    been studied in hopes of bypassing the safety issues with
    viral transduction.
    670

    Orthopaedic Knowledge Update 10

    Autologous cellbased therapy has shown promise


    because of its avoidance of viral vectors, multipotent
    differentiation, and proliferation potential. Exposing
    mesenchymal stem cells to various media conditions
    can initiate differentiation down different pathways, including that of the chondrogenic lineage, which shows
    similarities to that of intervertebral disk tissue. Researchers have demonstrated that rabbit mesenchymal
    stem cells transplanted into healthy rabbit disks can
    survive for up to 24 weeks,18 suggesting that long-term
    survival is realistic. Studies characterizing the strategies
    of disk regeneration currently are still in the early
    stages as more data are required to progress to clinical
    trials.

    Future Directions
    Interest is growing in the development of minimally invasive surgery, motion-preserving surgical procedures,
    and regenerative technologies. Spine surgery is an
    evolving field with pronounced interest in preventing

    2011 American Academy of Orthopaedic Surgeons

    Chapter 52: New Technologies in Spine Surgery

    This article presents early results for patients enrolled in


    two concurrent FDA IDE lumbar arthroplasty clinical
    trials at a single institution. The authors found no statistical significance between the two groups at 2-year
    follow-up, although the two-level arthroplasty group
    scored marginally lower on evaluations.

    adjacent-segment degeneration and disease as well as


    avoiding revision surgeries. With many new technologies in clinical trials, future data regarding the safety
    and efficacy of these devices and techniques can be anticipated.

    Kanayama M, Hashimoto T, Shigenobu K, Togawa D,


    Oha F: A minimum 10-year follow-up of posterior dynamic stabilization using Graf artificial ligament. Spine
    (Phila Pa 1976) 2007;32(18):1992-1996, discussion
    1997.
    The authors present a retrospective review of 56 patients showing improvement in outcomes for patients
    with degenerative spondylolisthesis and flexion instability. Results for those with laterolisthesis and degenerative scoliosis were poor.

    1.

    Pimenta L, McAfee PC, Cappuccino A, Cunningham


    BW, Diaz R, Coutinho E: Superiority of multilevel cervical arthroplasty outcomes versus single-level outcomes: 229 consecutive PCM prostheses. Spine (Phila
    Pa 1976) 2007;32(12):1337-1344.
    In a prospective series, multilevel cervical arthroplasty
    demonstrated significantly improved clinical outcomes
    in comparison with single-level outcomes, while reoperation rates leveled at 3-year follow-up. Level of evidence: II.

    8.

    Schaeren S, Broger I, Jeanneret B: Minimum four-year


    follow-up of spinal stenosis with degenerative spondylolisthesis treated with decompression and dynamic
    stabilization. Spine (Phila Pa 1976) 2008;33(18):E636E642.
    This prospective study reported a minimum 4-year
    follow-up of single-level spondylolisthesis. Good clinical
    outcomes that hold up after 4 years were reported, but a
    21% rate of screw loosening and breakage and a 47%
    rate of adjacent-level degeneration were seen.

    2.

    Goffin J, Van Calenbergh F, van Loon J, et al: Intermediate follow-up after treatment of degenerative disc disease with the Bryan Cervical Disc Prosthesis: Singlelevel and bi-level. Spine (Phila Pa 1976) 2003;28(24):
    2673-2678.

    3.

    Sasso RC, Smucker JD, Hacker RJ, Heller JG: Artificial


    disc versus fusion: A prospective, randomized study
    with 2-year follow-up on 99 patients. Spine (Phila Pa
    1976) 2007;32(26):2933-2940, discussion 2941-2942.
    In this prospective study, the authors demonstrated that
    single-level cervical arthroplasty was comparable to the
    gold standard ACDF in clinical outcomes and reoperation rates, while preserving motion at the index level.

    9.

    Wrgler-Hauri CC, Kalbarczyk A, Wiesli M, Landolt


    H, Fandino J: Dynamic neutralization of the lumbar
    spine after microsurgical decompression in acquired
    lumbar spinal stenosis and segmental instability. Spine
    (Phila Pa 1976) 2008;33(3):E66-E72.
    The authors report a high incidence of hardware failure
    and improved clinical outcomes mainly due to microscopic decompression in this prospective study. Thirty
    percent of patients had continued reports of lumbar
    pain at 1-year follow-up.

    4.

    5.

    6.

    David T: Long-term results of one-level lumbar arthroplasty: Minimum 10-year follow-up of the CHARITE
    artificial disc in 106 patients. Spine (Phila Pa 1976)
    2007;32(6):661-666.
    A retrospective chart review of 106 patients who underwent one-level arthroplasty at either L4-5 or L5-S1 is
    presented. This study revealed durability at minimum
    10-year follow-up and a low reoperation rate for
    adjacent-level disease.

    10.

    Zhu Q, Larson CR, Sjovold SG, et al: Biomechanical


    evaluation of the Total Facet Arthroplasty System:
    3-dimensional kinematics. Spine (Phila Pa 1976) 2007;
    32(1):55-62.
    A biomechanical evaluation of the TFAS is presented.
    Range of motion was 81% of the intact spine in flexion,
    68% in extension, 88% in lateral bending, and 128% in
    axial rotation.

    Siepe CJ, Mayer HM, Heinz-Leisenheimer M, Korge A:


    Total lumbar disc replacement: Different results for different levels. Spine (Phila Pa 1976) 2007;32(7):782790.
    This article presents midterm clinical results from a prospective study of lumbar total disk replacement at different segments (L4-5, L5-S1, and bilevel L4-5 and L5-S1).
    The results note significant differences between singlelevel and bilevel arthroplasty. Outcomes were reported
    to be significantly lower in bilevel total disk replacement
    with higher complication rates.

    11.

    Wilke HJ, Schmidt H, Werner K, Schmlz W, Drumm J:


    Biomechanical evaluation of a new total posteriorelement replacement system. Spine (Phila Pa 1976)
    2006;31(24):2790-2796, discussion 2797.

    12.

    McAfee P, Khoo LT, Pimenta L, et al: Treatment of lumbar spinal stenosis with a total posterior arthroplasty
    prosthesis: Implant description, surgical technique, and
    a prospective report on 29 patients. Neurosurg Focus
    2007;22(1):E13.
    A prospective, multicenter, pilot study performed outside the United States assessed 29 patients who underwent TOPS implantation. Visual analog scale for leg
    pain improved from 88 to 12 points, ODI dropped from

    Hannibal M, Thomas DJ, Low J, Hsu KY, Zucherman J: ProDisc-L total disc replacement: A comparison
    of 1-level versus 2-level arthroplasty patients with a
    minimum 2-year follow-up. Spine (Phila Pa 1976)
    2007;32(21):2322-2326.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    5: Spine

    7.

    Annotated References

    671

    Section 5: Spine

    13.

    14.

    16.

    Kondrashov DG, Hannibal M, Hsu KY, Zucherman JF:


    Interspinous process decompression with the X-STOP
    device for lumbar spinal stenosis: A 4-year follow-up
    study. J Spinal Disord Tech 2006;19(5):323-327.

    Richards JC, Majumdar S, Lindsey DP, Beaupr GS,


    Yerby SA: The treatment mechanism of an interspinous
    process implant for lumbar neurogenic intermittent
    claudication. Spine (Phila Pa 1976) 2005;30(7):744749.

    17.

    Chung KJ, Hwang YS, Koh SH: Stress fracture of bilateral posterior facet after insertion of interspinous implant. Spine (Phila Pa 1976) 2009;34(10):E380-E383.

    Zucherman JF, Hsu KY, Hartjen CA, et al: A multicenter, prospective, randomized trial evaluating the X
    STOP interspinous process decompression system for
    the treatment of neurogenic intermittent claudication:
    Two-year follow-up results. Spine (Phila Pa 1976) 2005;
    30(12):1351-1358.
    Siddiqui M, Smith FW, Wardlaw D: One-year results of
    X Stop interspinous implant for the treatment of lumbar
    spinal stenosis. Spine (Phila Pa 1976) 2007;32(12):
    1345-1348.
    This prospective study looks at a small group of patients
    with lumbar stenosis treated with the X-STOP device.
    Results are from 12-month follow-up. The data reported showed 71% clinical improvement, but 7 of 24
    patients (29%) had recurrence of symptoms at 1 year.

    The authors present a case report of stress fractures of


    bilateral inferior articular processes of L4 6 years after
    insertion of an interspinous spacer at L4-5.
    18.

    Sobajima S, Vadala G, Shimer A, Kim JS, Gilbertson


    LG, Kang JD: Feasibility of a stem cell therapy for intervertebral disc degeneration. Spine J 2008;8(6):888896.
    This two-part in vitro and in vivo study looked at the
    feasibility of stem cell therapy for disk disease. Results
    showed extracellular matrix production in vitro by human stem cells, and incorporation of transplanted stem
    cells in rabbit intervetebral disks at 24 weeks. It was
    concluded that stem cells may have multiple mechanisms to confer therapeutic effect in disc degeneration.

    5: Spine

    15.

    57% to 16%, and the Zurich Claudication Questionnaire dropped from 57% to 26% at 1-year follow-up.
    No cases of slip progression and no signs of screw loosening were found.

    672

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    This page intentionally left blank

    This page intentionally left blank

    Chapter 53

    Shoulder, Upper Arm, and Elbow


    Trauma: Pediatrics
    J. Michael Wattenbarger, MD

    Steven L. Frick, MD

    Injuries to the Sternoclavicular Joint and Clavicle


    The sternoclavicular joint connects the upper extremity
    to the axial skeleton. This joint is susceptible to injury
    from a direct blow or other force applied laterally to
    the clavicle, acromion, or shoulder. The medial clavicle
    ossification center appears during the late teenage
    years, and the physis closes between age 20 and 25
    years. As a result, sternoclavicular injuries in teenagers
    and young adults often are physeal injuries that mimic
    dislocations. A delay in diagnosis is common because
    physical examination and plain radiography can be unreliable for assessing displacement. For a patient with
    pain and swelling near the sternoclavicular joint, axial
    CT is recommended to assess for dislocation or physeal
    injury and to clarify the direction and magnitude of any
    displacement. An injury with anterior instability usually is treated nonsurgically. A posteriorly displaced
    fracture or dislocation can cause injury or compression
    to the great vessels, trachea, and esophagus, and usually it is treated with closed or open reduction to restore anatomic alignment (Figure 1). Although some
    authors believe that medial physeal injuries have remodeling potential and can be treated nonsurgically,
    others have noted a high frequency of persistent instability after reduction and recommend open reduction
    and stabilization with suture or wires.1-3 Pin fixation in
    this region is not recommended because of the risk of
    pin migration and injury to nearby vital structures. It is
    recommended that a vascular or cardiothoracic surgeon
    be notified and available during the reduction because
    of the potential for catastrophic hemorrhage. Closed

    2011 American Academy of Orthopaedic Surgeons

    Clavicle Fractures
    Diaphyseal clavicle fractures occur in patients of any
    age, including newborn infants. Clavicle fracture in a
    newborn is treated with immobilization that can be as
    simple as pinning the sleeve covering the affected arm
    into the desired position. Brachial plexus injury may
    occur in conjunction with clavicle fracture in a newborn. A child with a clavicle fracture may have pseudoparalysis of the upper extremity from pain, however.
    If the clinician is unable to assess the neurovascular sta-

    6: Pediatrics

    Dr. Wattenbarger or an immediate family member


    serves as a board member, owner, officer, or committee
    member of the Pediatric Orthopaedic Society of North
    America and has received research or institutional support from Biomet. Dr. Frick or an immediate family
    member serves as a board member, owner, officer, or
    committee member of the American Orthopaedic Association, the J. Robert Gladden Society, the Pediatric Orthopaedic Society of North America, and the American
    Academy of Orthopaedic Surgeons; and has received research or institutional support from Biomet.

    reduction probably should not be attempted for a


    chronic injury (an injury of more than 2 weeks duration) because the clavicle may be adhering to mediastinal vascular structures. Instead, open reduction should
    be performed with careful circumferential dissection
    around the medial clavicle.

    Figure 1

    CT showing a posteriorly displaced fracture of the


    sternoclavicular joint (arrow).

    Orthopaedic Knowledge Update 10

    675

    Section 6: Pediatrics

    Figure 2

    Schematic drawings showing features of the lateral elbow. A, The hourglass shape formed by the olecranon and
    coronoid fossa. B, The humeral-capitellar angle, which is 40 in children of all ages. C, The anterior humeral line,
    which in most children should bisect the capitellum; in young children, the anterior humeral line should intersect
    the anterior third of the capitellum. D, A smooth arc from the anterior humerus capitellum and coronoid process
    should be present. (Adapted from Herring JA, Tachdijan MO, eds: Tachdjians Pediatric Orthopedics, ed 4. Philadelphia, PA, Saunders, 2008, p 2461.)

    tus of the upper extremity at the time of injury, the


    child should be examined several weeks later to rule
    out a brachial plexus injury.
    More than 80% of clavicle fractures in children are
    diaphyseal, and almost all of them will heal with nonsurgical treatment. A review of pediatric clavicle fractures over a 20-year period in a busy trauma center
    found that only 15 children were surgically treated.4
    The indications for surgical treatment of a pediatric
    clavicle fracture included tenting of the skin, an open
    fracture, severe shortening of the shoulder girdle, and
    risk to the neurologic or vascular structures.
    A distal clavicle fracture also can usually be treated
    nonsurgically in children. The strong periosteal sleeve
    typically is not displaced with the fracture. Therefore, a
    distal fracture often heals with what appears to be two
    clavicles in bayonet apposition, and this so-called double clavicle usually remodels.

    Proximal Humerus Fractures

    6: Pediatrics

    The growth potential of the proximal humeral physis


    (which contributes 80% of the humerus length) and the
    range of motion of the shoulder joint mean that most
    proximal humerus fractures in children and adolescents
    can be treated nonsurgically with excellent functional
    results. Most fractures of the proximal humerus are in
    the Salter-Harris type II pattern, with the distal shaft
    fragment displaced through the thinner anterior periosteal sleeve. In the Neer-Horowitz classification, which
    is most commonly used, type I is a minimally displaced
    fracture, type II is displaced less than one third of the
    width of the shaft, type III is displaced one third to two
    thirds of the width of the shaft, and type IV is displaced
    more than two thirds of the width of shaft.5
    The treatment of proximal humerus fractures in children age 6 years or younger is not controversial. Even a
    type III or IV fracture can be treated nonsurgically with
    676

    Orthopaedic Knowledge Update 10

    a good functional outcome. Concern about the lack of


    remodeling potential in adolescents has led some to recommend surgical treatment of these fractures. According to an early report, surgically treated patients had a
    higher rate of complications than patients treated with
    closed reduction.6 However, a later study found that
    proximal humerus fractures in adolescents can be
    treated safely with open reduction and fixation with either pins or screws.7 Because of complications related
    to wires, the use of retrograde flexible nails has been
    recommended for the surgical treatment of these fractures.8 It should be noted that most studies have reported good functional results even after closed treatment of severely displaced and angulated proximal
    humerus fractures in adolescents.9
    Nerve and vascular injuries are uncommon in association with proximal humerus fractures. One study
    found associated nerve injuries in only 4 of 578 patients with proximal humerus fracture (0.7%), all of
    them with valgus displacement (shaft is displaced medially).10 These nerve deficits resolved within 9 months
    without treatment.

    Elbow Injuries
    Elbow injuries are common in children. The radiographic evaluation should include AP and lateral radiographs. An internal oblique radiograph is helpful for
    evaluating a minimally displaced lateral condyle fracture.11 An understanding of the normal radiographic
    appearance of a childs elbow anatomy is necessary for
    the initial evaluation and may help in determining the
    treatment. A true lateral radiograph should show the
    hourglass appearance of the olecranon fossa and supracondylar area (Figure 2), but the medial epicondyle
    should not be seen, and there should be no widening of

    2011 American Academy of Orthopaedic Surgeons

    Chapter 53: Shoulder, Upper Arm, and Elbow Trauma: Pediatrics

    the metaphyseal area. The humeral condylar angle,


    formed by a line along the shaft of the humerus and a
    line perpendicular to the capitellar physis, is 40 in children of all ages.12 The anterior humeral line is drawn
    down the anterior shaft of the humerus and should bisect the capitellum; however, in children younger than 4
    years it should intersect the anterior third of the capitellum.12 In all radiographic views, the radius should be
    aligned with the capitellum, as shown by the radiocapitellar line (a line drawn down the radial shaft should intersect the capitellum). On an AP radiograph, the Baumann angle is formed by a line drawn through the long
    axis of the humerus and a line drawn along the flat
    metaphyseal region adjacent to the capitellar physis.
    The Baumann angle averages 72 in children, but it can
    range from 64 to 8113 (Figure 3). This angle can be
    useful in assessing the coronal alignment of the elbow
    after reduction of a supracondylar humerus fracture.14
    The presence of the posterior fat pad sign was associated with an occult fracture in 76% of children
    whose radiographs were otherwise negative.15 Thus,
    most children with a posterior fat pad sign are assumed
    to have a nondisplaced elbow fracture. Typically these
    children receive cast treatment for 3 weeks.
    Supracondylar fracture accounts for as many as
    60% of elbow fractures in children; it is the most common type of elbow fracture in children. The lateral condyle fracture represents approximately half of the remaining 40% of elbow fractures in children. Medial
    epicondyle, medial condyle, olecranon, and transphyseal fractures occur much less frequently.

    Supracondylar Humerus Fractures

    2011 American Academy of Orthopaedic Surgeons

    Schematic drawing showing the Baumann angle,


    which is formed by a line parallel to the humeral shaft and a line parallel to the lateral
    condyle physis. (Reproduced with permission
    from Yen YM, Kocher MS: Lateral entry compared with medial and lateral entry pin fixation
    for completely displaced supracondylar humeral
    fractures in children: Surgical technique. J Bone
    Joint Surg Am 2008;90[suppl 2, pt 1]:20-30.)

    The techniques for the treatment of displaced supracondylar humerus fracture include skeletal traction,
    closed reduction, and casting. With the advent of intraoperative fluoroscopy, closed reduction and pinning
    have become the treatment of choice for a type II or III
    supracondylar humerus fracture.16,19,20 In the past, type
    II fractures were often treated with closed reduction
    and casting, but concern about loss of reduction and
    malunion have led to recommendations for surgical
    treatment of these fractures. A study of displaced type
    II fractures after closed reduction found that a third of
    the fractures lost position and 17% ultimately needed
    secondary reduction and pinning.21 There also are concerns that deformities in the sagittal plane of a childs
    elbow will not remodel well. A study of the long-term
    effects of elbow malreduction found that 50% had radiographic abnormalities and 50% had limited elbow
    motion.22 The practice of flexing the elbow to 120
    during treatment to avoid loss of reduction has been
    questioned by recent studies; these studies found an
    increase in forearm compartment pressure and a loss of
    the radial pulse when the elbow was flexed past
    90.23,24

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    A supracondylar humerus fracture can occur in extension or flexion. An extension injury to the humerus
    represents 97% of supracondylar humerus fractures.
    The Gartland classification of extension-type fractures
    has been modified to include flexion-type fractures.16 A
    Gartland type I fracture is minimally displaced. A type
    II fracture is incomplete; one cortex is intact, there is either posterior (extension) or anterior (flexion) angulation, and fracture displacement is more than 3 mm. A
    type III fracture is completely displaced. A recently proposed type IV fracture has multidirectional instability,
    often diagnosed when the flexion reduction maneuver
    for an extension-type fracture causes the distal fragment to move anterior to the proximal fragment.17
    There is little disagreement on the treatment of a
    type I fracture, which is with casting, usually for 3
    weeks. The initial evaluation of these fractures should
    include a careful evaluation of the medial distal humerus, with consideration of the need for contralateral
    comparison radiographs. Subtle comminution of the
    medial distal humerus in an otherwise minimally displaced fracture can lead to cubitus varus. Fractures
    with medial comminution and varus malalignment
    should be treated surgically18 (Figure 4). Physical examination and radiographs of the contralateral elbow can
    help determine whether a minimally displaced supracondylar fracture is in varus.

    Figure 3

    677

    Section 6: Pediatrics

    Figure 4

    AP radiograph showing a minimally displaced supracondylar fracture with medial comminution.


    The fracture was not reduced, and the patient
    developed cubitus varus requiring supracondylar
    osteotomy.

    6: Pediatrics

    Closed reduction and percutaneous pinning of type


    II fractures had a low complication rate in 189 patients
    treated at one institution.19 There were no malunions,
    no surgical complications, and no anesthesia complications. Four patients (2.1%) had an infection; three of
    the infections were superficial and were treated with
    oral antibiotics. The patient with a deep infection was
    the only one requiring reoperation. The authors concluded that surgical treatment of type II supracondylar
    fractures is safe. Other authors also stressed the low
    complication rate associated with closed reduction and
    pinning, and they recommend this treatment of angulated type II fractures.16,20
    Type III fractures are treated surgically with closed
    reduction under fluoroscopic guidance and pin fixation. Modern pinning techniques have been well studied and found to have low complication rates.19,20,25-27
    Volkmann ischemia is rarely seen with fracture pinning
    and postoperative elbow immobilization at less than
    90 of flexion. Malunion also rarely occurs. Only 1
    malunion was reported in a study of 622 surgically
    treated supracondylar fractures.20 No malunions occurred in 189 surgically treated type II fractures,19 and
    only 1 malunion occurred in 203 surgically treated
    fractures.28 In a good-quality reduction, the anterior
    humeral line should bisect the capitellum, and the humerocondylar and Baumann angles should be close to
    normal. Mild rotational malalignment is well tolerated
    because of shoulder motion, and translational deformi678

    Orthopaedic Knowledge Update 10

    ties have good remodeling potential. Intraoperative internal and external oblique radiographs are helpful for
    judging the reduction.
    The most common complications in most large studies are pin migration (approximately 2% of patients)
    and infection (1% to 2.4%).19,20,27 The infections associated with closed reduction and pinning usually are superficial and can be treated with oral antibiotics.
    Rarely, the infection is deep and requires surgical dbridement. A comparison of semisterile technique and
    full surgical preparation found no difference in infection rates; the infection rate remained low even if preoperative antibiotics were not used.20,27 Three weeks of
    pin fixation is sufficient for almost all supracondylar
    humerus fractures in children. A longer period of pin
    fixation provides bacteria and foreign material with an
    entry portal for a longer period of time and thereby fosters infection. In an adolescent with supracondylar humerus fracture, the duration of pin fixation is 4 to 6
    weeks, and the rate of deep infection is correspondingly
    higher. In these patients, burying the pins beneath the
    skin may decrease the infection risk.
    Studies of the pin configuration for supracondylar
    fractures have compared the use of medial- and lateralentry crossed pins with the use of lateral-entry pins
    alone. Biomechanical studies found that crossed pins
    are stronger in torsion than a lateral-entry construct.
    Proponents of lateral-only pins cite a lower incidence of
    iatrogenic nerve injury with these pins. A systematic review of 35 studies that included 2,054 children found
    that an iatrogenic nerve injury was 1.84 times more
    likely when medial- and lateral-entry pins were used,
    compared with lateral-entry pins alone.29 The probability of loss of reduction was 0.58 times lower when
    medial- and lateral- entry crossed pins were used than
    with lateral-entry-only pins. Recent prospective studies
    found no difference in loss of reduction or iatrogenic
    nerve injury based on pin configuration.30,31
    The incidence of iatrogenic ulnar nerve injury may
    be lower in more recent studies because of a better understanding of its cause and the use of safer techniques
    for medial pinning. For instance, it is known that the
    ulnar nerve will subluxate anteriorly when the elbow is
    hyperflexed in some children.32,33 Therefore, most surgeons who use medial- and lateral-entry pins reduce an
    extension-type fracture in flexion before placing one or
    two lateral pins, and they extend the elbow before placing the medial pin30,31,34,35 (Figure 5). If palpating the
    cubital tunnel is difficult because of swelling, a small
    medial incision is recommended to make sure the ulnar
    nerve is out of the way before the medial pin is
    placed.20 The medial pin should be removed if the patients hand moves as it is being placed.
    More recent studies have described the technique of
    using lateral entry pins to decrease the risk of loss of reduction. Loss of reduction in 9 of 322 fractures (2.9%)
    was caused by failure to engage both fragments with
    two or more pins, failure to achieve bicortical fixation
    with two or more pins, or failure to achieve adequate
    pin separation (more than 2 mm) at the fracture site.36
    The researchers now use three lateral pins for a type III

    2011 American Academy of Orthopaedic Surgeons

    Chapter 53: Shoulder, Upper Arm, and Elbow Trauma: Pediatrics

    Figure 5

    Radiograph showing two lateral pins and a


    medial pin for fixation of a supracondylar humerus fracture. The medial pin should be placed
    with the elbow extended to avoid entrapment
    of the ulnar nerve.

    2011 American Academy of Orthopaedic Surgeons

    Figure 6

    A, Fluoroscopic images showing improper placement of lateral entry pins for fixation of a supracondylar fracture. There is very little spread
    between the pins. B, Radiographs showing loss
    of reduction 2 weeks after pinning.

    difficult to achieve. The argument that a delay in treatment can lead to a need for open reduction is difficult
    to assess because the indications for open reduction
    have not been defined. Although nonemergent treatment is often implemented, one study found that compartment syndrome developed in 11 patients with a
    low-energy fracture although they had no initial sign of
    vascular compromise; there was an average delay to
    surgery of 22 hours.44 The authors recommended early
    surgical treatment of patients with a red-flag warning
    sign such as severe elbow swelling, ecchymosis, neurologic deficit, or diminished or absent radial pulse. Patients with an ipsilateral forearm or wrist fracture also
    are at increased risk for developing a compartment syndrome and should be carefully monitored.45
    In a patient with a supracondylar fracture and absent radial and ulnar pulses, distal perfusion is determined to be adequate (a pink hand) or inadequate (a
    white hand). A patient with a white hand often has a
    ruptured or entrapped brachial artery with inadequate
    collateral circulation, and the surgical team should be

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    fracture (Figures 6 and 7). Other researchers state that


    one lateral pin must engage the lateral column and the
    other pin must engage the central column.34 A prospective study of intraoperative internal and external
    oblique fluoroscopy used to assess rotational stability
    after pinning found that only 26% of type III fractures
    were stable after two lateral-only pins were used.37 A
    third pin was added to the unstable fractures, with resulting stability in an additional 50%. In the fractures
    that remained unstable, a medial pin was added.
    Flexion-type fractures are rare and are more difficult
    to treat than extension-type fractures. Open reduction
    is more often required, and preoperative ulnar nerve
    symptoms are more common.38,39 A type IV fracture
    has multidirectional instability, with no intact periosteum to help with the reduction. These fractures can often be treated closed by using pins as a joystick in the
    distal fragment and by rotating the C-arm rather than
    the patients arm to obtain orthogonal views during
    pinning.17,19
    It has been established that closed supracondylar humerus fractures without vascular injury or severe softtissue swelling can be managed as surgical urgencies,
    requiring prompt but not immediate treatment.40-43 According to many protocols, the fracture should be
    splinted in 30 to 40 of elbow flexion; the patient
    should be admitted for observation, with closed reduction and pinning as soon as the patients stomach is
    empty and an expert surgical team is available. There is
    concern that swelling may lead to vascular compromise
    or a compartment syndrome if treatment is delayed, or
    that an acceptable closed reduction may become more

    679

    Section 6: Pediatrics

    Figure 7

    A and B, Fluoroscopic images showing proper placement of lateral entry pins for fixation of a type III lateral condyle
    fracture. The spread between the pins at the fracture site is adequate, and the pins engage both cortices.

    prepared to explore and repair or reconstruct the brachial artery after reducing and pinning the fracture. Arteriography is not indicated for an isolated injury. A patient with a pink hand should undergo closed reduction
    and pinning. A near-anatomic reduction with no gapping should be obtained to avoid artery entrapment or
    tethering by soft tissues pulled into the fracture. If an
    acceptable closed reduction cannot be obtained, an anterior approach should be used for open reduction to
    allow visualization of the artery. If the pulse returns after closed reduction, the patient is admitted for observation. If the pulse does not return but there is a Doppler signal at the wrist and the hand remains well
    perfused, the recommendation is to admit the patient
    and carefully monitor perfusion and active finger motion over the next 48 hours. Some authors recommend
    a more aggressive approach, with earlier exploration of
    the brachial artery if the pulse does not return after reduction. If the pulse is lost after closed reduction and
    pinning in a patient with an intact preoperative pulse,
    open reduction usually is indicated to assess the artery.
    The elbow should not be flexed more than 90 for
    postoperative cast immobilization.

    Lateral Condyle Fractures


    6: Pediatrics

    Treatment of a lateral condyle fracture is based on the


    amount of displacement seen on radiographs and
    whether there is an intact articular cartilage hinge. Internal oblique radiographs are useful in assessing the
    amount of displacement in a lateral condyle fracture11
    (Figure 8). An intact articular surface can be expected if
    there is less than 2 mm of displacement in any radiographic view. An incomplete fracture should have an
    intact articular cartilage surface, which suggests a relatively stable fracture.
    Lateral condyle fractures traditionally are classified
    using the Milch system; however, it is not useful for
    guiding modern treatments. A new classification system
    680

    Orthopaedic Knowledge Update 10

    for lateral condyle fractures has been proposed based


    on the amount of displacement of the fracture and
    whether the articular cartilage is intact on arthrogram.46 A type I fracture has less than 2 mm of displacement, a type II fracture has more than 2 mm of
    displacement and intact articular cartilage, and a type
    III fracture has more than 2 mm of displacement and
    incongruent articular cartilage. Intraoperative arthrography is recommended for fractures with more than 2
    mm of displacement if it is unclear whether the articular surface is intact. With an intact articular surface,
    closed reduction and pinning are recommended. An
    open reduction and pinning are performed if the articular surface is not intact.46 There were three times as
    many complications among type III fractures as among
    type II fractures; all type III fractures had displacement
    of at least 4 mm.
    In a study of treatment for lateral condyle fractures,
    closed reduction was attempted for all fractures. If the
    fracture could be reduced to less than 2 mm of displacement, closed pinning was performed. Fractures
    that could not be reduced to less then 2 mm of displacement were treated with open reduction and internal fixation. Although severely displaced fractures were
    most likely to require open reduction and internal fixation, many of these fractures could be treated closed.
    There was no osteonecrosis, nonunion, or physeal arrest.47
    Lateral overgrowth or a lateral bump sometimes appears, regardless of whether a lateral condyle fracture
    was treated surgically or with casting alone. A 10% incidence of lateral overgrowth was reported in surgically
    treated lateral condyle fractures. The possibility of lateral overgrowth should be discussed with the family before surgery.
    Fractures that are minimally displaced (less than
    2 mm) can be treated with a cast and close follow-up.
    Only a small percentage of minimally displaced frac-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 53: Shoulder, Upper Arm, and Elbow Trauma: Pediatrics

    Figure 8

    A, AP radiograph of a lateral condyle fracture showing minimal displacement. B, Internal oblique radiograph of the
    same elbow, clearly showing a displaced lateral condyle fracture. (Reproduced with permission from Song KS, Kang
    CH, Min BW, Bae KC, Cho CH: Internal oblique radiographs for diagnosis of nondisplaced or minimally displaced
    lateral condylar fractures of the humerus in children. J Bone Joint Surg Am 2007;89[1]:58-63.)

    uated for the presence of an entrapped medial


    epicondyle. There is agreement that fractures with less
    than 5 mm of displacement can be treated with 1 to 2
    weeks of immobilization, followed by resumption of
    activities. The treatment of fractures with more than 5
    mm of displacement is more controversial. For a highdemand athlete, surgical treatment may be recommended to avoid the possibility of instability. A study
    with long-term follow-up of medial epicondyle fractures displaced 5 to 15 mm found that patients had
    similar results regardless of whether they were treated
    with casting or with open reduction and internal fixation.49

    Transphyseal Fractures

    Monteggia Fracture-Dislocations

    Transphyseal fractures are relatively uncommon, usually occurring in children younger than 2 years. Half of
    these fractures are associated with child abuse. The differential diagnosis includes lateral condyle fracture and
    elbow dislocation. In a transphyseal fracture, the relationship of the radial head and capitellum is intact. The
    fracture usually is treated with closed reduction and
    pinning. Casting alone has a higher rate of cubitus
    varus.

    Late recognition of Monteggia fracture-dislocations


    still occurs and necessitates difficult reconstructive procedures. Closed treatment after early recognition usually is successful and typically leads to healing in an anatomic position, with good function. To prevent
    missing the diagnosis, the radiocapitellar line should be
    assessed on every lateral radiograph of the elbow; a line
    down the radial shaft should pass through the center of
    the capitellar ossification center (Figure 9). Closed reduction of the ulnar shaft deformity usually results in
    reduction of the dislocated radial head. If closed reduction is not possible, open reduction through a lateral
    approach is indicated, with preservation or repair of
    the annular ligament. In patients age 8 years and older

    Medial Epicondyle Fractures


    Fifty percent of medial epicondyle fractures are associated with a dislocated elbow. Postreduction radiographs of an elbow dislocation always should be eval-

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    tures go on to nonunion. If a minimally displaced fracture does not heal, pinning is recommended.
    Nonunion of lateral condyle fractures can lead to cubitus valgus and tardy ulnar nerve palsy. There have
    been historically high rates of osteonecrosis in fractures
    treated with late open reduction and internal fixation
    (more than 3 weeks after initial injury). Open reduction
    and internal fixation has been recommended for lateidentified fractures, with a goal of union of the fragment rather than anatomic reduction.48 Such a fracture
    should be fixed in the position that provides the best
    range of motion and carrying angle. Soft-tissue stripping should be avoided.

    681

    Section 6: Pediatrics

    Figure 9

    A, Radiograph showing a greenstick ulna fracture. The radial head is dislocated (a line drawn through the proximal
    radius does not line up with the capitellum). This Monteggia fracture was initially missed. B, Lateral radiograph of
    the same fracture 3 months later, clearly showing the dislocated radial head. The ulna is not straight; this characteristic suggests the possibility of a dislocated radial head.

    with a length-unstable ulna fracture, plate fixation may


    be indicated to maintain the length and reduction of
    the radiocapitellar joint. Late reconstruction of a
    missed Monteggia injury is considered if the radial
    head retains its concave structure; typically it involves
    osteotomy of the ulna to correct the angular and length
    deformity, with or without annular ligament reconstruction.

    6: Pediatrics

    Completely Displaced Radial Neck Fractures

    Figure 10

    682

    Radiograph showing a displaced radial neck


    fracture, which requires surgical treatment.
    The fracture has almost 90 of angulation.

    Orthopaedic Knowledge Update 10

    A radial neck fracture with less than 30 of angulation


    and less than 3 to 5 mm of translation is managed with
    2 to 3 weeks of immobilization followed by a gradual
    return to function (Figure 10). Healing with greater angulation or translation can result in a cam effect that
    disrupts the rotational arc of the radius around the
    ulna, limiting forearm supination and pronation. Open
    reduction of a displaced radial neck fracture is associated with several complications, including stiffness and
    osteonecrosis. Because of these risks, there should be an
    attempt at closed reduction with percutaneous pin reduction, intramedullary pin reduction, or manipulation
    of the radial neck with a curved elevator, while avoiding opening the fracture or radiocapitellar joint. Multi-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 53: Shoulder, Upper Arm, and Elbow Trauma: Pediatrics

    ple methods of closed manipulation can be attempted


    before a more invasive method is used. A stout pin
    placed distal and posterior to the fracture can be used
    to lever the radial head back onto the neck, or the pin
    can be used to directly push on the radial head. If such
    a reduction method is successful, stability is tested with
    supination and pronation under fluoroscopy. If necessary, the fracture is stabilized with obliquely directed
    wires. Excellent success and functional results have
    been reported with the use of a retrograde intramedullary rod, which is driven up to the fracture, rotated,
    and driven into the radial neck-head fragment.50 Rotation of the rod reduces the fracture and provides internal fixation.
    If these techniques are not successful, a formal open
    reduction is done with a lateral approach to the radiocapitellar joint. Usually the radial head fragment is displaced laterally and distally, and care is taken during
    exposure to preserve any intact soft-tissue attachments,
    which may provide vascularity to the fragment. The annular ligament should be evaluated; it may need to be
    divided and repaired later to reposition the radial head
    in anatomic position in the joint. Fixation is done using
    obliquely placed wires, small screws, or an intramedullary rod.

    Rajan RA, Hawkins KJ, Metcalfe J, Konstantoulakis C,


    Jones S, Fernandes J: Elastic stable intramedullary nailing for displaced proximal humeral fractures in older
    children. J Child Orthop 2008;2(1):15-19.
    Fourteen older patients with displaced proximal humerus fractures were treated with open or closed reduction and stabilization with elastic nails. The procedure
    was safe and resulted in good outcomes as measured by
    outcomes scores and patient satisfaction.

    9.

    Bahrs C, Zipplies S, Ochs BG, et al: Proximal humeral


    fractures in children and adolescents. J Pediatr Orthop
    2009;29(3):238-242.
    Of 43 proximal humerus fractures in patients age 6 to
    16 years, 33 were treated surgically. An anatomic closed
    reduction was obtained in 16 of the 33 patients after reduction under general anesthesia. Open reduction was
    then performed in 17 patients. Soft tissue including periosteum (two patients) and biceps tendon with periosteum (seven patients) was found in the fracture site. All
    patients had an excellent result. Level of evidence: IV.

    10.

    Hwang RW, Bae DS, Waters PM: Brachial plexus palsy


    following proximal humerus fracture in patients who
    are skeletally immature. J Orthop Trauma 2008;22(4):
    286-290.
    Neurologic injury is extremely uncommon in patients
    with proximal humerus fractures. In this series, 0.4% of
    patients had a neurologic deficit, and all resolved with
    observation. Level of evidence: IV.

    11.

    Song KS, Kang CH, Min BW, Bae KC, Cho CH: Internal oblique radiographs for diagnosis of nondisplaced
    or minimally displaced lateral condylar fractures of the
    humerus in children. J Bone Joint Surg Am 2007;89(1):
    58-63.
    In a prospective study of 54 minimally displaced lateral
    condyle fractures, the efficacy of internal oblique views
    for determining the amount of displacement and, therefore, instability in lateral condyle fractures was assessed.
    Different displacement was seen on the AP and internal
    oblique radiographs in 70% of the fractures. Level of
    evidence: I.

    12.

    Simanovsky N, Lamdan R, Hiller N, Simanovsky N:


    The measurements and standardization of humerocondylar angle in children. J Pediatr Orthop 2008;28(4):
    463-465.
    A study of humerocondylar angle in normal children divided the children by age group as younger than 5 years,
    5 to 10 years, and 10 to 15 years. In all age groups the
    humerocondylar angle was found to be 40.

    13.

    Herman MJ, Boardman MJ, Hoover JR, Chafetz RS:


    Relationship of the anterior humeral line to the capitellar ossific nucleus: Variability with age. J Bone Joint
    Surg Am 2009;91(9):2188-2193.
    The anterior humeral line passes through the middle
    third of the capitellum in most children. However, the
    location of this line is more variable in children who are
    younger than 4 years, passing almost equally through either the middle third or the anterior third of the capitellum.

    Annotated References
    1.

    Wirth MA, Rockwood CA Jr: Acute and chronic traumatic injuries of the sternoclavicular joint. J Am Acad
    Orthop Surg 1996;4(5):268-278.

    2.

    Lewonowski K, Bassett GS: Complete posterior sternoclavicular epiphyseal separation: A case report and review of the literature. Clin Orthop Relat Res 1992;281:
    84-88.

    3.

    Waters PM, Bae DS, Kadiyala RK: Short-term outcomes


    after surgical treatment of traumatic posterior sternoclavicular fracture-dislocations in children and adolescents.
    J Pediatr Orthop 2003;23(4):464-469.

    4.

    Kubiak R, Slongo T: Operative treatment of clavicle


    fractures in children: A review of 21 years. J Pediatr Orthop 2002;22(6):736-739.

    5.

    Neer CS II, Horwitz BS: Fractures of the proximal humeral epiphysial plate. Clin Orthop Relat Res 1965;41:
    24-31.

    6.

    Beringer DC, Weiner DS, Noble JS, Bell RH: Severely


    displaced proximal humeral epiphyseal fractures: A
    follow-up study. J Pediatr Orthop 1998;18(1):31-37.

    7.

    Dobbs MB, Luhmann SL, Gordon JE, Strecker WB,


    Schoenecker PL: Severely displaced proximal humeral
    epiphyseal fractures. J Pediatr Orthop 2003;23(2):208215.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    8.

    683

    Section 6: Pediatrics

    14.

    Williamson DM, Coates CJ, Miller RK, Cole WG: Normal characteristics of the Baumann (humerocapitellar)
    angle: An aid in assessment of supracondylar fractures.
    J Pediatr Orthop 1992;12(5):636-639.

    15.

    Skaggs DL, Mirzayan R: The posterior fat pad sign in


    association with occult fracture of the elbow in children. J Bone Joint Surg Am 1999;81(10):1429-1433.

    16.

    Omid R, Choi PD, Skaggs DL: Supracondylar humeral


    fractures in children. J Bone Joint Surg Am 2008;90(5):
    1121-1132.
    This is an excellent review of the literature on the evaluation, treatment, and complications of supracondylar
    humerus fractures.

    17.

    18.

    19.

    6: Pediatrics

    20.

    21.

    684

    Leitch KK, Kay RM, Femino JD, Tolo VT, Storer SK,
    Skaggs DL: Treatment of multidirectionally unstable supracondylar humeral fractures in children: A modified
    Gartland type-IV fracture. J Bone Joint Surg Am 2006;
    88(5):980-985.
    De Boeck H, De Smet P, Penders W, De Rydt D: Supracondylar elbow fractures with impaction of the medial
    condyle in children. J Pediatr Orthop 1995;15(4):444448.
    Skaggs DL, Sankar WN, Albrektson J, Vaishnav S, Choi
    PD, Kay RM: How safe is the operative treatment of
    Gartland type 2 supracondylar humerus fractures in
    children? J Pediatr Orthop 2008;28(2):139-141.
    This is a retrospective review of 189 type II supracondylar fractures treated at one institution with closed reduction and pinning. Three superficial infections were
    treated with oral antibiotics. One patient had a deep infection. The authors recommend surgical treatment of
    type II fractures based on the complication rate in other
    studies of similar fractures.
    Bashyal RK, Chu JY, Schoenecker PL, Dobbs MB, Luhmann SJ, Gordon JE: Complications after pinning of supracondylar distal humerus fractures. J Pediatr Orthop
    2009;29(7):704-708.
    This review of complications associated with pinning of
    622 supracondylar humerus fractures at one institution
    specifically compared the infection rate with various
    types of preparations. A minimal preparation without
    preoperative antibiotics did not lead to a higher infection rate. The authors describe a technique for placing a
    medial pin, if needed. Only one iatrogenic ulnar nerve
    injury was found in 311 patients treated with a medial
    pin (0.3%). Preoperative nerve deficit was most common in flexion and type III fractures. Level of evidence:
    III.
    Parikh SN, Wall EJ, Foad S, Wiersema B, Nolte B: Displaced type II extension supracondylar humerus fractures: Do they all need pinning? J Pediatr Orthop 2004;
    24(4):380-384.
    A study of 24 type II fractures treated with closed reduction and casting found that 7 fractures lost position, and
    4 of the 7 required secondary reduction and pinning.
    Two fractures had an unsatisfactory outcome.

    Orthopaedic Knowledge Update 10

    22.

    Simanovsky N, Lamdan R, Mosheiff R, Simanovsky N:


    Underreduced supracondylar fracture of the humerus in
    children: Clinical significance at skeletal maturity. J Pediatr Orthop 2007;27(7):733-738.
    At final follow-up, 50% of 22 patients with a supracondylar humerus fracture that was initially underreduced
    in the sagittal plane had radiographic abnormality of
    the humerocondylar angle, 50% had limited elbow flexion, and 31% were aware of their limited elbow flexion
    at skeletal maturity. Only three patients felt minor functional disability. Ten patients had an unsatisfactory result. The authors recommend surgical treatment with
    pinning for a moderately displaced fracture to avoid late
    deformity and loss of motion.

    23.

    Battaglia TC, Armstrong DG, Schwend RM: Factors affecting forearm compartment pressures in children with
    supracondylar fractures of the humerus. J Pediatr Orthop 2002;22(4):431-439.

    24.

    Mapes RC, Hennrikus WL: The effect of elbow position


    on the radial pulse measured by Doppler ultrasonography after surgical treatment of supracondylar elbow
    fractures in children. J Pediatr Orthop 1998;18(4):441444.

    25.

    Skaggs DL, Cluck MW, Mostofi A, Flynn JM, Kay RM:


    Lateral-entry pin fixation in the management of supracondylar fractures in children. J Bone Joint Surg Am
    2004;86(4):702-707.

    26.

    Skaggs DL, Hale JM, Bassett J, Kaminsky C, Kay RM,


    Tolo VT: Operative treatment of supracondylar fractures of the humerus in children: The consequences of
    pin placement. J Bone Joint Surg Am 2001;83(5):735740.

    27.

    Iobst CA, Spurdle C, King WF, Lopez M: Percutaneous


    pinning of pediatric supracondylar humerus fractures
    with the semisterile technique: The Miami experience.
    J Pediatr Orthop 2007;27(1):17-22.
    A review of 304 supracondylar humerus fractures
    treated with a semisterile technique found an overall infection rate of 2.34%, with a deep infection rate of
    0.47%. Perioperative antibiotics were not used in 68%
    of the patients. Level of evidence: IV.

    28.

    Bahk MS, Srikumaran U, Ain MC, et al: Patterns of pediatric supracondylar humerus fractures. J Pediatr Orthop 2008;28(5):493-499.
    The coronal and sagittal angle of supracondylar humerus fractures was studied in 203 fractures. Fractures
    with a coronal obliquity of more than 10 had greater
    comminution and rotational malunion. Similarly, fractures with a sagittal obliquity of more than 20 were associated with a higher incidence of additional injuries
    and malunion in extension than fractures with less than
    20 of sagittal obliquity.

    29.

    Brauer CA, Lee BM, Bae DS, Waters PM, Kocher MS: A
    systematic review of medial and lateral entry pinning
    versus lateral entry pinning for supracondylar fractures
    of the humerus. J Pediatr Orthop 2007;27(2):181-186.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 53: Shoulder, Upper Arm, and Elbow Trauma: Pediatrics

    Medial-lateral pin configuration and lateral pin configuration were systematically reviewed using data from 35
    studies including 2,054 children. Iatrogenic nerve injury
    was 1.84 times more common with medial- and lateralentry pins than with lateral-entry pins alone. The probability of loss of reduction was 0.58 times lower with
    medial- and lateral-entry pinning. In recent prospective
    studies there was no difference in loss of reduction and
    iatrogenic nerve injury between medial- and lateralentry pins and lateral-entry pins alone. Medial- and
    lateral-entry pinning was found to be more stable.
    30.

    31.

    Kocher MS, Kasser JR, Waters PM, et al: Lateral entry


    compared with medial and lateral entry pin fixation for
    completely displaced supracondylar humeral fractures
    in children: A randomized clinical trial. J Bone Joint
    Surg Am 2007;89(4):706-712.
    A prospective study compared the use of crossed pins
    (n = 24) and lateral-entry pins (n = 28) in type III
    extension-type supracondylar fractures. There was no
    significant difference in mild loss of reduction (one in
    the crossed-pins patient group and six in the lateral pin
    patient group) or radiographic parameters. There were
    no iatrogenic ulnar nerve injuries in either group. Both
    lateral-entry and crossed-pin fixation are effective in the
    treatment of type III supracondylar humerus fractures.
    Level of evidence: I.
    Tripuraneni KR, Bosch PP, Schwend RM, Yaste JJ: Prospective, surgeon-randomized evaluation of crossed pins
    versus lateral pins for unstable supracondylar humerus
    fractures in children. J Pediatr Orthop B 2009;18(2):9398.
    In a prospective review of supracondylar fractures
    treated with crossed pins (n = 20) and those treated with
    lateral pins only (n = 20), patients were randomized
    based on surgeon preference. There was no betweengroup difference in outcome with regard to final range
    of motion or radiographic parameters. One patient in
    each group had a change in treatment plan: in the lateral
    pin only group, the surgeon chose to use a medial pin
    because of medial comminution, and in the crossed-pin
    group the surgeon used only lateral pins because of a
    subluxating ulnar nerve.
    Zaltz I, Waters PM, Kasser JR: Ulnar nerve instability in
    children. J Pediatr Orthop 1996;16(5):567-569.

    33.

    Belhan O, Karakurt L, Ozdemir H, et al: Dynamics of


    the ulnar nerve after percutaneous pinning of supracondylar humeral fractures in children. J Pediatr Orthop B
    2009;18(1):29-33.
    The authors prospectively studied ulnar nerve morphology and dynamics using ultrasound in patients treated
    with either cross-pinning or lateral-entry-only pinning.
    They recommend lateral-entry pinning as the safer procedure.

    34.

    Yen YM, Kocher MS: Lateral entry compared with medial and lateral entry pin fixation for completely displaced supracondylar humeral fractures in children: Surgical technique. J Bone Joint Surg Am 2008;90(suppl 2,
    pt 1):20-30.
    The technique for pinning supracondylar humerus fractures is reviewed.

    2011 American Academy of Orthopaedic Surgeons

    Eidelman M, Hos N, Katzman A, Bialik V: Prevention


    of ulnar nerve injury during fixation of supracondylar
    fractures in children by flexion-extension cross-pinning
    technique. J Pediatr Orthop B 2007;16(3):221-224.
    Sixty-seven supracondylar fractures were treated with
    two lateral pins and one medial pin. The lateral pins
    were placed with the patients arm flexed, and the medial pin was placed with the arm extended. There were
    no iatrogenic ulnar nerve injuries.

    36.

    Sankar WN, Hebela NM, Skaggs DL, Flynn JM: Loss of


    pin fixation in displaced supracondylar humeral fractures in children: Causes and prevention. J Bone Joint
    Surg Am 2007;89(4):713-717.
    A study of 322 supracondylar humerus fractures examined the incidence and causes of postoperative displacement. All of the eight fractures that lost reduction
    (2.9%) were Gartland type III; seven were treated with
    two lateral pins, and one was treated with crossed pins.
    Loss of reduction was more often avoided when three
    lateral pins were used. Three types of pin fixation errors
    were identified.

    37.

    Zenios M, Ramachandran M, Milne B, Little D, Smith


    N: Intraoperative stability testing of lateral-entry pin
    fixation of pediatric supracondylar humeral fractures.
    J Pediatr Orthop 2007;27(6):695-702.
    A prospective study of 21 patients with a type III supracondylar humerus fracture found that only 26% of the
    fractures were stable after two lateral pins were used,
    based on a comparison of lateral intraoperative fluoroscopic views in internal and external rotation. Stability
    was achieved with a third lateral pin in 48% of patients.
    An additional medial pin and medial-entry wire were
    placed and if the fracture was not stable after three lateral wires were used. Twenty-four percent of the fractures needed a medial pin to achieve stability. After the
    stability testing protocol was instituted, no patient had a
    return to the operating room for loss of reduction.

    38.

    Mahan ST, May CD, Kocher MS: Operative management of displaced flexion supracondylar humerus fractures in children. J Pediatr Orthop 2007;27(5):551-556.
    A retrospective review found that type III flexion-type
    supracondylar humerus fractures were more likely to require open reduction (31%) than type III extension-type
    fractures (10%). Patients with a flexion-type fracture
    had more preoperative ulnar nerve symptoms (19%)
    than those with an extension-type fracture (3%).
    Flexion-type fractures are more difficult to treat than
    extension-type fractures and should be recognized preoperatively.

    39.

    Steinman S, Bastrom TP, Newton PO, Mubarak SJ: Beware of ulnar nerve entrapment in flexion-type supracondylar humerus fractures. J Child Orthop 2007;1(3):
    177-180.
    A retrospective study of supracondylar fractures requiring open reduction found that, although flexion-type
    fractures accounted for only 2% to 3% of the supracondylar fractures, 20% of the fractures requiring open reduction were of the flexion type; in half of those, the ulnar nerve was entrapped in the fracture.

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    32.

    35.

    685

    Section 6: Pediatrics

    40.

    Iyengar SR, Hoffinger SA, Townsend DR: Early versus


    delayed reduction and pinning of type III displaced supracondylar fractures of the humerus in children: A
    comparative study. J Orthop Trauma 1999;13(1):51-55.

    41.

    Mehlman CT, Strub WM, Roy DR, Wall EJ, Crawford


    AH: The effect of surgical timing on the perioperative
    complications of treatment of supracondylar humeral
    fractures in children. J Bone Joint Surg Am 2001;83(3):
    323-327.

    42.

    Gupta N, Kay RM, Leitch K, Femino JD, Tolo VT, Skaggs DL: Effect of surgical delay on perioperative complications and need for open reduction in supracondylar
    humerus fractures in children. J Pediatr Orthop 2004;
    24(3):245-248.

    43.

    Leet AI, Frisancho J, Ebramzadeh E: Delayed treatment


    of type 3 supracondylar humerus fractures in children.
    J Pediatr Orthop 2002;22(2):203-207.

    44.

    Ramachandran M, Skaggs DL, Crawford HA, et al: Delaying treatment of supracondylar fractures in children:
    Has the pendulum swung too far? J Bone Joint Surg Br
    2008;90(9):1228-1233.
    In a multicenter retrospective study, 11 pediatric patients with an isolated supracondylar humerus fracture
    and no vascular initial compromise later developed a
    compartment syndrome. Significant swelling at presentation and delay in fracture reduction may be important
    warning signs for the development of a compartment
    syndrome in children with a supracondylar humerus
    fracture.
    Blakemore LC, Cooperman DR, Thompson GH,
    Wathey C, Ballock RT: Compartment syndrome in ipsilateral humerus and forearm fractures in children. Clin
    Orthop Relat Res 2000;376:32-38.

    Weiss JM, Graves S, Yang S, Mendelsohn E, Kay RM,


    Skaggs DL: A new classification system predictive of
    complications in surgically treated pediatric humeral
    lateral condyle fractures. J Pediatr Orthop 2009;29(6):
    602-605.
    A proposed classification of lateral condyle fractures
    was based on a retrospective review of children treated
    at one institution over a 7-year period. The overall complication rate was 25%.

    47.

    Song KS, Kang CH, Min BW, Bae KC, Cho CH, Lee
    JH: Closed reduction and internal fixation of displaced
    unstable lateral condylar fractures of the humerus in
    children. J Bone Joint Surg Am 2008;90(12):26732681.
    A prospective study reviewed the results of closed reduction with percutaneous Kirschner wire fixation in unstable fractures of the lateral condyle. Fractures were classified into five types based on AP and internal oblique
    radiographs. Fractures were pinned closed if the fracture
    gap after reduction was less than 2 mm. There were no
    major complications after 63 fractures. Level of evidence: IV.

    48.

    Wattenbarger JM, Gerardi J, Johnston CE: Late open


    reduction internal fixation of lateral condyle fractures.
    J Pediatr Orthop 2002;22(3):394-398.

    49.

    Farsetti P, Potenza V, Caterini R, Ippolito E: Long-term


    results of treatment of fractures of the medial humeral
    epicondyle in children. J Bone Joint Surg Am 2001;
    83-A:1299-1305.

    50.

    Schmittenbecher PP, Haevernick B, Herold A, Knorr P,


    Schmid E: Treatment decision, method of osteosynthesis, and outcome in radial neck fractures in children: A
    multicenter study. J Pediatr Orthop 2005;25(1):45-50.

    6: Pediatrics

    45.

    46.

    686

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 54

    Forearm, Wrist, and Hand


    Trauma: Pediatrics
    Howard R. Epps, MD

    Michelle S. Caird, MD

    Introduction

    Dr. Epps or an immediate family member serves as a


    board member, owner, officer, or committee member of
    the Pediatric Orthopaedic Society of North America, the
    Houston Orthopedic Society, and the Texas Orthopedic
    Hospital. Neither Dr. Caird nor any immediate family
    member has received anything of value from or owns
    stock in a commercial company or institution related directly or indirectly to the subject of this chapter.

    2011 American Academy of Orthopaedic Surgeons

    Forearm Diaphyseal Fractures


    Forearm fractures are very common in children. These
    injuries can be plastic deformation of the forearm,
    greenstick fractures, or complete fractures of both
    bones. As with other pediatric fractures, treatment depends on fracture type and location, adequacy of reduction, associated soft-tissue injuries, and the age of
    the patient.7 A thorough evaluation includes assessment
    for associated injuries, especially to the wrist or elbow.
    Most fractures in the diaphysis of the forearm in
    children can be treated with closed reduction and immobilization in a cast.8,9 Plastic deformation is a deforming injury to the bone without frank fracture and
    results in painful, visibly bent bones. If reduction is required (greater than 20 of angulation), steady threepoint bend pressure sustained over minutes may be
    needed. Cast immobilization provides protection and
    pain reduction. Greenstick fractures are well treated
    with closed reduction and well-molded casting (Figure 1).
    Patient age and fracture location help define acceptable alignment with more remodeling potential in
    younger children and in those with more distal fractures. Ten degrees of angulation, bayonet apposition,
    and 30 of malrotation are well tolerated in complete
    diaphyseal fractures in children age 10 years or
    younger.10 Children younger than 8 years can tolerate
    up to 20 of angulation, full translation, and up to 45
    of malrotation.11 Except for obvious malrotation, the
    assessment of rotation is challenging and may be detected on forearm radiographs as a mismatch of cortical thickness at the fracture site or in the relationship
    between the bicipital tuberosity and the radial styloid
    on an AP radiograph, which should be 180 from each
    other. Close monitoring in the cast with weekly radiographs for the first 3 to 4 weeks following reduction allows identification and treatment of unstable fractures.
    A full treatment course is often 6 to 12 weeks of immobilization. Complications can occur with these injuries.
    Malunion may decrease forearm rotation and, if insuf-

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Trauma of the forearm and hand are among the most


    common injuries sustained in children, representing
    over 40% of all fractures. Injuries are slightly more
    common in boys and usually result from falls, sports
    participation, or the use of playground equipment.1
    Most injuries occur in isolation. In the multitrauma setting, management becomes prioritized by the primary
    and secondary survey.
    Management of fractures depends on the fracture
    pattern (torus, greenstick, complete, or plastic deformation), the fracture location, and the age of the patient.
    Historically, it was widely believed that practically all
    forearm and hand fractures could be managed primarily with closed techniques. It is currently recognized
    that certain fractures are best managed with surgical intervention, yet the bulk of these fractures are managed
    closed.
    The age of the patient and the amount of displacement still guide the treatment plan, but other factors
    also play a prominent role. The surgeon must consider
    the remodeling potential of the fracture,2,3 the cost to
    the family of surgical care, patient and family expectations, and the familys personal beliefs. Guidelines for
    acceptable alignment provide some direction but are
    not evidence based. These other factors must be considered during shared decision making for each patient.
    Counseling from the outset and careful monitoring of
    unstable fractures should lead to a final result that
    meets the expectations of all parties.
    When fractures require reduction, multiple options
    exist for anesthesia in the emergency department. Options include conscious sedation with nitrous oxide,
    ketamine, or short-acting benzodiazepines with possi-

    ble hematoma block supplementation.4,5 Intravenous


    regional anesthesia has the advantage of avoiding the
    systemic effects of conscious sedation.6

    687

    Section 6: Pediatrics

    Figure 1

    Radiographic studies of a 6-year-old girl with a


    greenstick fracture of the diaphysis of the radius and ulna with approximately 15 of angulation. A, The fracture was treated with closed
    reduction and casting. This resulted in return of
    full forearm motion and good alignment on AP
    (B) and lateral (C) radiographs.

    6: Pediatrics

    ficient growth and remodeling potential remains, corrective osteotomies may be required.12 Refractures occur in 8% of children and often require open reduction
    with internal fixation.
    Indications for surgical intervention include open
    fractures, fractures with significant soft-tissue injury or
    swelling, unstable fractures, and fractures with unacceptable alignment after reduction attempts. Surgical
    techniques include reduction with intramedullary stabilization of both bones, fixation with plating of both
    bones, a hybrid construct with plating of one bone and
    intramedullary fixation of the other, or single-bone fixation combined with long arm casting until union is
    achieved13,14 (Figure 2). When properly executed each
    method provides similar results.
    Compartment syndrome can occur in association
    with forearm fractures treated operatively15 and nonsurgically. Multiple passes with flexible intramedullary
    nails in attempted reduction increases the risk for compartment syndrome.15 A high index of suspicion in
    high-energy injury patterns and early recognition of
    signs including increasing requirement for pain medication can lead to prompt treatment with forearm fasciotomies.16 All open forearm fractures require thorough irrigation and dbridement at the time of injury
    and may be stabilized safely at the same time if deemed
    necessary.17 Healing time may be delayed in 4% to 5%
    of open fractures, but nonunion is rare.
    Galeazzi fractures are fractures of the distal third of
    the radial diaphysis with dislocation at the distal radioulnar joint (DRUJ). The injury occurs infrequently in
    the pediatric population and is most often seen in adolescents. Many of these injuries go unrecognized. Good
    688

    Orthopaedic Knowledge Update 10

    Figure 2

    Radiographic studies of an 8-year-old boy with


    a midshaft forearm fracture of the radius and
    ulna. The ulna fracture, which was open, was
    treated with irrigation and dbridement and
    intramedullary nailing of the ulna combined
    with cast immobilization. A, Radiograph at
    operation. AP (B) and lateral (C) radiographs
    after healing.

    results are achieved with anatomic reduction of the radius fracture (either closed or with open reduction and
    internal fixation) and immobilization of the DRUJ in a
    reduced position. This often requires supination of the
    forearm, or in very rare instances, pinning of the DRUJ
    in a reduced position.18

    Distal Radius and Ulna Metaphyseal Fractures


    Fractures of the distal radius metaphysis occur in all
    age groups, but the peak incidence occurs during the
    adolescent growth spurt.1,19 High-resolution peripheral
    quantitative CT has shown transient changes in the
    bone architecture during the latter half of puberty. The
    proportion of load borne by cortical bone decreases
    and the porosity of the cortex increases, which may explain this phenomenon.20
    Torus fractures of the metaphysis are inherently stable. They heal uneventfully in 3 weeks with treatment in
    a below-elbow cast or a removable splint. Previous
    studies reported comparable outcomes but superior patient and parent satisfaction when patients were treated
    with a removable device that could be discontinued at
    home.21-23 More recent work, however, showed that patients treated with a removable splint experienced pain
    for a longer period of time and required more time to

    2011 American Academy of Orthopaedic Surgeons

    Chapter 54: Forearm, Wrist, and Hand Trauma: Pediatrics

    Table 1

    Acceptable Angulation for Distal Radius Fractures in Degrees


    Age (Years)

    Sagittal Plane, Boys

    Sagittal Plane, Girls

    Frontal Plane

    4-9

    20

    15

    15

    9-11

    15

    10

    11-13

    10

    10

    >13

    (Data from Waters PM, Mih AD: Fractures of the distal radius and ulna, in Beaty JH, Kasser JR, eds: Rockwood and Wilkins Fractures in Children, ed 6. Philadephia, PA,
    Lippincott Williams & Wilkins, 2006, p 370.)

    2011 American Academy of Orthopaedic Surgeons

    redisplacement is higher and the potential for remodeling is lower. Percutaneous fixation also provides stability when excessive swelling, soft-tissue concerns, or
    neurologic symptoms preclude immobilization with a
    snug cast.7 Pin configurations include metaphyseal pins,
    smooth transphyseal pins, and transradioulnar pin fixation.29,30 Rare considerations with these methods include early physeal arrest with transphyseal pinning31
    and formation of a radioulnar synostosis with transradioulnar pin fixation.

    Distal Radius and Ulna Physeal Fractures


    Physeal fractures of the distal radius and ulna are 20%
    of the physeal fractures sustained by children.7 This
    area has the largest remodeling potential of all forearm
    fractures, but growth disturbance remains a concern.
    The fractures occur most commonly in adolescents, so
    the proximity to skeletal maturity becomes an important factor in guidelines for acceptable alignment.
    Fractures requiring reduction should be reduced as
    gently as possible with adequate sedation and muscle
    relaxation to minimize injury to the physis. Fractures
    present longer than 1 week should not be reduced because of the risk of iatrogenic injury to the physis.32 In
    children with significant growth remaining at the time
    of injury, fractures can be followed after healing to detect growth arrest, which occurs in approximately 1%
    to 7% of these injuries. If growth potential is preserved, the patient can still benefit from fracture remodeling, and a corrective osteotomy can be performed
    at skeletal maturity if the deformity remains excessive.
    Fractures determined to be markedly unstable at reduction can be supplemented with smooth wire fixation to
    enhance stability. Though rare, displaced intra-articular
    fractures of the distal radial epiphysis require anatomic
    reduction and stabilization.
    Ulnar styloid fractures have a low rate of union. A
    review of 46 ulnar styloid fractures associated with distal radius fractures revealed a nonunion rate of 80%
    (Figure 3). Seven patients developed symptomatic nonunions, and all were found to have pathology involving
    the triangular fibrocartilage complex (TFCC).33 Persistent symptoms on the ulnar side of the wrist warrant
    investigation of the integrity of the TFCC. Physeal frac-

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    resume their normal activity level.24 Parents can thus


    choose between the convenience of a removable splint
    with the possibility of some increased discomfort early
    in the healing process, or better control of pain but potentially more difficulties related to a cast. Careful interpretation of radiographs is mandatory to differentiate
    between a true torus fracture that is amenable to this
    treatment protocol and a subtle nondisplaced greenstick
    fracture that has a higher risk of displacement.
    Greenstick fractures and complete fractures of the
    metaphyseal region may be unstable and require close
    monitoring. Acceptable alignment for metaphyseal
    fractures with displacement depends on age (Table 1).
    Greenstick fractures of the metaphysis are potentially
    unstable and should be monitored closely. The proximity to the physis gives the surgeon some leeway in the
    amount of acceptable displacement. Recent work suggests that fractures with minimal displacement (15 or
    less of angulation on the sagittal view and 0.5 cm of
    displacement) have low risk of displacement when
    monitored closely and managed in an appropriately
    molded cast.3 With this protocol more than 85% of patients fractures healed with less than 20 of angulation,
    and all patients had normal function at 6 weeks. The
    potential for displacement, however, is well established.
    Close observation with weekly radiographs can help
    prevent the unpleasant surprise of a deformed arm
    when the cast is removed after several weeks (Figure 3).
    Complete metaphyseal fractures requiring reduction
    have a high risk of redisplacement, particularly in children older than 10 years. Loss of reduction remains
    problematic and exceeds 30% in some series. Short arm
    casts and long arm casts are equally effective provided
    they are appropriately applied with careful molding.9,25
    A prospective study of 75 distal radial fractures requiring reduction showed that initial complete displacement, the degree of obliquity of the fracture line, and
    the quality of casting technique are correlated with loss
    of reduction.26 Defined as the ratio of the width of the
    cast in the sagittal view to the width of the cast in the
    coronal view at the fracture, a cast index of less than
    0.7 was associated with a low rate of remanipulation.27
    Closed reduction with percutaneous fixation has
    been shown to reduce the rate of redisplacement of
    fractures requiring reduction.28 This approach has been
    recommended for older children because their risk of

    689

    Section 6: Pediatrics

    Figure 3

    AP (A) and lateral (B) radiographs of the wrist of a 13-year-old boy with distal metaphyseal fractures of the radius
    and ulna with an associated ulnar styloid fracture. Good reduction was achieved on AP (C) and lateral (D) radiographs, but reduction was lost over the first 2 weeks of sugar tong splint treatment as shown on the lateral radiograph (E). The patient underwent closed reduction and percutaneous pin fixation as seen on AP (F) and lateral (G)
    radiographs. he fracture healed and the patient returned to full activities without pain despite ulnar styloid nonunion (H and I).

    6: Pediatrics

    tures of the distal ulna have a significantly higher risk


    of growth arrest (50%) than fractures of the distal radius.34 This fact should be conveyed to families of children with this injury, and the patients should be followed after healing to detect growth disturbance.

    Carpal Injuries

    Scaphoid Fractures
    Injuries to the carpal bones are rare in children. Most
    carpal injuries in children are scaphoid fractures and occur after age 11 years. Wrist and snuffbox tenderness
    are suggestive of fracture. Early plain radiographs may
    not reveal the fracture, and inadequate treatment can
    690

    Orthopaedic Knowledge Update 10

    lead to nonunion. Therefore, children with suspected


    injury should be immobilized in a thumb spica cast with
    repeat radiographs at 10 to 14 days after injury, and
    cast wear should be continued if there is evidence of
    fracture. Authors of a 2009 study found that 30% of
    pediatric patients with suspected injury treated in this
    manner went on to have radiographic evidence of scaphoid fracture at follow-up. 35 According to results from
    a 2007 study, 94% of pediatric patients with scaphoid
    fractures had good or excellent results by objective and
    self-assessment scores.36 Treatment of documented fractures follows the general recommendations of immobilization for nondisplaced fractures, closed or open reduction with compression screw fixation for displaced
    fractures, and surgical treatment of nonunions.37

    2011 American Academy of Orthopaedic Surgeons

    Chapter 54: Forearm, Wrist, and Hand Trauma: Pediatrics

    Table 2

    Hand Fractures Requiring Surgical Treatment in Children


    Potential Complications
    of Missed Injury

    Fracture

    Treatment

    Phalangeal neck fracture

    Reduction of the extension at the fracture


    and pin fixation

    Loss of flexion

    Phalangeal condyle fracture

    Reduction of intra-articular fracture with


    pin fixation

    Malunion and loss of motion

    Seymour fracture (open Salter-Harris type I or II


    fracture of distal phalanx with interposition
    of germinal matrix into physis)

    Nail plate removal, irrigation and


    dbridement, reduction of open
    fracture, nail bed repair

    Osteomyelitis and nail


    abnormalities

    Metacarpal and phalangeal shaft fractures

    Reduction of malrotation and pin fixation

    Malrotation

    Bennett fracture (intra-articular fracture of the


    thumb metacarpal base)

    Reduction of the shortening, angulation,


    and malrotation at the fracture and pin
    fixation

    Malunion and arthritis

    Gamekeepers fracture (Salter-Harris type III


    intra-articular fracture at thumb proximal
    phalanx)

    Open reduction of intra-articular fracture


    with pin fixation

    Nonunion and instability

    Fractures of Other Carpal Bones


    Fractures and injuries to other carpal bones are rare,
    and mainly case reports exist. These include transscaphoid perilunate dislocations, pisiform fracturedislocations associated with distal radius fractures,38
    and trapezial fractures associated with first carpal
    metacarpal dislocations.39 Many of these fractures are
    associated with other wrist injuries, and treatment is individualized.

    Hand Injuries
    The hand is the most frequently injured part of the
    body in children. The patterns and mechanisms of injury differ between age groups, with more soft-tissue
    crush injuries in toddlers and primarily bony sports injuries in older children.40 The small finger and its metacarpal are most commonly fractured followed by the
    thumb. Phalangeal fractures are slightly more common
    than metacarpal fractures. Most of these injuries are
    best treated nonsurgically.41

    Hand Fractures and Dislocations

    2011 American Academy of Orthopaedic Surgeons

    6: Pediatrics

    Most phalangeal fractures occur at the base or the


    proximal metaphysis, are minimally displaced, and require nonsurgical treatment with buddy taping or
    splinting. Metacarpal fractures most commonly are diaphyseal and should be scrutinized for malrotation.
    Some pediatric hand fractures require surgical intervention, and these are detailed in Table 2. Phalangeal
    neck fractures frequently have a rotation and extension
    deformity that requires closed reduction and pin fixation to prevent loss of flexion.41-43 Phalangeal condyle
    fractures are intra-articular, and most require reduction
    and pinning (Figure 4). Seymour fractures are open

    Figure 4

    A 15-year-old boy presented for treatment 6


    weeks after sustaining a unicondylar fracture
    of the middle phalanx. AP (A) and oblique (B)
    radiographs show intra-articular displacement
    and moderate healing. When unrecognized, this
    fracture will heal with limited motion at the
    distal interphalangeal joint.

    Orthopaedic Knowledge Update 10

    691

    Section 6: Pediatrics

    patients younger than 5 years, complete laceration, or


    zone I, II, or III injury). Mallet finger injuries occur
    more commonly in adolescents and are treated in the
    same manner as in adults.

    Flexor Tendon Injuries


    Flexor tendon injuries in children most often occur as a
    result of a cut by glass. These injuries may be difficult
    to diagnose depending on patient age and cooperation.
    Complete laceration can alter the resting posture of the
    hand. Early diagnosis and repair with techniques used
    in adults leads to good results in children.45-47 There is
    controversy surrounding postoperative protocols, with
    both full immobilization and early mobilization methods showing good results.48

    Annotated References

    Figure 5

    A nondisplaced fracture of the base of the thumb


    metacarpal in a 9-year-old boy healed with
    closed treatment and weekly monitoring with
    radiographs. These fractures may displace and
    then require reduction and percutaneous pin
    fixation until union.

    6: Pediatrics

    Salter-Harris type I or II fractures of the distal phalanx


    with a tear of the germinal matrix and interposition of
    soft tissue into the physis. These fractures should be
    treated with nail plate removal; irrigation and dbridement; reduction of the open fracture; nail bed repair;
    and replacement of the nail plate into the eponychial
    fold. Phalangeal and metacarpal fractures associated
    with malrotation should be reduced and stabilized until
    healed. Intra-articular fractures of the first metacarpal
    base (Bennett fractures) may displace due to the pull of
    the abductor pollicus longus on the distal radial fragment. Displaced fractures here require reduction of the
    shortened, angled, and rotated fragments with percutaneous pins until fracture union (Figure 5). Although
    older children and teens may sustain an ulnar collateral
    ligament injury at the thumb metacarpophalangeal
    joint, more commonly the same mechanism results in a
    Salter-Harris type III intra-articular fracture at the
    thumb proximal phalanx. If the fracture is displaced,
    open reduction and pinning are necessary.

    1.

    Beaty J, Kasser J, eds: Rockwood and Wilkins Fractures in Children, ed 6. Philadelphia, PA, Lippincott
    Williams & Wilkins, 2006.

    2.

    Do TT, Strub WM, Foad SL, Mehlman CT, Crawford


    AH: Reduction versus remodeling in pediatric distal
    forearm fractures: A preliminary cost analysis. J Pediatr
    Orthop B 2003;12(2):109-115.

    3.

    Al-Ansari K, Howard A, Seeto B, Yoo S, Zaki S, Boutis


    K: Minimally angulated pediatric wrist fractures: Is immobilization without manipulation enough? CJEM
    2007;9(1):9-15.
    This retrospective cohort study examined bicortical distal radius fractures with minimal angulation (15 of
    sagittal plane angulation and 0.5 cm of displacement).
    Most patients (89%) healed with less than 20 of angulation. Level of evidence: IV.

    4.

    Marcus RJ, Thompson JP: Anaesthesia for manipulation of forearm fractures in children: A survey of current practice. Paediatr Anaesth 2000;10(3):273-277.

    5.

    Cimpello LB, Khine H, Avner JR: Practice patterns of


    pediatric versus general emergency physicians for pain
    management of fractures in pediatric patients. Pediatr
    Emerg Care 2004;20(4):228-232.

    6.

    Werk LN, Lewis M, Armatti-Wiltrout S, Loveless EA:


    Comparing the effectiveness of modified forearm and
    conventional minidose intravenous regional anesthesia
    for reduction of distal forearm fractures in children.
    J Pediatr Orthop 2008;28(4):410-416.
    Sixty-two patients with acute forearm fractures requiring reduction in the emergency department were randomized to conventional minidose or modified forearm
    intravenous regional anesthesia. Outcomes were similar.
    Level of evidence: I.

    7.

    Bae DS: Pediatric distal radius and forearm fractures.


    J Hand Surg Am 2008;33(10):1911-1923.
    A comprehensive review of the literature is presented.

    Extensor Tendon Injuries


    Extensor tendon injuries are much less common than
    flexor tendon injuries in children. They can be detected
    with loss of tenodesis of the fingers with flexion and
    extension of the wrist. In a retrospective study of primary repair and outcome, 98% of patients had good or
    excellent total active motion.44 Twenty-two percent had
    some extension lag or loss of flexion (more likely with
    692

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 54: Forearm, Wrist, and Hand Trauma: Pediatrics

    Eberl R, Singer G, Schalamon J, Petnehazy T, Hoellwarth ME: Galeazzi lesions in children and adolescents:
    Treatment and outcome. Clin Orthop Relat Res 2008;
    466(7):1705-1709.
    In this retrospective study of Galeazzi fractures in children, 31% were initially recognized. Twenty-two of 26
    patients were treated with reduction and a long or short
    arm cast, and 4 of 26 were treated surgically. Outcomes
    were good (3 patients) or excellent (23 patients) in all
    cases. Level of evidence: IV.

    19.

    Hove LM, Brudvik C: Displaced paediatric fractures of


    the distal radius. Arch Orthop Trauma Surg 2008;
    128(1):55-60.
    The authors examined incidence, fracture pattern, treatment, and radiologic outcome of all pediatric distal radius fractures treated in a single city in 1 year.

    20.

    Kirmani S, Christen D, van Lenthe GH, et al: Bone


    structure at the distal radius during adolescent growth.
    J Bone Miner Res 2009;24(6):1033-1042.
    The authors performed high-resolution peripheral quantitative CT on healthy children 6 to 21 years of age.
    Bone strength increased with age, but the porosity of
    cortical bone peaked transiently during puberty.

    21.

    Abraham A, Handoll HH, Khan T: Interventions for


    treating wrist fractures in children. Cochrane Database
    Syst Rev 2008;2:CD004576.
    The authors performed a systematic review of 10 randomized controlled trials treating pediatric distal radius
    fractures to determine risks and benefits of various
    methods of treatment. Level of evidence: II.

    22.

    Reinhardt KR, Feldman DS, Green DW, Sala DA, Widmann RF, Scher DM: Comparison of intramedullary
    nailing to plating for both-bone forearm fractures in
    older children. J Pediatr Orthop 2008;28(4):403-409.

    Plint AC, Perry JJ, Correll R, Gaboury I, Lawton L: A


    randomized, controlled trial of removable splinting versus casting for wrist buckle fractures in children. Pediatrics 2006;117(3):691-697.

    23.

    This study retrospectively compared functional and radiographic outcomes of length-stable both-bone forearm
    fractures that were treated with intramedullary fixation
    or compression plating in children 10 to 16 years of age,
    Outcomes and rates of complications were comparable.
    Level of evidence: III.

    Symons S, Rowsell M, Bhowal B, Dias JJ: Hospital versus home management of children with buckle fractures
    of the distal radius: A prospective, randomised trial.
    J Bone Joint Surg Br 2001;83(4):556-560.

    24.

    Oakley EA, Ooi KS, Barnett PL: A randomized controlled trial of 2 methods of immobilizing torus fractures of the distal forearm. Pediatr Emerg Care 2008;
    24(2):65-70.
    Children with distal radius torus fractures were randomized to a volar fiberglass splint or a short arm plaster cast.
    Patients treated with a splint had increased duration of
    pain (P = 0.009) and took more time to resume normal
    activities (P = 0.001). Patients wearing a cast had significantly more problems with the appliance (P = 0.004).
    Level of evidence: II.

    25.

    Bohm ER, Bubbar V, Yong Hing K, Dzus A: Above and


    below-the-elbow plaster casts for distal forearm fractures in children: A randomized controlled trial. J Bone
    Joint Surg Am 2006;88(1):1-8.

    26.

    Alemdaroglu KB, Iltar S, Cimen O, Uysal M, Alagz E,


    Atlihan D: Risk factors in redisplacement of distal ra-

    Zionts LE, Zalavras CG, Gerhardt MB: Closed treatment of displaced diaphyseal both-bone forearm fractures in older children and adolescents. J Pediatr Orthop 2005;25(4):507-512.

    9.

    Webb GR, Galpin RD, Armstrong DG: Comparison of


    short and long arm plaster casts for displaced fractures
    in the distal third of the forearm in children. J Bone
    Joint Surg Am 2006;88(1):9-17.

    10.

    Price CT, Scott DS, Kurzner ME, Flynn JC: Malunited


    forearm fractures in children. J Pediatr Orthop 1990;
    10(6):705-712.

    11.

    Ploegmakers JJ, Verheyen CC: Acceptance of angulation


    in the non-operative treatment of paediatric forearm
    fractures. J Pediatr Orthop B 2006;15(6):428-432.

    12.

    Price CT, Knapp DR: Osteotomy for malunited forearm


    shaft fractures in children. J Pediatr Orthop 2006;26(2):
    193-196.
    The authors performed radius and ulna osteotomies for
    nine malunited forearm fractures in this retrospective
    case series. The average improvement in forearm rotation was 102 after correction. Level of evidence: IV.

    13.

    Garg NK, Ballal MS, Malek IA, Webster RA, Bruce CE:
    Use of elastic stable intramedullary nailing for treating
    unstable forearm fractures in children. J Trauma 2008;
    65(1):109-115.
    In this retrospective study of children with unstable
    forearm fractures that were treated with flexible intramedullary nails, the authors found a delayed union
    and a nonunion. Overall, complications were considered
    few, and functional outcome was good. Level of evidence: IV.

    14.

    15.

    Yuan PS, Pring ME, Gaynor TP, Mubarak SJ, Newton


    PO: Compartment syndrome following intramedullary
    fixation of pediatric forearm fractures. J Pediatr Orthop
    2004;24(4):370-375.

    16.

    Bae DS, Kadiyala RK, Waters PM: Acute compartment


    syndrome in children: Contemporary diagnosis, treatment, and outcome. J Pediatr Orthop 2001;21(5):680688.

    17.

    Luhmann SJ, Schootman M, Schoenecker PL, Dobbs


    MB, Gordon JE: Complications and outcomes of open
    pediatric forearm fractures. J Pediatr Orthop 2004;
    24(1):1-6.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    18.

    8.

    693

    Section 6: Pediatrics

    In this retrospective study, 30% of pediatric patients


    with suspected but radiographically negative scaphoid
    fractures went on to show radiographic evidence of
    fracture at 1.5 to 2-week follow-up. The authors recommend thumb spica immobilization of suspected scaphoid fractures until follow-up radiographs are normal.
    Level of evidence: IV.

    dial fractures in children. J Bone Joint Surg Am 2008;


    90(6):1224-1230.
    The authors prospectively analyzed 75 displaced or severely angulated pediatric wrist fractures. Completely
    displaced fractures were 11.7 times more likely to redisplace after reduction than angulated fractures. The degree of obliquity of the fracture line was also strongly
    correlated with redisplacement. Level of evidence: I.
    27.

    28.

    McLauchlan GJ, Cowan B, Annan IH, Robb JE: Management of completely displaced metaphyseal fractures
    of the distal radius in children: A prospective, randomised controlled trial. J Bone Joint Surg Br 2002;
    84(3):413-417.

    29.

    Jung HJ, Jung YB, Jang EC, et al: Transradioulnar single Kirschner-wire fixation versus conventional
    Kirschner-wire fixation for unstable fractures of both of
    the distal forearm bones in children. J Pediatr Orthop
    2007;27(8):867-872.
    The authors describe a technique to treat unstable distal
    both-bone forearm fractures with a single Kirschner
    wire traversing the radius and the ulna without violating
    the physis. Cases were compared with a historical group
    treated with conventional pinning techniques. Outcomes
    were similar. Level of evidence: III.

    30.

    Choi KY, Chan WS, Lam TP, Cheng JC: Percutaneous


    Kirschner-wire pinning for severely displaced distal radial fractures in children: A report of 157 cases. J Bone
    Joint Surg Br 1995;77(5):797-801.

    31.

    Boyden EM, Peterson HA: Partial premature closure of


    the distal radial physis associated with Kirschner wire
    fixation. Orthopedics 1991;14(5):585-588.

    32.

    Waters PM, Bae DS, Montgomery KD: Surgical management of posttraumatic distal radial growth arrest in
    adolescents. J Pediatr Orthop 2002;22(6):717-724.

    6: Pediatrics

    33.

    34.

    35.

    694

    36.

    Chess DG, Hyndman JC, Leahey JL, Brown DC, Sinclair AM: Short arm plaster cast for distal pediatric
    forearm fractures. J Pediatr Orthop 1994;14(2):211213.

    Abid A, Accadbled F, Kany J, de Gauzy JS, Darodes P,


    Cahuzac JP: Ulnar styloid fracture in children: A retrospective study of 46 cases. J Pediatr Orthop B 2008;
    17(1):15-19.
    Forty-six ulnar styloid fractures associated with distal
    radius fractures were reviewed retrospectively. Eighty
    percent failed to unite. All patients with chronic symptoms had pathology involving the TFCC. Level of evidence: IV.
    Golz RJ, Grogan DP, Greene TL, Belsole RJ, Ogden JA:
    Distal ulnar physeal injury. J Pediatr Orthop 1991;
    11(3):318-326.
    Evenski AJ, Adamczyk MJ, Steiner RP, Morscher MA,
    Riley PM: Clinically suspected scaphoid fractures in
    children. J Pediatr Orthop 2009;29(4):352-355.

    Orthopaedic Knowledge Update 10

    Huckstadt T, Klitscher D, Weltzien A, Mller LP, Rommens PM, Schier F: Pediatric fractures of the carpal scaphoid: A retrospective clinical and radiological study.
    J Pediatr Orthop 2007;27(4):447-450.
    In this retrospective study, 22 pediatric patients with
    scaphoid fractures were reviewed, with 17 receiving cast
    immobilization and 5 requiring open reduction and
    screw fixation for displacement or nonunion. A total of
    94% were scored good or excellent by the Cooney score
    and by patient self-assessment. Level of evidence: IV.

    37.

    Henderson B, Letts M: Operative management of pediatric scaphoid fracture nonunion. J Pediatr Orthop
    2003;23(3):402-406.

    38.

    Mancini F, De Maio F, Ippolito E: Pisiform bone


    fracture-dislocation and distal radius physeal fracture in
    two children. J Pediatr Orthop B 2005;14(4):303-306.

    39.

    Parker WL, Czerwinski M, Lee C: First carpalmetacarpal joint dislocation and trapezial fracture
    treated with external fixation in an adolescent. Ann
    Plast Surg 2008;61(5):506-510.
    This case report describes this extremely rare injury in a
    teenager who had a good outcome and recommends external fixation as a possible treatment in the pediatric
    population. Level of evidence: V.

    40.

    Vadivelu R, Dias JJ, Burke FD, Stanton J: Hand injuries


    in children: A prospective study. J Pediatr Orthop 2006;
    26(1):29-35.

    41.

    Valencia J, Leyva F, Gomez-Bajo GJ: Pediatric hand


    trauma. Clin Orthop Relat Res 2005;432(432):77-86.

    42.

    Cornwall R, Ricchetti ET: Pediatric phalanx fractures:


    Unique challenges and pitfalls. Clin Orthop Relat Res
    2006;445:146-156.

    43.

    Waters PM: Operative carpal and hand injuries in children. J Bone Joint Surg Am 2007;89(9):2064-2074.
    The authors present a review of surgically treated injuries in children. Level of evidence: V.

    44.

    Fitoussi F, Badina A, Ilhareborde B, Morel E, Ear R,


    Penneot GF: Extensor tendon injuries in children. J Pediatr Orthop 2007;27(8):863-866.
    This retrospective study of extensor tendon repairs in
    children showed 98% good or excellent total active motion. Twenty-two percent had extension lag or flexion
    loss that was more likely in patients younger than 5
    years, complete laceration, or zone I, II, or III injury.
    Level of evidence: IV.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 54: Forearm, Wrist, and Hand Trauma: Pediatrics

    45.

    Nietosvaara Y, Lindfors NC, Palmu S, Rautakorpi S,


    Ristaniemi N: Flexor tendon injuries in pediatric patients. J Hand Surg Am 2007;32(10):1549-1557.
    This retrospective study of children who underwent
    flexor tendon repair showed good subjective and objective outcomes with multistrand repair at all levels with
    an active-motion rehabilitation program. Level of evidence: IV.

    46.

    Darlis NA, Beris AE, Korompilias AV, Vekris MD, Mitsionis GI, Soucacos PN: Two-stage flexor tendon reconstruction in zone 2 of the hand in children. J Pediatr Orthop 2005;25(3):382-386.

    47.

    Kato H, Minami A, Suenaga N, Iwasaki N, Kimura T:


    Long-term results after primary repairs of zone 2 flexor
    tendon lacerations in children younger than age 6 years.
    J Pediatr Orthop 2002;22(6):732-735.

    48.

    Moehrlen U, Mazzone L, Bieli C, Weber DM: Early mobilization after flexor tendon repair in children. Eur J
    Pediatr Surg 2009;19(2):83-86.
    This retrospective study of children who underwent
    flexor tendon repair and an age-adapted early motion
    rehabilitation protocol showed 93% total active motion
    and 93% good or excellent results. Level of evidence:
    IV.

    6: Pediatrics

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    695

    Chapter 55

    Upper Extremity Disorders:


    Pediatrics
    Dan A. Zlotolow, MD

    Scott H. Kozin, MD

    Introduction

    Dr. Zlotolow or an immediate family member is an unpaid consultant to Arthrex and serves as a board member, owner, officer, or committee member of the American Society for Surgery of the Hand. Dr. Kozin or an
    immediate family member serves as a board member,
    owner, officer, or committee member of the American
    Society for Surgery of the Hand.

    2011 American Academy of Orthopaedic Surgeons

    Figure 1

    6: Pediatrics

    Upper limb deformities make up a full 10% of all congenital anomalies, second only in incidence to cardiac
    anomalies.1 Although teratogens often are blamed for
    such congenital differences, most occur spontaneously
    or are genetically determined. Many deformities, such
    as thrombocytopenia-absent radius, follow a set pattern, and others, such as central deficiencies and symbrachydactyly, have a spectrum of phenotypic variants
    that make them difficult to classify.
    Recent advances in cell-signaling research have enriched our understanding of anomalous limb development. The limb bud begins to develop 26 days after fertilization, when the embryo is smaller than a grain of
    rice. By the eighth week, the embryo is approximately
    1 inch in length, and the upper limb is fully formed
    (Figure 1). Congenital deformities that affect limb formation occur during this period. Further differentiation
    and growth of the limbs occurs during the subsequent
    fetal period. Longitudinal growth of the limb is coordinated by the apical ectodermal ridge (AER), an ectodermal condensation that forms a cap over the lengthening
    limb. Lateral plate mesoderm (destined to become
    bone, cartilage, and tendon) and somatic mesoderm
    (muscle, nerve, and vasculature) grow out from the embryo under the AER.2 Anteroposterior radioulnar differentiation is determined by the zone of polarizing activity (ZPA) through the sonic hedgehog pathway.
    Duplication of the ZPA results in mirror-image duplication of the limb. Dorsoventral development is coordinated by the wingless-type signaling pathway in the
    dorsal non-AER ectoderm. Removal of the AER results
    in a truncated limb, but its influence on the underlying
    mesoderm can be overcome by the addition of fibroblast growth factors to the apex of the limb bud.3 The

    ZPA also is necessary for longitudinal growth via induction of the gremlin protein. Both gremlin and bone
    morphogenetic proteins are produced in the growing
    limb mesoderm. The antagonistic effects of gremlin on
    bone morphogenetic proteins prevent premature limb
    maturation and cessation of longitudinal development.4
    The wingless-type signaling pathway also is necessary
    for longitudinal growth because it influences the establishment and maintenance of the AER.5
    The most commonly used classification scheme is
    based on the understanding of embryogenesis, but it is
    limited because of its reliance on clinical judgment as
    well as the overlap of deformities (Table 1). Great variations in the clinical appearance of the same embryologic malformation can challenge the clinician who is
    trying to identify an anomaly. Often, the pattern of deformity (one or all limbs affected) and its associations
    (for example, Poland syndrome in symbrachydactyly)
    offer clues to accurate diagnosis and classification. At
    initial diagnosis, the primary goal of the surgeon is to

    Schematic drawings showing the development of


    the limb bud in a proximal-to-distal direction
    coordinated by the apical ectodermal ridge
    (AER). The zone of polarizing activity (ZPA) signals the differentiation of radius- and ulna-side
    structures. A, The limb bud in the frontal plane.
    B, A cross section of the limb bud at the dashed
    line shown in A. (Adapted with permission from
    Daluiski A, YiS E, Lyons KM: The molecular control of upper extremity development: Implications for congenital hand anomalies. J Hand
    Surg Am 2001;26[1]:8-22.)

    Orthopaedic Knowledge Update 10

    697

    Section 6: Pediatrics

    assist the family in understanding and coping with the


    childs condition.

    Failure of Formation

    Radial Longitudinal Deficiencies


    Two thirds of all radial longitudinal deficiencies are diagnosed as part of a syndrome, often involving the

    Table 1

    The Embryologic Classification


    of Congenital Anomalies
    Primary Classification

    Secondary Classification

    I. Failure of formation

    A. Transverse arrest
    B. Longitudinal arrest

    II. Failure of differentiation

    A. Soft tissue
    B. Skeletal
    C. Tumorous

    III. Duplication

    A. Whole limb
    B. Humeral
    C. Radial
    D. Ulnar
    E. Digit

    IV. Overgrowth

    A. Whole limb
    B. Partial limb
    C. Digit

    V. Undergrowth

    A. Whole limb
    B. Whole hand
    C. Metacarpal
    D. Digit

    VI. Constriction band


    syndrome
    VII. Generalized skeletal
    abnormality

    heart, kidney, bone marrow, or gastrointestinal tract.


    The more severe the deficiency, the more likely it is to
    be associated with a syndrome.6 Half of these deficiencies are bilateral. Boys are more often affected than
    girls, by a ratio of 3 to 2. The occurrence usually is sporadic, with minimal influence of family history. Radial
    longitudinal deficiency may be the only observable sign
    of a syndrome, and its presence should trigger a full
    workup of the heart, kidney, bone marrow, and gastrointestinal tract, as well as a general pediatric orthopaedic examination. A chromosomal challenge test should
    be performed to detect Fanconi anemia before bone
    marrow failure can occur.7
    The classification is based upon the extent of deficiency, from thumb hypoplasia to complete absence of
    the radius (Table 2). Complete absence of the radius is
    most common, accompanied by a shortened forearm
    segment and a radial deviation of the wrist. The ulna is
    typically 60% shorter on the affected side than on the
    contralateral side, and often it is bowed and thickened8
    (Figure 2).
    Thrombocytopenia-Absent Radius Syndrome
    Thrombocytopenia-absent radius syndrome is characterized by complete bilateral absence of the radii and
    preservation of the thumbs (Figure 2). Its incidence is
    1 to 2 per 1 million live births.9 Although the phenotype is well understood, the predominantly autosomal
    recessive genotype is only beginning to be determined.
    Transient hypomegakaryotic thrombocytopenia is present at birth and tends to improve if the child survives
    the first year of life.
    Fanconi Anemia
    Fanconi anemia is a pancytopenia associated with radial longitudinal deficiency. Unlike thrombocytopeniaabsent radius syndrome, this hematologic disorder appears when the child is age 3 to 12 years. The diagnosis

    Table 2

    The Global Classification of Radial Longitudinal Deficiencies

    6: Pediatrics

    Type

    Thumb

    Carpusa

    Distal Radius

    Proximal Radius

    Absence or hypoplasia

    Normal

    Normal

    Normal

    Absence or hypoplasia

    Absence, hypoplasia,
    or coalition

    Normal

    Normal, radioulnar synostosis,


    or radial head dislocation

    Absence or hypoplasia

    Absence, hypoplasia,
    or coalition

    >2 mm shorter than ulna

    Normal, radioulnar synostosis,


    or radial head dislocation

    Absence or hypoplasia

    Absence, hypoplasia,
    or coalition

    Hypoplasia

    Hypoplasia

    Absence or hypoplasia

    Absence, hypoplasia,
    or coalition

    Physis absence

    Variable hypoplasia

    Absence or hypoplasia

    Absence, hypoplasia,
    or coalition

    Absence

    Absence

    A carpal anomaly implies hypoplasia, coalition, absence, or bipartite carpal bones. Hypoplasia and absence are more common on the radial side of the carpus, and
    coalitions are more frequent on the ulnar side. Radiographic findings are valid only if the child is older than 8 years, to allow for ossification of the carpal bones.

    698

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 55: Upper Extremity Disorders: Pediatrics

    Figure 2

    A child with thrombocytopenia-absent radius syndrome. Ulnar bowing at the forearm and preservation of the
    thumb can be seen in the AP radiograph of the hand and lateral forearm (A) and a photograph (B). (Courtesy of
    Shriners Hospital for Children, Philadelphia, PA.)

    can easily be missed, with tragic consequences. Every


    child with any radial longitudinal deficiency should undergo a chromosomal challenge test to rule out Fanconi
    anemia. Unless bone marrow transplantation is successful, the pancytopenia is progressive and lethal. Children
    with Fanconi anemia are susceptible to acute myelogenous leukemia as well as solid tumors of the head,
    neck, breast, liver, esophagus, and vulva. The pancytopenia may be accompanied by anomalies in other organ systems, including the skin and kidneys.10

    Holt-Oram Syndrome
    With an incidence of 1 per 100,000 live births, HoltOram syndrome is the most common of all heart-limb
    syndromes.10 The severity of the limb deformity is not
    predictive of the extent of cardiac involvement and can
    vary greatly across generations. Most deformities are
    limited to thumb hypoplasia, but more severe radial de-

    2011 American Academy of Orthopaedic Surgeons

    Thumb Hypoplasia
    Radial longitudinal deficiencies may occur without affecting the thumb, as in thrombocytopenia-absent radius syndrome, or may affect only the thumb. As with
    any radius-side deficiency, the presence of an associated
    syndrome or anomaly should be suspected and ruled
    out. Evaluation of a hypoplastic thumb primarily
    hinges on the status of the basal joint. A thumb with a
    stable basal joint usually can be salvaged with a combination of skin flaps, ligament reconstructions, and tendon transfers. An unstable thumb will not function
    well, and the best treatment is ablation and pollicization. The Manske modification of the Blauth classification differentiates types IIIA and IIIB based on basal
    joint stability (Table 3).

    6: Pediatrics

    VACTERL Association
    The term VACTERL association is commonly used to
    include cardiac malformations and limb anomalies in
    association with vertebral defects, anal atresia, tracheoesophageal fistula with esophageal atresia, renal anomalies, and radial dysplasia. At least three systems must
    be affected for the diagnosis of VACTERL association
    to be made. The limb deformities include the spectrum
    of radial longitudinal deficiencies as well as syndactyly
    and polydactyly. No reliable inheritance pattern or teratogenic exposure has been identified for the
    VACTERL association, possibly because it represents a
    common but highly variable phenotypic terminus for
    various chromosomal or environmental insults.

    ficiencies and even ulna-side deficiencies can occur.


    More than 70 mutations in the TBX5 transcription factor gene have been associated with Holt-Oram syndrome. Not all people with a TBX5 mutation have the
    disease, however, and only 35% of patients with the
    syndrome have a TBX5 mutation.11 The inheritance
    pattern is autosomal dominant with variable expression.

    Treatment
    As soon as the diagnosis of radial longitudinal deficiency is made, a passive stretching protocol should be
    instituted under the supervision of a therapist. Tight
    radius-side structures should be stretched every time
    the childs diaper is changed and at bedtime. Progressive splinting can begin as soon as the limb is long
    enough to accommodate it. A severely affected patient

    Orthopaedic Knowledge Update 10

    699

    Section 6: Pediatrics

    Table 3

    The Classification of Thumb Deficiency


    Type

    Clinical Findings

    Treatment

    Minor generalized hypoplasia Augmentation

    II

    Absence of intrinsic thenar


    muscles
    Narrowing of first web space
    Ulnar collateral ligament
    insufficiency

    III

    IIIA: Reconstruction
    Absence of intrinsic thenar
    IIIB: Pollicization
    muscles
    Narrowing of first web space
    Ulnar collateral ligament
    insufficiency
    Extrinsic muscle and tendon
    abnormalities
    Skeletal deficiency
    IIIA: Stable carpometacarpal
    joint
    IIIB: Unstable carpometacarpal
    joint

    IV

    Floating thumb

    Pollicization

    Absence of thumb

    Pollicization

    Opponensplasty
    First web release
    Ulnar collateral
    ligament
    reconstruction

    6: Pediatrics

    or a patient who has undergone unsuccessful nonsurgical management may benefit from centralization procedures to correct the radial deviation of the wrist. An
    older patient who has functionally compensated for the
    deformity, a patient with a proximate terminal condition, or a patient with an extension contracture of the
    elbow who relies on the radial deviation to reach the
    mouth is a poor candidate for any surgical procedure.
    A supposedly successful operation may make such a
    patients condition worse. The results of centralization
    remain unpredictable despite recent technical advances.
    Even when an excellent correction is achieved, recurrence of the deformity is common. An alternative may
    be gradual distraction lengthening of the tight radiusside structures using an Ilizarov-type ring fixator (Figure 3). When correction of the wrist position is
    achieved, a centralization procedure can be performed
    with little to no tension on the radius side. The results
    of this technique have been promising, although recurrence remains a concern.12,13 Ulna lengthening via distraction osteogenesis may need to be performed several
    times to achieve adequate length at maturity. Despite
    high complication rates, ulna lengthening remains appealing because it can improve the use of the hand if
    near-normal length is achieved.14
    The treatment of thumb hypoplasia hinges on the
    stability of the carpometacarpal joint. The child typically does not use the thumb if the basal joint is unstable because insufficient power is available for pinching
    and grasping. As the child grows, he or she will learn to
    bypass the thumb in favor of scissor grasping between
    the index and long fingers. Cortical representation will
    not develop in an unused thumb, and heroic measures
    700

    Orthopaedic Knowledge Update 10

    Figure 3

    Photograph showing the use of a hybrid fixator


    to slowly correct soft-tissue balance before surgical centralization in a child with radial dysplasia. (Courtesy of Shriners Hospital for Children,
    Philadelphia, PA.)

    to salvage such a thumb will not lead to its use. Pollicization is the preferred option because it effectively
    takes advantage of the childs developing indexlong
    finger pinch pattern.
    A type I thumb requires no treatment. A type II
    thumb has deficient intrinsic musculature and can be
    reconstructed with an opponensplasty and a four-flap
    Z-plasty for web space deepening. Ulnar collateral ligament reconstruction and, if necessary, radial collateral
    ligament reconstruction may be accomplished at the
    same time. Pollex abductus (an interconnection between the flexor and extensor systems along the radial
    aspect of the thumb) can occur with a type II or IIIA
    thumb. These thumbs require a pulley reconstruction
    and recentralization of the flexor tendon. A type IIIA
    thumb is missing extrinsic motors and requires tendon
    transfers to provide extensor pollicis longus and/or
    flexor pollicis longus function. A type IIIB, IV, or V
    thumb is best treated with ablation and pollicization
    (Figure 4). The results of pollicization are correlated
    with the condition of the index finger and its associated
    musculature before pollicization.15-17 Children who develop a good grip-and-pinch pattern after pollicization
    are likely to maintain the pattern into adulthood.16

    Ulnar Deficiencies
    Unlike a radius-side deficiency, the loss of ulna-side
    structures in the upper limb rarely is accompanied by
    abnormalities in other organ systems. Concomitant

    2011 American Academy of Orthopaedic Surgeons

    Chapter 55: Upper Extremity Disorders: Pediatrics

    Figure 4

    Type IIIB thumb hypoplasia before (A) and after (B) thumb ablation and index pollicization. It can be difficult for
    parents to understand the need for surgery, particularly if the thumb is of adequate size. However, the function
    and appearance of the hand can be dramatically improved through a well-done pollicization. (Courtesy of Shriners
    Hospital for Children, Philadelphia, PA.)

    Central Deficiencies
    A cleft hand results from a failure of formation of the
    center of the limb. The inherited forms typically become more severe with each generation, and affected
    families should undergo genetic counseling. Sporadic
    incidences may represent a spontaneous mutation. Bi-

    2011 American Academy of Orthopaedic Surgeons

    lateral foot and hand involvement (split handsplit foot


    syndrome) has been located on chromosome 719 (Figure
    6). The clinical deformity ranges from a slightly shortened third ray to only one ulnar digit (in the monodactylous type). Bizarre combinations and orientations of
    the carpals, metacarpals, and phalanges can occur, as
    well as syndactyly and synostoses. The presence of nubbins suggests the diagnosis of an atypical cleft hand
    (symbrachydactyly).
    The cleft hand has been called a functional triumph, yet a social disaster.20 The cleft in a mildly affected hand can be closed to optimize its appearance
    and help the child use the hand to carry small objects
    and liquids. A two-digit hand is cosmetically challenging for most children, but its function is excellent if the
    length of the digits is adequate. Length augmentation
    of the thumb or short finger may be of benefit. Syndactyly releases may be indicated as well. The reconstructive options are limited for a monodactylous hand.
    6: Pediatrics

    skeletal abnormality can exist, however, including preaxial abnormality, fibular hemimelia, or proximal focal
    femoral deficiency (Figure 5). Bilaterality occurs only in
    approximately one quarter of patients.
    The classification is based on the severity of elbow
    and forearm involvement, as well as the condition of
    the thumb and thumbindex finger web space18 (Table
    4). Hand involvement varies greatly, with almost all
    children having absent ulna-side digits, and some children having absent or anomalous radius-side digits.
    The wrist is in mild to moderate ulnar deviation, and
    the forearm segment may be markedly shortened. Elbow range of motion can be limited or absent.
    As with a radial deficiency, the progression of deformity can be limited by early stretching and splinting.
    Corrective procedures can be considered when the child
    is at least 6 months of age. Syndactyly releases and
    deepening of the thumbindex finger web space can improve the appearance and function of the hand. Creation of a one-bone forearm occasionally is necessary
    to stabilize the forearm, but it results in the loss of any
    forearm rotation. Correction of the ulnar deviation
    posture is rarely necessary. No predictable procedures
    exist for restoring elbow motion in these children.

    Symbrachydactyly
    The diagnosis of symbrachydactyly includes a wide
    range from transverse deficiency above the elbow to
    mild hypoplasia of the hand. Unlike cleft hand, symbrachydactyly predominantly affects only one limb.
    The monodactylous form preserves the thumb (Figure
    7). The etiology is believed to be an interruption of the
    vascular supply to the end of the limb, resulting in loss
    of the mesodermal cells destined to become terminal
    limb structures. Transverse deficiencies with nubbin
    formation may indicate that, although the AER contin-

    Orthopaedic Knowledge Update 10

    701

    Section 6: Pediatrics

    Table 4

    The Classification of Ulnar Deficiencies (0-IV)


    and Subgroup Classification by Abnormality of
    the First Web Space (A-D)
    Type

    Grade

    Figure 5

    6: Pediatrics

    Normal forearm
    Deficiencies in hand and carpus

    Hypoplasia

    Hypoplasia of the ulna with


    presence of distal and
    proximal ulnar epiphysis
    Minimal shortening

    II

    Partial aplasia

    Partial aplasia with absence of


    the distal or middle third of
    the ulna

    III

    Complete aplasia Total agenesis of the ulna

    IV

    Synostosis

    Fusion of the radius to the


    humerus

    Subtype Grade

    Characteristics

    Normal

    Normal first web space and


    normal thumb

    Mild

    Mild first web space deficiency


    and mild thumb hypoplasia
    with intact opposition and
    extrinsic tendon function

    Moderate to
    severe

    Moderate to severe first web


    space deficiency and similar
    thumb hypoplasia with
    malrotation into the plane
    of the digits
    Loss of opposition
    Dysfunction of the extrinsic
    tendons

    Absence

    Absence of the thumb

    AP upper (A) and lower (B) extremity radiographs


    of a child with ulnar dysplasia with thumb duplication, as well as associated fibular hemimelia
    and proximal focal femoral deficiency. (Courtesy
    of Shriners Hospital for Children, Philadelphia,
    PA.)

    ued to signal the limb to grow, only the ectoderm was


    available for forming terminal structures. A transverse
    deficiency without nubbins is believed to result from a
    loss of the AER with truncation of limb growth.21
    In the short-finger type of symbrachydactyly, the
    triad of syndactyly, brachydactyly, and symphalangism
    is most common (Figure 8). A severely affected hand
    can resemble a cleft hand, but the presence of nubbins
    and the involvement of only one limb differentiates the
    two diagnoses. Poland syndrome may be present, with
    absence of the sternal head of the pectoralis major, and
    the patient also may have a loss of breast tissue and a
    chest wall deficiency (Figure 9). The monodactylous
    702

    Characteristics

    Orthopaedic Knowledge Update 10

    Figure 6

    Photograph showing a childs split hands (central


    deficiency). The childs feet had a similar deformity. (Courtesy of Shriners Hospital for Children,
    Philadelphia, PA.)

    2011 American Academy of Orthopaedic Surgeons

    Chapter 55: Upper Extremity Disorders: Pediatrics

    Figure 7

    Photographs showing the dorsal (A) and volar (B)


    aspects of a hand with short-finger symbrachydactyly, which is characterized by the triad of
    syndactyly, brachydactyly, and symphalangism.
    (Courtesy of Shriners Hospital for Children, Philadelphia, PA.)

    Figure 10

    Photograph showing a transverse deficiency just


    below the elbow with terminal nubbins (peromelic symbrachydactyly). (Courtesy of Shriners
    Hospital for Children, Philadelphia, PA.)

    Photograph showing a childs hand with monodactylous symbrachydactyly, with the thumb
    preserved. (Courtesy of Shriners Hospital for
    Children, Philadelphia, PA.)

    Photograph of a girl with severe Poland syndrome. The absence of the pectoralis muscles
    and a nipple can be seen. More commonly, only
    the sternal head of the pectoralis major is absent. (Courtesy of Shriners Hospital for Children,
    Philadelphia, PA.)

    2011 American Academy of Orthopaedic Surgeons

    form can be differentiated from a cleft hand by preservation of the thumb. Nubbins may be absent. The peromelic form is a transverse deficiency with loss of all
    digits (Figure 10). Nubbins can be seen at the terminus
    of the limb.
    Syndactyly releases are indicated for a child with the
    short-finger type. Redundant soft tissue at the end of
    the limb allows nonvascularized toe proximal phalanges to be transferred to gain digital length. The growth
    of these transferred phalanges has been variable, although preservation of the periosteum and collateral
    ligaments appears to improve the results.22 Vascularized
    toe transfers are technically more challenging than nonvascularized phalangeal transfers, but they can add
    greater length and provide more mobile joints. Vascu-

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Figure 9

    Figure 8

    703

    Section 6: Pediatrics

    of radius, ulna, and combined deficiencies.25 Severe


    forms of Holt-Oram syndrome are similar in appearance, and associated cardiac anomalies therefore
    should be ruled out. The truncated limb length means
    that a prosthesis can provide substantial functional improvement. Early fitting is indicated to optimize acceptance of the prosthesis.

    Failure of Differentiation

    Syndactyly

    Figure 11

    Photograph of a child with phocomelia, with severe hypoplasia of the limb. (Courtesy of Shriners Hospital for Children, Philadelphia, PA.)

    6: Pediatrics

    larized toe transfers can be used for some monodactylous and peromelic-type hands.23 Distraction osteogenesis is another option; a 30% to 100% increase in
    phalangeal length has been reported, with no donor site
    morbidity.24 Prosthesis fitting at age 6 months was considered mandatory for a child with the peromelic type
    of syndactyly, particularly at the midforearm or aboveelbow level. However, the children rarely rely on the
    prosthesis for functioning unless the deficiencies are bilateral, and the adage fit when they sit may no longer
    apply.
    Phocomelia
    Phocomelia became famous as a consequence of maternal thalidomide use to treat pregnancy-related nausea,
    but otherwise it is quite rare. The syndrome is characterized by short or absent long bones and a flipperlike
    appearance of the hands and/or feet. Intercalary aplasia
    results in the loss of forearm segments or the entire
    arm. The hands and feet sometimes arise directly from
    the trunk (Figure 11). Phocomelia may be the most severe form of longitudinal deficiency along the spectrum
    704

    Orthopaedic Knowledge Update 10

    Failure of separation of the digits occurs in 3 per


    10,000 live births. Although an autosomal dominant
    inheritance pattern is common, the expression is variable and penetrance is incomplete. The genetic defect
    has been localized to chromosome 2 (2q34-q36).26 Syndromic associations are relatively uncommon, although
    Apert syndrome (Figure 12), Poland syndrome, symbrachydactyly, amnionic disruption sequence, cleft
    hand, and ulnar longitudinal deficiency can occur. Amnionic bands cause a fenestrated type of syndactyly
    known as acrosyndactyly, with retention of a narrow
    remnant of the proximal web space.
    The classification of syndactyly is straightforward.
    The presence or absence of a synostosis determines
    whether the syndactyly is simple or complex. The term
    synonychia refers to a joint nail plate and indicates a
    synostosis of the distal phalanges. A complete syndactyly extends to the fingertip, and an incomplete syndactyly does not. Apert syndrome is classified as a complete or complicated syndactyly.
    Reconstruction to obtain an adequate web space
    usually is indicated for functional and aesthetic reasons. The timing of surgery is controversial, but most
    surgeons agree that early separation of a complete syndactyly is warranted for border digits, particularly the
    thumb and index finger. Because of the disparity in
    length between the ring and small fingers and the
    thumb and index finger, the shorter digit will tether the
    longer digit, creating joint contractures and rotational
    deformities. Release of the thumbindex finger web
    should be performed by age 6 months to allow development of prehensile grasp-and-pinch patterns. Separation of the long and ring fingers can be delayed until
    the hand is larger and easier to reconstruct. At least 3
    months should be allowed between procedures to separate adjacent digits.
    The commissure and the lateral nail fold are the
    most challenging areas to reconstruct in simple syndactyly. The commissure should be free of any suture lines
    and grafts to prevent later scarring and contracture
    (web creep). A full-thickness skin graft is almost always
    necessary to cover any remaining defects, and harvesting can be easily done from the wrist crease, with virtually no harvest site morbidity (Figure 13). A complex
    syndactyly may require soft-tissue transfers. The digital
    neurovascular bundles may be abnormal or absent if a
    synostosis is present.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 55: Upper Extremity Disorders: Pediatrics

    Figure 12

    Photograph (A) and AP radiograph (B) showing a complicated syndactyly in a child with Apert syndrome. (Courtesy
    of Shriners Hospital for Children, Philadelphia, PA.)

    Figure 13

    Photographs showing the location of full-thickness skin graft harvesting and flaps used for the release of a syndactyly. The wrist crease is an excellent source of skin graft (A), with minimal postoperative morbidity (B). Dorsal (C)
    and volar (D) flaps should be designed to minimize suturing at the commissure. (Courtesy of Shriners Hospital for
    Children, Philadelphia, PA.)

    Camptodactyly

    Kirner Deformity

    Proximal interphalangeal joint contractures can result


    from a fracture or a tendon laceration or avulsion, or
    they may occur spontaneously or as part of a syndrome. It may be difficult to differentiate camptodactyly from posttraumatic proximal interphalangeal joint
    contractures or boutonniere deformities, particularly in
    young children. True camptodactyly occurs in as many
    as 1% of the population. When familial, it has an autosomal dominant inheritance pattern.27 The congenital
    type has no sex predilection, but the adolescent type
    occurs more often in girls. The small finger is most
    commonly affected.

    Kirner deformity is a combined flexion and radial deviation deformity of the small finger that occurs spontaneously or may have a genetic component. The finger
    has an angulated distal interphalangeal joint with a
    curved, beak-shaped nail similar to that found in nail
    clubbing. However, the deformity itself is at the distal
    phalanx and not at the joint. Treatment is rarely necessary.

    Partial damage to the physis as a result of trauma, a


    thermal injury, or a physeal abnormality inherited as an
    autosomal dominant trait can lead to progressive radioulnar angular deformity. The middle phalanx of the
    small finger is most commonly affected, with a typical
    bend toward the ring finger. Radiographs may reveal a
    C-shaped physis that results in a triangular delta phalanx (Figure 14). The curvature begins to interfere with
    daily activities when the deformity reaches 30 to 40.28

    2011 American Academy of Orthopaedic Surgeons

    Synostosis Across the Elbow


    Humeroradial synostosis can occur with ulnar hypoplasia (type I), or with a normal ulna (type II). Although
    type II is more commonly familial than type I, both
    types occur in a variety of genetic syndromes or with
    other skeletal or extraskeletal anomalies.29 The child
    should be referred to a geneticist as well as to appropriate pediatric subspecialists. In type I humeroradial
    synostosis, the elbow usually is fused in extension,
    making some daily tasks difficult. When the elbow is
    fused in a flexed position, as is more common in type
    II, patients are better able to perform bimanual tasks
    and to feed and groom themselves. Severe hyperexten-

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Clinodactyly

    Congenital Synostoses

    705

    Section 6: Pediatrics

    Figure 14

    Photograph (A) and PA radiograph (B) showing the hand of a child with bilateral clinodactyly. (Courtesy of Shriners Hospital for Children, Philadelphia, PA.)

    sion may warrant a corrective osteotomy to improve


    function.

    6: Pediatrics

    Radioulnar Synostosis
    The most common upper extremity synostosis is found
    between the radius and ulna. The diagnosis is often
    missed because function is maintained through compensatory hyperrotation at the wrist (sometimes of
    more than 100) as well as and rotation at the shoulder.30 Although there is an autosomal dominant transmission pattern, penetrance is variable and the synostosis can occur sporadically. Radiographs show a wellformed fusion mass across the proximal radius and
    ulna, often with a radial head dislocation (Figure 15).
    Most synostoses are in a near-neutral position and are
    well tolerated, requiring no treatment unless the child is
    limited in specific daily activities. Takedown of the
    synostosis to achieve forearm motion is almost always
    unsuccessful.31 Rotational osteotomies can position the
    arm in a more favorable position. The optimal position
    for function is controversial, although slight pronation
    of both arms may be most useful for computer use. Supination of the nondominant side may facilitate
    perineal care.

    Sprengel Deformity
    Failure of the scapula to descend during embryogenesis
    results in a congenital elevation of the scapula. The deformity is sporadic and typically unilateral. An omovertebral band almost always is present. The treatment
    remains controversial. If functional or cosmetic consid706

    Orthopaedic Knowledge Update 10

    erations warrant surgical intervention, procedures


    ranging from soft-tissue releases to scapular osteotomies can be considered.

    Duplication

    Thumb (Preaxial) Polydactyly


    Thumb duplication most commonly occurs in white
    children and typically is unilateral and sporadic. The
    etiology is a split rather than a true duplication. Both
    thumbs are smaller than the thumb on the unaffected
    contralateral side. The ulnar-sided thumb tends to be
    larger and better formed than the radial-sided thumb
    (Figure 16). A simple count of the abnormal bones
    yields the Wassel stage. In a Wassel type IV thumb (the
    most common duplication), there are four abnormal
    bones including two distal and two proximal phalanges.32
    Surgical reconstruction is indicated for most patients. Because the thumb to be preserved is usually
    smaller than the unaffected contralateral thumb, bulk
    from the thumb to be ablated should be preserved to
    augment the final reconstruction. The collateral ligaments should be preserved or repaired and reconstructed.

    Ulnar Polydactyly
    Postaxial polydactyly is most common in children of
    African descent; it has an autosomal dominant transmission pattern with high penetrance.33 Often one of

    2011 American Academy of Orthopaedic Surgeons

    Chapter 55: Upper Extremity Disorders: Pediatrics

    Figure 15

    AP (A) and lateral (B) radiographs showing a radioulnar synostosis. (Courtesy of Shriners Hospital for Children,
    Philadelphia, PA.)

    Figure 16

    Photograph (A) and PA radiograph (B) showing a type II thumb duplication. Note that two phalanges are affected.
    (Courtesy of Shriners Hospital for Children, Philadelphia, PA.)

    2011 American Academy of Orthopaedic Surgeons

    In type A, the extra digit is well formed; in type B, it


    is little more than a skin tag (Figure 17). A type A digit
    requires surgical excision; in-office ablation should not
    be attempted. A type B digit traditionally has been tied
    off with clips or suture ligature. Surgical ablation may
    be preferred to obtain a better long-term cosmetic result and avoid the necessity of the parents observing
    the digit necrosis and eventual autoamputation.33 A
    type B ablation can be performed in the office with a
    portable electrocautery device, under local anesthesia.

    6: Pediatrics

    the childs parents will have bilateral bumps on the ulnar side of the hand because a polydactylous digit was
    tied off at a young age. The child should receive a routine physical examination to detect any other skeletal
    system abnormalities. An extra digit on the ulnar side
    of the hand of a child of European descent should trigger an evaluation to detect a possible cardiac septal defect, thoracic dystrophy, hypogenitalism or ambiguous
    genitalia, ocular disorder, cleft lip or palate, mental retardation, cutaneous and nail dysplasia, or renal anomaly. Ellisvan Creveld syndrome should be suspected in
    a child from a genetically isolated population such as
    the Amish. Genetic counseling is recommended if the
    polydactyly is associated with other findings.

    Ulnar Dimelia
    Mirror hand is a rare duplication centered about the index finger. The hand has as many as eight fingers but

    Orthopaedic Knowledge Update 10

    707

    Section 6: Pediatrics

    Figure 17

    Photographs showing a type A (A) and a type B (B) postaxial duplication. A well-formed digit should be excised in
    the operating room, but a vestigial digit with a small skin and vascular pedicle can be excised in the office. (Courtesy of Shriners Hospital for Children, Philadelphia, PA.)

    Overgrowth

    Macrodactyly

    6: Pediatrics

    Figure 18

    Photograph showing the classic appearance of


    ulnar dimelia (mirror hand). The ulna-side
    structures are duplicated, and the thumb is absent. (Courtesy of Shriners Hospital for Children, Philadelphia, PA.)

    no thumb (Figure 18). The radius is absent, and two ulnae are present instead. Duplication of the ZPA is
    thought to lead to the formation of two ulnar halves of
    the limb. The treatment involves pollicization of the
    best radial digit and ablation of the rest to create a
    thumb and four fingers. The supranumerary digits often yield viable tendons for transfer, which may be
    needed particularly if wrist extensors are absent. The
    elbow, forearm, and wrist motion is limited because of
    the double ulnae.
    708

    Orthopaedic Knowledge Update 10

    Overgrowth of one or more digits occurs sporadically or


    as part of neurofibromatosis or Klippel-TrenaunayWeber, Ollier-Maffucci, or Proteus syndrome. All components of the digit are enlarged, commonly with angular deformity and joint contracture (Figure 19). In static
    macrodactyly, a congenital finger enlargement grows
    proportionally to the other digits. Progressive macrodactyly is more common. The finger is of normal size at birth
    but exhibits disproportionate growth that leads to worsening joint stiffness. Type I is the most common, with
    fatty infiltration of the median nerve within the carpal
    tunnel extending distally to the digital nerves. Type II is
    associated with neurofibromatosis and skeletal enlargement with osteochondromas. Type II is characterized by
    digital hyperostosis, periarticular osteochondromas, stiff
    joints, and no nerve hypertrophy. Type IV is macrodactyly in the setting of hemihypertrophy of the entire
    limb.34 Debulking procedures can lead to further joint
    stiffness and may need to be repeated. Closing-wedge osteotomies through the physis can halt longitudinal
    growth and correct angulation of the digit, but they do
    not arrest appositional growth and may result in further
    joint stiffness. Ray amputation may be the most viable
    option for a stiff finger that interferes with functioning.

    Constriction Band Syndrome


    Strands of the amnionic membrane can detach from the
    innermost layer of the placenta and entrap the develop-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 55: Upper Extremity Disorders: Pediatrics

    Figure 19

    Photographs showing macrodactyly of the long finger. A, The typical angulation and joint contractures can be seen.
    B, Ray amputation and index transposition yielded a more functional hand. (Courtesy of Shriners Hospital for
    Children, Philadelphia, PA.)

    ing fetus. The result is constricting rings that can lead


    to amputations and syndactyly. Facial or cranial clefts
    can result if the fetus swallows these bands. There is no
    consensus as to the nomenclature, and the phenomenon
    has been called constriction ring syndrome, amnionic
    band syndrome, Streeter dysplasia, or annular constriction rings. Differentiating amnionic disruption sequence from symbrachydactyly or a central deficiency
    can be difficult. Constriction bands and acrosyndactyly
    are pathognomonic (Figure 20). Inclusion cysts sometimes are seen at the level of an amputation. An impending amputation in a neonate is a surgical emergency. The constriction should be released with
    Z-plasties as soon as possible. In contrast, a minor
    band that does not place the limb at risk can be observed, and typically it requires no treatment.

    6: Pediatrics

    Brachial Plexus Injury


    The incidence of neonatal brachial plexus palsy is approximately 1 to 2 per 1,000 live births, although it
    may be declining despite an overall increase in fetal
    weight at term delivery. In addition to fetal macrosomia, the risk factors include prolonged or difficult labor, shoulder dystocia, breech presentation, forceful extraction with the aid of vacuum or forceps, a uterine
    anomaly, and a previous child with a brachial plexus
    injury. A caesarian delivery decreases but does not eliminate the risk of a brachial plexus injury.

    2011 American Academy of Orthopaedic Surgeons

    Figure 20

    Photograph showing vessel loops through the


    remnant of the web space in a child with
    acrosyndactyly from constriction band syndrome. (Courtesy of Shriners Hospital for Children, Philadelphia, PA.)

    The right side is most often injured. An upper trunk


    injury at C5-C6 is most common (Erb palsy). An extended upper plexus lesion involves C7, and a global

    Orthopaedic Knowledge Update 10

    709

    Section 6: Pediatrics

    Table 5

    Patterns of Brachial Plexus Injuries


    Pattern

    Involved Nerve Roots

    Primary Deficiency

    Erb-Duchenne lesion
    Upper brachial plexus

    C5-C6

    Shoulder abduction and external rotation


    Elbow flexion

    Extended Erb lesion


    Upper and middle plexus

    C5-C7

    Shoulder abduction and external rotation


    Elbow flexion
    Elbow and finger extension

    Dejerine-Klumpke lesion
    Lower brachial plexus

    C8-T1

    Hand intrinsic muscles


    Finger flexors

    Total or global lesion


    Entire brachial plexus

    C5-T1

    Entire extremity

    6: Pediatrics

    plexus injury continues to C8-T1 (Table 5). An isolated


    lower plexus injury (Klumpke palsy) is rare. Involvement of the lower plexus can result in a Horner syndrome, characterized by ptosis, miosis, enophthalmos,
    and anhidrosis. Most neonatal palsies are neurapraxic
    injuries that improve within 2 months. Axonometric injuries undergo Wallerian degeneration and require
    nerve regeneration within an intact nerve sheath. Functional recovery of elbow flexion by age 4 to 6 months
    indicates that at least a portion of the nerve is in continuity. Limited or absent elbow flexion at age 6 months
    suggests a neurotmetic injury. Because the nerves have
    been disrupted, spontaneous recovery in the long term
    is unlikely.
    Patients with a neurotmetic rupture require excision
    of the neuroma and cable grafting of the defect with
    autograft nerve (most commonly the sural nerve). Direct repair usually is not possible. Nerve root avulsion
    from the spinal cord is a preganglionic injury and is not
    repairable by any means. Nerve grafting from viable
    roots and/or delayed tendon transfers are required to
    improve function. An avulsion injury should be suspected if the child has phrenic nerve dysfunction with
    an elevated hemidiaphragm on inspiratory imaging,
    Horner syndrome, or scapular winging.
    Incomplete recovery in the shoulder typically favors
    the C6-C7 innervated internal rotators and adductors
    over the C5-C6 innervated external rotators and abductors. Untreated, a posterior moment is placed across
    the glenohumeral joint, resulting in anterior capsular
    and muscular tightness, posterior glenohumeral subluxation, posterior glenoid version, and eventually formation of a pseudoglenoid on the posterior surface of the
    scapula. The process is similar to that of developmental
    dysplasia of the hip joint.
    The treatment begins during the neonatal period
    with passive abduction and external rotation stretching
    by the caretaker at every diaper change. If the shoulder
    contracture persists after stretching, botulinum toxin
    injections can be used. Late-appearing or resistant contractures require an open or arthroscopic glenohumeral
    reduction, with or without tendon transfers. A humeral
    rotational osteotomy can be considered to orient the
    710

    Orthopaedic Knowledge Update 10

    forearm into a better position for feeding and grooming.

    Developmental Conditions

    Pediatric Trigger Thumb


    Trigger thumb in children is no longer believed to be
    congenital, but its etiology is unknown.35-37 At age 1
    year, the prevalence is 3 per 1,000 children.36 Although
    the rate of spontaneous resolution is undefined, surgical release remains the mainstay of treatment.37-40

    Trigger Finger
    Trigger finger in adults and trigger thumb in children
    and adults respond predictably to A1 pulley release,
    but trigger finger in children does not. Unlike pediatric
    trigger thumb, in pediatric trigger finger there is often
    an anatomic variance that leads to the triggering effect.
    Abnormal interconnections between the superficialis
    and profundus tendons have been implicated. Surgical
    release requires a more extensive exposure than for an
    adult trigger finger and may require exposure of the entire flexor system in the hand and finger. Release of the
    A1 pulley with resection of one slip of the flexor digitorum superficialis tendon has been recommended.41

    Madelung Deformity
    The cause of Madelung deformity is controversial. The
    characteristic feature is undergrowth of the volar-ulnar
    corner of the distal radius (Figure 21).Tension from a
    restraining Vickers ligament may limit growth at that
    portion of the distal radius.42 Most incidences are sporadic, but mutations in the SHOX gene can lead to
    Leri-Weill dyschondrosteosis, in which the patient has
    short stature, mesomelic upper and lower limb shortening, and Madelung deformity. Mutations can occur
    spontaneously or be inherited via autosomal dominant
    transmission. Girls are more often affected than boys.43
    A similar deformity can result from repetitive ballistic
    loading of the wrist and is common in young female
    gymnasts.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 55: Upper Extremity Disorders: Pediatrics

    Figure 21

    Photograph (A) and AP and lateral radiographs (B) showing Madelung deformity. (Courtesy of Shriners Hospital for
    Children, Philadelphia, PA.)

    Madelung deformity usually requires no treatment,


    and even a gross deformity is well tolerated. Early release of the Vickers ligament and physiolysis has been
    recommended to prevent worsening of the deformity
    and allow some spontaneous correction.44 Gymnasts
    should cease weight-bearing activities until the pain resolves. The indications for surgical correction include
    pain and aesthetic concerns. A dome osteotomy can
    correct the increased tilt and inclination and can restore
    a more neutral ulnar variance.45 If the childs symptoms
    are primarily from ulnocarpal impaction, ulnar shortening may be added to a radial osteotomy or used primarily.46,47
    Figure 22

    A neonatal compartment syndrome always is accompanied by a skin lesion over the affected limb (Figure
    22).48 The telltale signs usually are visible at birth, although they often are missed. The limb is edematous
    with tip necrosis or ischemia. If the compartments are
    not released, the limb progresses to necrosis and digital
    contractures. The late appearance of this syndrome is
    typical of a Volkmann ischemic contracture. The differential diagnosis includes amnionic disruption sequence
    (identified by the presence of a band proximal to the

    2011 American Academy of Orthopaedic Surgeons

    Photograph showing neonatal compartment syndrome, with the pathognomonic skin lesion
    and peripheral ischemia. (Courtesy of Shriners
    Hospital for Children, Philadelphia, PA.)

    6: Pediatrics

    Vasculocutaneous Catastrophe of the Newborn


    (Intrauterine Compartment Syndrome)

    level of the ischemia or necrosis), cord strangulation,


    arterial thrombosis, and cellulitis. Emergency compartment release is the only treatment in the acute setting.
    A child with a late-appearing syndrome may benefit
    from release of the entire flexor-pronator origin, neurolysis, and dbridement of necrotic tissue.

    Orthopaedic Knowledge Update 10

    711

    Section 6: Pediatrics

    dial deficiency in children. J Pediatr Orthop 2005;25(3):


    377-381.

    Annotated References
    1.

    Bamshad M, Watkins WS, Dixon ME, et al: Reconstructing the history of human limb development: Lessons from birth defects. Pediatr Res 1999;45(3):291299.

    2.

    Daluiski A, Yi SE, Lyons KM: The molecular control of


    upper extremity development: Implications for congenital hand anomalies. J Hand Surg Am 2001;26(1):8-22.

    3.

    Riddle RD, Tabin C: How limbs develop. Sci Am 1999;


    280(2):74-79.

    4.

    Lyons K, Ezaki M: Molecular regulation of limb


    growth. J Bone Joint Surg Am 2009;91(suppl 4):47-52.
    The known molecular regulators of limb development are
    concisely and clearly reviewed. The clinical sequelae of
    breakdowns in the regulatory pathways are considered.

    6: Pediatrics

    5.

    6.

    Goldfarb CA, Wall L, Manske PR: Radial longitudinal


    deficiency: The incidence of associated medical and
    musculoskeletal conditions. J Hand Surg Am 2006;
    31(7):1176-1182.

    7.

    Auerbach AD, Rogatko A, Schroeder-Kurth TM: International Fanconi Anemia Registry: Relation of clinical
    symptoms to diepoxybutane sensitivity. Blood 1989;
    73(2):391-396.

    8.

    Lourie GM, Lins RE: Radial longitudinal deficiency: A


    review and update. Hand Clin 1998;14(1):85-99.

    9.

    Hall JG: Thrombocytopenia and absent radius (TAR)


    syndrome. J Med Genet 1987;24(2):79-83.

    10.

    Klopocki E, Schulze H, Strauss G, et al: Complex inheritance pattern resembling autosomal recessive inheritance involving a microdeletion in thrombocytopeniaabsent radius syndrome. Am J Hum Genet 2007;80(2):
    232-240.
    A microdeletion of chomosome 1q21.1 was consistently
    found in 30 patients with TAR syndrome. The deletion
    occurred de novo in 25% of cases.

    11.

    12.

    13.

    712

    Barrow JR, Thomas KR, Boussadia-Zahui O, et al: Ectodermal Wnt3/beta-catenin signaling is required for the
    establishment and maintenance of the apical ectodermal
    ridge. Genes Dev 2003;17(3):394-409.

    Brassington AM, Sung SS, Toydemir RM, et al: Expressivity of Holt-Oram syndrome is not predicted by TBX5
    genotype. Am J Hum Genet 2003;73(1):74-85.
    Goldfarb CA, Murtha YM, Gordon JE, Manske PR:
    Soft-tissue distraction with a ring external fixator before
    centralization for radial longitudinal deficiency. J Hand
    Surg Am 2006;31(6):952-959.
    Sabharwal S, Finuoli AL, Ghobadi F: Pre-centralization
    soft tissue distraction for Bayne type IV congenital ra-

    Orthopaedic Knowledge Update 10

    14.

    Pickford MA, Scheker LR: Distraction lengthening of


    the ulna in radial club hand using the Ilizarov technique. J Hand Surg Br 1998;23(2):186-191.

    15.

    Kozin SH, Weiss AA, Webber JB, Betz RR, Clancy M,


    Steel HH: Index finger pollicization for congenital aplasia or hypoplasia of the thumb. J Hand Surg Am 1992;
    17(5):880-884.

    16.

    Clark DI, Chell J, Davis TR: Pollicisation of the index


    finger: A 27-year follow-up study. J Bone Joint Surg Br
    1998;80(4):631-635.

    17.

    Manske PR, McCaroll HR Jr: Index finger pollicization


    for a congenitally absent or nonfunctioning thumb.
    J Hand Surg Am 1985;10(5):606-613.

    18.

    Cole RJ, Manske PR: Classification of ulnar deficiency


    according to the thumb and first web. J Hand Surg Am
    1997;22(3):479-488.

    19.

    Buss PW: Cleft hand/foot: Clinical and developmental


    aspects. J Med Genet 1994;31(9):726-730.

    20.

    Flatt AE: Cleft hand and central defects, in Flatt AE, ed:
    The Care of Congenital Hand Anomalies, ed 2. St.
    Louis, MO, Quality Medical Publishing, 1994, pp 337365.

    21.

    Summerbell D: A quantitative analysis of the effect of


    excision of the AER from the chick limb-bud. J Embryol Exp Morphol 1974;32(3):651-660.

    22.

    Radocha RF, Netscher D, Kleinert HE: Toe phalangeal


    grafts in congenital hand anomalies. J Hand Surg Am
    1993;18(5):833-841.

    23.

    Kay SP, Wiberg M: Toe to hand transfer in children:


    Part 1. Technical aspects. J Hand Surg Br 1996;21(6):
    723-734.

    24.

    Dhalla R, Strecker W, Manske PR: A comparison of


    two techniques for digital distraction lengthening in
    skeletally immature patients. J Hand Surg Am 2001;
    26(4):603-610.

    25.

    Goldfarb CA, Manske PR, Busa R, Mills J, Carter P,


    Ezaki M: Upper-extremity phocomelia reexamined: A
    longitudinal dysplasia. J Bone Joint Surg Am 2005;
    87(12):2639-2648.

    26.

    Kozin SH: Syndactyly. J Am Soc Surg Hand 2001;1:


    1-13.

    27.

    Engber WD, Flatt AE: Camptodactyly: An analysis of


    sixty-six patients and twenty-four operations. J Hand
    Surg Am 1977;2(3):216-224.

    28.

    Burke F, Flatt A: Clinodactyly: A review of a series of


    cases. Hand 1979;11(3):269-280.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 55: Upper Extremity Disorders: Pediatrics

    29.

    McIntyre JD, Benson MK: An aetiological classification


    for developmental synostoses at the elbow. J Pediatr Orthop B 2002;11(4):313-319.

    30.

    Ogino T, Hikino K: Congenital radio-ulnar synostosis:


    Compensatory rotation around the wrist and rotation
    osteotomy. J Hand Surg Br 1987;12(2):173-178.

    31.

    Kanaya F, Ibaraki K: Mobilization of a congenital proximal radioulnar synostosis with use of a free vascularized fascio-fat graft. J Bone Joint Surg Am 1998;80(8):
    1186-1192.

    32.

    Wassel HD: The results of surgery for polydactyly of the


    thumb: A review. Clin Orthop Relat Res 1969;64:175193.

    33.

    Watson BT, Hennrikus WL: Postaxial type-B polydactyly: Prevalence and treatment. J Bone Joint Surg Am
    1997;79(1):65-68.

    41.

    Bae DS, Sodha S, Waters PM: Surgical treatment of the


    pediatric trigger finger. J Hand Surg Am 2007;32(7):
    1043-1047.
    A retrospective study of 18 consecutive patients found a
    91% resolution of trigger fingers in children treated
    with A1 pulley release and partial flexor digitorum superficialis resection. Level of evidence: IV.

    42.

    Stehling C, Langer M, Nassenstein I, Bachmann R,


    Heindel W, Vieth V: High resolution 3.0 Tesla MR imaging findings in patients with bilateral Madelungs deformity. Surg Radiol Anat 2009;31(7):551-557.
    MRI of three patients with Madelung deformity revealed a stout Vickers ligament and pyramidization of
    the proximal carpal row, along with an anomalous hypertrophied and elongated volar radiotriquetral ligament.

    43.

    Huber C, Rosilio M, Munnich A, Cormier-Daire V;


    French SHOX GeNeSIS Module: High incidence of
    SHOX anomalies in individuals with short stature.
    J Med Genet 2006;43(9):735-739.

    44.

    Vickers D, Nielsen G: Madelung deformity: Surgical


    prophylaxis (physiolysis) during the late growth period
    by resection of the dyschondrosteosis lesion. J Hand
    Surg Br 1992;17(4):401-407.

    45.

    Harley BJ, Brown C, Cummings K, Carter PR, Ezaki M:


    Volar ligament release and distal radius dome osteotomy for correction of Madelungs deformity. J Hand
    Surg Am 2006;31(9):1499-1506.

    34.

    ORahilly R: Morphological patterns in limb deficiencies and duplications. Am J Anat 1951;89(2):135-193.

    35.

    Slakey JB, Hennrikus WL: Acquired thumb flexion contracture in children: Congenital trigger thumb. J Bone
    Joint Surg Br 1996;78(3):481-483.

    36.

    Kikuchi N, Ogino T: Incidence and development of trigger thumb in children. J Hand Surg Am 2006;31(4):
    541-543.

    37.

    Rodgers WB, Waters PM: Incidence of trigger digits in


    newborns. J Hand Surg Am 1994;19(3):364-368.

    46.

    Dinham JM, Meggitt BF: Trigger thumbs in children: A


    review of the natural history and indications for treatment in 105 patients. J Bone Joint Surg Br 1974;56(1):
    153-155.

    Salon A, Serra M, Pouliquen JC: Long-term follow-up


    of surgical correction of Madelungs deformity with
    conservation of the distal radioulnar joint in teenagers.
    J Hand Surg Br 2000;25(1):22-25.

    47.

    McAdams TR, Moneim MS, Omer GE Jr: Long-term


    follow-up of surgical release of the A(1) pulley in childhood trigger thumb. J Pediatr Orthop 2002;22(1):
    41-43.

    Bruno RJ, Blank JE, Ruby LK, Cassidy C, Cohen G,


    Bergfield TG: Treatment of Madelungs deformity in
    adults by ulna reduction osteotomy. J Hand Surg Am
    2003;28(3):421-426.

    48.

    Ragland R III, Moukoko D, Ezaki M, Carter PR, Mills


    J: Forearm compartment syndrome in the newborn: Report of 24 cases. J Hand Surg Am 2005;30(5):9971003.

    38.

    39.

    40.

    Skov O, Bach A, Hammer A: Trigger thumbs in children: A follow-up study of 37 children below 15 years
    of age. J Hand Surg Br 1990;15(4):466-467.

    6: Pediatrics

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    713

    Chapter 56

    Spine Trauma and Disorders:


    Pediatrics
    Anthony Scaduto, MD

    Daniel Hedequist, MD

    Congenital Anomalies

    Dr. Scaduto or an immediate family member is a member of a speakers bureau or has made paid presentations on behalf of Abbott and Zimmer; serves as a paid
    consultant to or is an employee of Abbott and Zimmer;
    and has received research or institutional support from
    DePuy, a Johnson & Johnson Company. Dr. Hedequist or
    an immediate family member is a member of a speakers
    bureau or has made paid presentations on behalf of
    Medtronic Sofamor Danek.

    2011 American Academy of Orthopaedic Surgeons

    6: Pediatrics

    Congenital abnormalities of the spine are caused by an


    embryologic insult that occurs between the 8th and
    12th weeks of gestation. These anomalies traditionally
    are classified as a failure of formation, a failure of segmentation, or mixed. In clinical practice, defining the
    anomaly and trying to predict growth potential and
    potential curve progression have useful treatment implications. Plain radiographs remain the simplest means
    of classifying congenital spine deformities. Threedimensional CT provides greater clarity when defining
    specific anomalies (Figure 1). In a patient undergoing
    surgery, the anomaly is best studied and classified using
    three-dimensional CT.1 Routine use of CT is not warranted in patients with a nonprogressive deformity that
    does not require treatment.
    The spinal column develops at the same embryologic
    stage as the spinal cord and organ systems, including
    the genitourinary and cardiac systems. A spinal cord
    abnormality (tethered cord, diastematomyelia, or
    Chiari malformation) is present in as many as 30% of
    patients with congenital scoliosis. Patients who have associated cutaneous signs of dysraphism, a neurologic
    abnormality, or curve progression requiring surgery
    should undergo screening of the spinal axis. The genitourinary system should be evaluated with screening ultrasonography of the kidneys, ureters, and bladder; the
    cardiac system should be evaluated with a thorough
    cardiac examination, with imaging if necessary.
    The prognosis depends on the anomaly and its potential for progression. A wedge vertebra, unsegmented
    hemivertebra, or block vertebra has little potential for
    progression and requires only minimal observation. A

    simple deformity such as a hemivertebra (with healthy


    disks above and below) has a greater potential for progression and should be carefully observed. A tether to
    growth (a failure of segmentation) has a significant tendency to cause rapid and severe growth abnormalities
    including unilateral bars and bars associated with multiple concave rib fusions.
    The surgical treatment of congenital scoliosis or kyphosis revolves around early diagnosis and treatment,
    before the development of spinal decompensation. In
    order of importance, the goals of surgery are to prevent
    progression, safely correct the deformity, and maintain
    flexibility and balance. The surgical treatment ranges
    from in situ fusion to convex epiphysiodesis to
    hemivertebra resection. Fusion and instrumentation can
    be effectively done with spine instrumentation and allograft, even in very young patients.2 The use of neurologic monitoring through somatosensory- and motorevoked potentials is paramount because of the great
    risk of neurologic injury during surgery for a congenital
    spine deformity.

    Figure 1

    Three-dimensional CT of an isolated hemivertebra. The disk spaces above and below the
    hemivertebra can be clearly seen. A fully segmented hemivertebra is associated with a high
    risk of progressive scoliosis.

    Orthopaedic Knowledge Update 10

    715

    Section 6: Pediatrics

    Congenital spine deformities occasionally are seen


    in concert with congenital rib fusions. The disorder
    can lead to a hypoplastic chest on one side, with resultant respiratory decompensation (called thoracic insufficiency). The interrelationship between the congenital
    deformed spine and the deformed chest is well recognized, and it has treatment ramifications. The development of the vertical expandable prosthetic titanium
    rib (VEPTR) has allowed improvement in spine
    growth, curve control, and expansion of the hypoplastic chest in some patients with congenital spine deformities. The management of severe deformities continues to evolve, and long-term follow-up is needed to
    determine the efficacy of the VEPTR.

    Klippel-Feil Syndrome
    A patient with Klippel-Feil syndrome has congenital
    cervical fusions as well as a low posterior hairline and a
    short neck secondary to the cervical fusions. KlippelFeil syndrome sometimes is erroneously diagnosed as
    congenital muscular torticollis because of the head tilt
    and limited motion that characterizes both conditions.
    As many as a third of patients with Klippel-Feil syndrome also have an elevated scapula (Sprengel deformity) or partial hearing loss. In general, patients require little orthopaedic intervention beyond counseling
    to avoid activities that place the neck at high risk, such
    as football, gymnastics, and trampoline use. Some pediatric patients develop instability or degeneration of adjacent normal, unfused cervical spine segments because
    of increased biomechanical stress. These patients can be
    treated with an instrumented cervical arthrodesis of the
    affected spine area.3

    Os Odontoideum

    6: Pediatrics

    Os odontoideum is an anomaly of the axis that frequently appears during childhood with neck pain, transient paresthesias, or myelopathy. This disorder is believed to result from an unrecognized fracture of C2 in
    early childhood, with subsequent instability caused by
    nonunion. An os odontoideum is best recognized on
    CT; it is characterized by an ossicle at the top of the
    dens above the C1-C2 articulation, with sclerotic borders. Plain radiographs in flexion and extension are
    used to document the associated C1-C2 instability. Half
    of patients with an os odontoideum have myelopathy,
    and MRI frequently shows signal changes in the spinal
    cord (Figure 2). The treatment of os odontoideum is
    surgical. Patients treated nonsurgically may develop
    neurologic signs. The surgery entails a C1-C2 posterior
    arthrodesis using autograft wires, transarticular screws,
    or a C1-C2 screw rod construct.4

    716

    Orthopaedic Knowledge Update 10

    Idiopathic Scoliosis
    Idiopathic scoliosis is a curvature of the spine of unknown etiology. The three categories, based on the patients age at diagnosis, are infantile (before age 3
    years), juvenile (age 3 to 10 years), and adolescent (age
    11 years or older). Infantile scoliosis more commonly
    affects boys than girls. Most infantile curves are left
    thoracic, with little rotation in the spine, and most resolve spontaneously over time with no treatment. The
    incidence of a neural axis abnormality is higher in infantile scoliosis than in adolescent scoliosis, and therefore the physical examination should focus on detecting
    any neurologic signs and any signs of spinal dysraphism. Analysis of the coronal radiographs allows measurement of the Cobb angle, the rib-vertebral angle difference of Mehta, and rib overlap of the apical
    vertebral body. These measurements reveal the presence
    of spinal rotation and determine whether the child has
    structural scoliosis, which is most likely to progress.
    Untreated progressive infantile scoliosis can lead to restrictive lung disease, cor pulmonale, and early death.
    Treatment usually is reserved for a progressive infantile curve of more than 25. A thoracolumbosacral orthosis or derotation casting can be used. The curve can
    be completely resolved with casting in children younger
    than 20 months who have a Cobb angle of less than
    60.5 Derotation casting often is unsuccessful if the
    curve is more than 60 or the child is older than 20
    months. These patients are best treated surgically with a
    growing rod spine construct. The growing-rod or
    VEPTR method allows spine and lung growth until definitive fusion can be performed.6
    Juvenile scoliosis is more common in girls than in
    boys and tends to appear as a right-side thoracic curvature. The incidence of spinal dysraphism in these patients is higher than that of adolescent scoliosis. Large
    curves require MRI screening of the spinal axis. A progressive curve with a Cobb angle of more than 25 is
    best treated with bracing either for 18 hours a day or at
    nighttime. Surgical intervention is reserved for patients
    with a Cobb angle of more than 50 (Figure 3). Depending on the size and age of the patient, the surgical
    treatment may be definitive instrumented fusion, or fusion may be delayed in favor of initial treatment with
    growing rods.
    Adolescent idiopathic scoliosis is the most common
    type of scoliosis. Most patients are healthy girls. The
    likelihood of curve progression depends on the size of
    the Cobb angle and the amount of remaining growth.
    The amount of remaining growth can be correlated
    with a left hand-and-wrist radiograph to determine
    bone age. The stages of the adolescent growth spurt
    were recently correlated with the bone age.7 These findings are used to determine whether the best treatment is
    observation, bracing, or surgery. Observation is appropriate for a skeletally immature patient with a Cobb
    angle of less than 25 or for a skeletally mature patient
    with a Cobb angle of more than 25and a curve of less
    than 50 in the thoracic spine and less than 35 to 40
    in the thoracolumbar or lumbar spine.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 56: Spine Trauma and Disorders: Pediatrics

    Figure 2

    2011 American Academy of Orthopaedic Surgeons

    The surgical options include an open anterior fusion


    with instrumentation, a thoracoscopic fusion with instrumentation, a posterior fusion with instrumentation,
    and a circumferential fusion with instrumentation. An
    open anterior procedure with instrumentation is best
    performed for a thoracolumbar curve with a normal
    sagittal profile. This procedure is ideal if levels can be
    spared by performing an anterior instrumented fusion.
    Thoracoscopic instrumentation and fusion is efficacious and associated with improved subjective patient
    outcomes.9 The instrumentation choices for posterior
    segmental fixation include hooks, wires, cables, and
    pedicle screws. The off-label use of segmental pedicle
    screw fixation has improved coronal plane correction
    in posterior instrumented fusion, but it has not yet been
    established whether the additional coronal correction
    will improve the long-term outcome. Segmental screw
    fixation has allowed many large curves to be managed
    effectively without an anterior release10 (Figure 3).
    Neurologic monitoring is paramount during every
    procedure for spine deformity. Standard monitoring
    should include detection of changes in somatosensoryand motor-evoked potentials. Motor-evoked potentials
    in particular can provide an excellent warning of im-

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Brace treatment to prevent curve progression is generally warranted in a child with significant remaining
    growth and a curve of 25 to 40. Brace use is recommended for 18 to 22 hours a day, although some braces
    are designed for nighttime use only. Ideally, brace use
    should lead to a 50% correction of the curve. Brace use
    is less likely to be successful if the in-brace correction is
    poor; there is hypokyphosis; or the patient is male,
    obese, or noncompliant. A multicenter randomized
    brace study (the BrAIST study [www.clinicaltrials.gov])
    is under way to determine the efficacy of brace use. Idiopathic curves larger than 50 are at risk for progression even after skeletal maturity is achieved. Instrumented fusion can improve the cosmetic deformity and
    stabilize pulmonary function. The Lenke classification
    is used to identify the major structural curve and any
    minor curves.8 The major curve must be included in the
    instrumented fusion. The decision to include a minor
    curve depends on curve flexibility, as determined from
    side-bending radiographs, and the sagittal alignment of
    the spine on a lateral radiograph. The fusion should extend sufficiently distal to ensure sagittal and coronal
    balance, but otherwise it should be limited as much as
    possible to preserve motion.

    Os odontoideum in an 11-year-old gymnast who reported arm weakness after


    a fall. A, Lateral radiograph of the cervical spine. Note the position of the
    anterior ring of the atlas and its relation to the body of the axis. B, CT
    showing a well-demarcated os odontoideum and its anatomic location. C,
    MRI showing cord signal changes at
    the level of the os odontoideum. D,
    Lateral radiograph 1 year after fusion
    with transarticular screws and iliac
    crest bone graft and cable grafting.

    717

    Section 6: Pediatrics

    Figure 3

    6: Pediatrics

    Figure 4

    An atypical left-side thoracic curve in an 8-year-old girl who reported headaches. A, AP radiograph. Spinal dysraphism is more common in juvenile scoliosis than it is in adolescent scoliosis. MRI screening of the spinal axis is required for a curve requiring intervention. B, MRI showing the presence of a Chiari malformation and spinal cord
    syrinx. The curve progressed despite Chiari decompression and bracing. AP (C) and lateral (D) radiographs showing
    definitive fusion with segmental screw fixation.

    A 14-year-old girl with Scheuermann kyphosis.


    Lateral radiographs before (A) and after (B) posterior Ponte osteotomies and segmental pedicle
    screw fixation and fusion.

    pending spinal cord dysfunction.11 Triggered electromyography can aid the surgeon in determining the
    safety of placement for thoracic pedicle screws.

    Scheuermann Kyphosis
    The most common type of structural kyphosis in adolescents is Scheuermann kyphosis, which can have dif718

    Orthopaedic Knowledge Update 10

    ferent effects in the thoracic, thoracolumbar, and lumbar spine. Although the exact etiology is unknown, the
    result is an abnormality of the end plate apophysis that
    leads to vertebral wedging, Schmorl nodes, and sagittal
    plane kyphosis. In the thoracic spine, Scheuermann kyphosis is radiographically defined as three consecutive
    vertebral bodies with wedging of more than 5 each.
    Thoracic Scheuermann kyphosis appears in adolescents
    as pain, deformity, or both. An affected individual has
    back pain during daily life and a tendency toward jobs
    that require less physical labor. A significant curve in
    early adolescence tends to progress during peak height
    velocity, leading to fixed thoracic kyphosis, increased
    lumbar lordosis with resultant sagittal imbalance, and
    cervical lordosis.
    Brace treatment for Scheuermann kyphosis can be
    considered in a growing child who has 50 or more of
    thoracic kyphosis. A Milwaukee brace or a Boston
    brace is used, the latter with a superstructure to allow
    overall control of sagittal alignment. Surgical treatment
    is indicated if the patient has progressive deformity,
    back pain, and cosmetic deformity. The radiographic
    criterion usually is 75 of thoracic kyphosis or 40 of
    thoracolumbar kyphosis. The surgical treatment usually is posterior only, even for a severe deformity. Segmental pedicle screw fixation with foramen-to-foramen
    osteotomies is required to obtain correction12 (Figure 4). Overcorrection of the deformity in the thoracic
    spine should be avoided because it can lead to proximal
    or distal junctional kyphosis. Neurologic deficits are
    more common with correction of kyphosis than correction of scoliosis, and monitoring with somatosensoryand motor-evoked potentials is necessary.
    The term atypical Scheuermann kyphosis usually refers to end plate irregularities, vertebral wedging, and
    loss of alignment in the lumbar spine. Atypical Scheuer-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 56: Spine Trauma and Disorders: Pediatrics

    mann kyphosis can cause back pain and discomfort


    during adolescence, especially in active patients. The resultant spasms and hamstring tightness can be treated
    with physical therapy, nonsteroidal anti-inflammatory
    drugs (NSAIDs), and occasionally bracing. The disorder is self-limiting; usually the symptoms resolve after
    growth is complete, with no long-term consequences.

    Spondylolysis and Spondylolisthesis

    2011 American Academy of Orthopaedic Surgeons

    Back Pain
    Back pain is uncommon in children younger than 12
    years, but almost half of children have experienced an
    episode of low back pain by age 18 years.14 A thorough
    patient history and examination are essential for identifying pathologic back pain, which is continuous, limits walking, or interferes with sleep. Pathologic back
    pain differs from benign, mechanical back pain, which
    usually is activity related and improves with rest. An
    exhaustive evaluation is not required for all children
    with back pain, and the diagnosis usually is made from
    plain radiographs only.15 Spondylolysis and Scheuermann kyphosis are the common causes of pathologic
    back pain in children. Less common conditions include
    infection, neoplastic disorders, and juvenile arthritis.
    Laboratory studies (complete blood count, erythrocyte
    sedimentation rate, and C-reactive protein level), CT,
    MRI, or bone scanning may be necessary. MRI is best
    used if there is disk pathology or a neurologic finding.
    CT allows bony changes to be seen, as in spondylolysis
    or an osteoid osteoma. A technetium Tc 99m bone
    scan can allow detection of a tumor, infection, or fracture. Most patients with benign mechanical back pain
    respond to rest, NSAIDs, and a home training program
    or supervised physical therapy.16 School-age children
    should be counseled on proper backpack use.

    Pediatric Spine Trauma


    Spine injuries are rare in children; only 1% of all pediatric injuries involve the spine. The most common
    causes of spine injury in children are motor vehicle
    crashes, falls, sports injuries, and child abuse. Injury
    patterns in young children differ from those of adults,
    in part because of the childs greater spine elasticity,
    head size, and horizontal facet orientation. The cervical
    spine is the most frequently injured region, but thoracic
    or lumbar spine injury becomes more common with increasing age.17 In comparison to spine injuries in adolescents and adults, cord injury is more common and
    more lethal in children younger than 8 years, but the
    prognosis for recovery is better.18 Upper cervical spine
    injury (occiput to C3) is more common than lower cervical spine injury in children younger than 8 years.19
    A thorough examination is essential for any child
    with a spine injury because of the high incidence of associated injuries and noncontiguous spine trauma. In

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    The term spondylolysis refers to a fracture or defect of


    the pars interarticularis. This injury is a common cause
    of low back pain in children and especially in adolescent athletes. Spondylolysis is common among gymnasts, who are subjected to many hyperextension
    forces. The symptoms include activity-related back pain
    without a true radicular component. Usually the pain is
    nonradiating and increases with hyperextension because of impingement by the facet joint immediately
    above the fracture region. The diagnosis can be made
    using plain radiographs, although subsequent singlephoton emission CT bone scanning or CT may be required. The pars fracture can be acute, but a chronic
    defect should be suspected if CT reveals wide fracture
    lines and sclerosis of the fracture edges. In general, the
    goal of treatment is to resolve the symptoms. Nonsurgical treatment focuses on physical therapy to
    strengthen the core and relieve any associated hamstring or hip flexor tightness. NSAIDs are useful for
    reducing any acute inflammation, and bracing can minimize repetitive hyperextension forces that can aggravate the condition. Although the rate of defect healing
    with nonsurgical treatment is only 28%, 83% of patients were found to have symptom improvement.13 A
    patient who has no symptom relief after significant
    nonsurgical treatment may be a candidate for a localized fusion (if the pars fracture is at the last lumbar vertebra), or for a surgical repair of the pars (if the fracture involves a more cephalad lumbar vertebra).
    Spondylolisthesis is the anterior displacement of a
    vertebral segment relative to the next adjacent vertebral
    level. Spondylolisthesis develops from a pars defect or a
    congenital anomaly of the posterior elements. This condition sometimes is mild and self-limiting (low-grade
    spondylolisthesis), but it can cause significant back
    pain, neurologic symptoms, and cosmetic deformity
    (high-grade spondylolisthesis). The prognosis depends
    on the patients age and the extent of vertebral subluxation at presentation. The slippage can be measured by
    calculating the slip angle or measuring the percentage
    of subluxation. Patients with low-grade spondylolisthesis can be treated nonsurgically, with plain radiographic
    follow-up every 6 to 12 months.
    The surgical treatment of spondylolisthesis varies
    widely, depending on the overall deformity, the amount
    of slip, and the presence of neurologic symptoms. Patients with significant slippage usually develop neurologic symptoms similar to those of spinal stenosis.
    These patients require a posterior decompression, in
    which the posterior elements in the area of the slip are

    removed and the nerve roots are decompressed out to


    the foramina. Further progression of the slip is prevented by a fusion. Modern instrumentation techniques
    generally are used to provide stability to the arthrodesis
    bed and avoid casting. Partial surgical realignment may
    be indicated to improve the overall sagittal balance of
    the patient. Usually a realignment procedure entails anterior column support, sometimes in concert with a decompression, through a posterior interbody fusion with
    transpedicular segmental instrumentation. Spondylolisthesis also is discussed in chapter 50.

    719

    Section 6: Pediatrics

    an unconscious child, the only sign of injury may be a


    palpable defect between spinous processes, facial bruising, or passenger restraint contusions. The examination
    can be challenging even if the child is conscious. As
    many as 20% of children with a spine fracture from
    blunt trauma have a normal initial examination, and
    therefore repeated examination is warranted.20

    Anatomy and Radiographic Evaluation


    The cervical, thoracic, and lumbar vertebral bodies develop from three primary ossification centers; the lat-

    Figure 5

    Schematic drawings of the ossification centers of


    the atlas and axis. (Adapted from Copley LA,
    Dormans JP: Cervical spine disorders in infants
    and children. J Am Acad Orthop Surg 1998;
    6:205.)

    eral ossification centers form each side of the neural


    arch, and the vertebral body arises from a central ossification center (Figure 5). The posterior arches fuse to
    each other by age 3 years, and the neural arch fuses to
    the body by age 7 years. Radiographic findings suggestive of injury in an adult may be within normal limits in
    a child. These findings include prevertebral soft-tissue
    thickening, an increased atlantodens interval, pseudosubluxation of C2-C3 or C3-C4, wedging of cervical
    vertebral bodies, and loss of cervical lordosis (Table 1).
    The radiographic evaluation of a child suspected of
    having a spine injury begins with AP and lateral radiographs; if the child is older than 5 years, an openmouth odontoid radiograph is added. Although CT of
    the entire cervical spine is routinely used to rule out injury in an adult, the use of CT as the primary imaging
    modality for cervical spine injury in children remains
    controversial.21,22 On CT or a plain radiograph, a radiolucent synchondrosis can be mistaken for a fracture
    line. Conversely, a fracture through the physis may be
    overlooked. If the initial radiographic findings are
    equivocal, CT with three-dimensional reconstruction
    can accurately detect upper osseous cervical injuries.
    MRI is superior to CT for delineating the soft-tissue
    anatomy, and it alters the initial diagnosis based on
    plain radiography or CT in as many as two thirds of
    patients.23,24 MRI is best reserved for patients who are
    unconscious, have neurologic findings or a suspicious
    mechanism of injury; or if a standard clinical and radiographic evaluation cannot be performed.

    Spinal Cord Injury Without


    Radiographic Abnormality
    In as many as 34% of spinal cord injuries in children
    younger than 8 years, no abnormalities can be seen on
    the initial plain radiographs. Evidence of injury usually

    Table 1

    6: Pediatrics

    Pediatric Cervical Spine Characteristics That May Be Mistaken for a Sign of Injury

    720

    Radiographic Finding

    Patient Age
    (Range, in Years)

    Wide atlantodens interval

    0-8

    5 mm
    Space available for cord 13 mm

    Dentrocentral synchondrosis

    0-7

    Fusion line may be visible until age 11 years

    Secondary ossification center at tip of dens

    6-12

    Appears around age 6 years


    Fuses with dens by age 12 years

    C2-C3 or C3-C4 pseudosubluxation

    0-8

    <4 mm
    Smooth, contiguous posterior laminar line
    (Swischuk line)

    Prevertebral soft-tissue swelling

    0-8

    <2/3 of adjacent vertebral width on lateral film


    Prevertebral tissue is enlarged in a crying child

    Interspace angulation

    0-8

    Occurs in 16% of healthy children

    Wedging of vertebral body

    0-12

    Vertebral bodies are ovoid at birth


    7% of healthy children have a wedged C3 body

    Absence of cervical lordosis

    0-12

    Occurs in 14% of healthy children

    Orthopaedic Knowledge Update 10

    Physiologic Limits

    2011 American Academy of Orthopaedic Surgeons

    Chapter 56: Spine Trauma and Disorders: Pediatrics

    is apparent on MRI during the immediate postinjury


    period, but the MRI evidence is more specific after 48
    hours. The soft-tissue abnormalities can be intraneural,
    as in cord edema or hematoma, or extraneural, as in
    longitudinal or interspinous ligament edema. Approximately 40% of children who have a spinal cord injury
    without radiographic abnormality (SCIWORA) completely recover, but 40% do not recover neurologic
    function and 20% have partial recovery. The rigidity of
    immobilization influences recovery. If stabilization is
    unachievable through external means (a collar or halo),
    surgical stabilization should be undertaken. Recurrence
    of injury was reported in 17% of patients with SCIWORA who had external immobilization lasting no
    more than 8 weeks, but it did not recur with immobilization for 12 weeks.25

    Spine Fracture Management


    Initial and Nonsurgical Management
    The management of a cervical spine fracture begins
    with immobilization in a pediatric-size collar. The disproportionate head-to-torso ratio of young children
    can cause as much as 15 of cervical flexion in the supine position, even with a well-fitting cervical collar.
    Thus, transportation of children younger than 8 years
    requires a spine board with an occipital depression or
    sufficient thoracic elevation to align the cervical and
    thoracic spines.
    The National Acute Spinal Cord Injury Study protocol recommends administering methylprednisolone sodium succinate for 23 hours within 3 hours of a spinal
    cord injury.26 The drug is administered for 48 hours if it
    is started 3 to 8 hours after the injury. The initial bolus
    dose of 30 mg/kg over 15 minutes is followed by a
    maintenance infusion of 5.4 mg/kg/h. Few data exist on
    the use of methylprednisolone for pediatric patients,
    and its use as a standard treatment for spinal cord injury has recently been questioned.27,28
    Spine fractures in children often can be managed
    nonsurgically because of the childs bone quality and
    excellent potential for remodeling. Depending on the
    level of injury, halo vest immobilization and a thoracic
    lumbosacral orthosis may maintain spine alignment
    and prevent instability during healing.

    2011 American Academy of Orthopaedic Surgeons

    Cervical Spine Fractures


    Occipitoatlantal Dislocation
    Occipitoatlantal injuries often are fatal. If the child survives the initial injury, complete tetraplegia is likely,
    with ventilator dependence. Identifying this injury can
    be difficult. A Powers ratio higher than 1 or lower than
    0.55 is indicative, respectively, of anterior or posterior
    displacement of the occiput on the atlas. Immobilization without traction (in a halo or Minerva cast) is essential to initial treatment. Definitive stabilization requires fusion of the occiput to C1 or C2.
    Atlas Fracture
    A burst fracture of C1 (the Jefferson fracture) is rare
    but may be underappreciated in children.33 An atlas
    fracture occurs when an axial load of the head is transmitted through the occipital condyles to the lateral
    masses at C1. This injury is difficult to appreciate on
    radiographs. CT can be useful for assessing the injury
    or confirming healing. Neurologic injury is unlikely.
    The treatment usually is simple immobilization with a
    halo vest or cast for 2 to 3 months.
    Odontoid Fracture
    An odontoid fracture in a child younger than 7 years
    occurs through the synchondrosis at the base of the
    dens. In older children, odontoid fractures are similar
    to those in adults. The common symptoms are neck
    and occipital pain or a limited cervical range of motion.
    Neurologic deficits are rare. Plain radiographs may
    show an anterior angulation and translation of the
    odontoid, but spontaneous reduction is possible and
    may lead to a missed diagnosis. CT or MRI should be
    used if the diagnosis is questionable.
    The injury heals well with adequate immobilization
    for 8 to 10 weeks. The choice of a rigid collar or a halo
    vest depends on the stability of the fracture and the size
    of the patient. Anterior displacement is reduced with
    mild extension and posterior translation when the halo
    is applied. Halo pin insertion into the thin calvaria of a
    young child is most safely accomplished by using 8 to
    12 pins and limiting the insertional torque of each pin.
    In general, the insertional torque of each halo pin
    should equal the age of the child (for example, 4 ft-lb
    of torque are used for a 4-year-old child); the upper
    limit is 8 ft-lb. A thermoplastic Minerva body jacket
    can be used as an alternative to halo immobilization in
    a very young child.34 This device avoids the possibility

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Pediatric Spine Instrumentation


    Brace management may be insufficient to impart stability after a severe pediatric spine injury. Ideally, surgery
    with instrumentation should restore stability, enhance
    fusion, and lead to as little loss in mobility as possible.
    Pediatric cervical spine instrumentation in the past consisted of wire constructs augmented with halo vest immobilization. There is growing interest in applying the
    rigid fixation techniques developed for adults to pediatric patients. In the cervical spine, the options include
    occipital plates, transarticular screws (C1-C2), pedicle
    screws, lateral mass screws, pars screws, and intralaminar screws (Figure 6). Several recent studies found that
    these techniques can be safely applied in children as
    young as 3 years. Proper surgical planning is essential,

    including CT to confirm favorable bone size and rule


    out atypical anatomy.4,29,30 Pedicle screw fixation is a
    powerful means of reducing and stabilizing fractures of
    the thoracic and lumbar spine in children. Its advantages include the possibility of limiting fusion to one or
    two levels above and below the fracture and reducing
    or eliminating the need for a brace. Additional study is
    needed to determine whether the use of pedicle screws
    that cross an open neurocentral synchondrosis in a
    young child can lead to iatrogenic spinal stenosis or
    scoliosis.31,32

    721

    Section 6: Pediatrics

    Figure 6

    Imaging studies of a 17-year-old girl. A, MRI showing an injury to the upper cervical spine resulting from a motor
    vehicle crash and complicated by the presence of congenital stenosis at C1. B, CT showing a high-riding vertebral
    artery at C2, which precluded the use of transarticular C1-C2 screws. CT is essential in planning cervical instrumentation in children. Lateral radiograph (C) and CT (D) showing occiput-to-C2 fusion with an occipital plate and intralaminar C2 screws.

    of pin complications and pin artifact on MRI or CT,


    but it allows slightly more motion.35

    6: Pediatrics

    Atlantoaxial Instability and Rotatory Subluxation


    Isolated rupture of the transverse ligament of the atlas
    is an uncommon injury in children. The resultant
    C1-C2 instability is suggested by an atlantodens interval greater than 5 mm on a lateral radiograph. Treatment of an acute rupture is possible with halo cast immobilization for 8 to 12 weeks. Marked instability is
    best managed with C1-C2 fusion.36
    Atlantoaxial rotatory subluxation is an acquired alteration of the articulation between the atlas and axis.
    It can result from minor trauma but more commonly
    occurs after an upper respiratory infection (Grisel syndrome) or a nasopharyngeal procedure. Head movement causes pain, and C1-C2 rotation is significantly
    limited or completely fixed. The child has torticollis, in
    which the chin is rotated to one side and the head is
    722

    Orthopaedic Knowledge Update 10

    tilted to the opposite side. Unlike congenital muscular


    torticollis, which is caused by a tight sternocleidomastoid, this condition is characterized by tenseness in the
    muscle that opposes the head position on the long side.
    Rotatory subluxation is suggested by asymmetry of
    the C1 lateral masses on an open-mouth odontoid radiograph or overlapping of C1 onto C2 on a lateral radiograph. Dynamic CT can confirm the diagnosis by
    revealing a loss of the normal atlantoaxial rotation
    with attempted maximal head rotation. Many atlantoaxial rotatory displacements resolve spontaneously.
    The treatment depends on the duration of symptoms.37
    During the first week, the treatment consists of immobilization with a soft collar, NSAIDs, and range-ofmotion exercises. If symptoms persist, inpatient cervical
    halter traction, muscle relaxants, and analgesics are
    used. A halo cast sometimes is applied for 4 to 6 weeks
    after reduction is achieved. If painful rotatory subluxation persists or recurs, fusion of C1-C2, with or without reduction, is indicated.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 56: Spine Trauma and Disorders: Pediatrics

    Hangmans Fracture
    Spondylolisthesis secondary to a bilateral pedicle fracture at C2 results from forced hyperextension and is
    called a hangmans fracture. Anterior displacement of
    the posterior arch of C2 more than 2 mm from the
    spinolaminar line (the Swischuk line) suggests injury.
    This fracture heals with immobilization for 12 weeks
    and rarely requires C1-C3 fusion.
    Subaxial Fracture
    Subaxial injury (C3-C7) is most common in children
    age 9 years or older, and usually occurs between C5
    and C7.38 The most common injury patterns involve
    compression fracture of the vertebral body or facet dislocation. These injuries often are managed with initial
    traction to realign the kyphosis and reduce any dislocated facet. Approximately two thirds of children with
    a subaxial injury can be treated with a rigid collar or
    halo vest only. Excessive cervical flexion or extension in
    children can also lead to the separation of the cartilaginous end plate from the vertebral body. This injury is
    extremely unstable and may require surgical fixation.

    Thoracolumbar Spine Injuries

    2011 American Academy of Orthopaedic Surgeons

    Annotated References
    1.

    Kawakami N, Tsuji T, Imagama S, Lenke LG, Puno


    RM, Kuklo TR; Spinal Deformity Study Group: Classification of congenital scoliosis and kyphosis: A new approach to the three-dimensional classification for progressive vertebral anomalies requiring operative
    treatment. Spine (Phila Pa 1976) 2009;34(17):17561765.
    Three-dimensional CT led to a more comprehensive understanding of anomalies than the classic classification
    scheme.

    2.

    Hedequist DJ: Instrumentation and fusion for congenital spine deformities. Spine (Phila Pa 1976) 2009;
    34(17):1783-1790.
    Modern instrumentation and fusion techniques for congenital scoliosis are reviewed.

    3.

    Hedequist D, Hresko T, Proctor M: Modern cervical


    spine instrumentation in children. Spine (Phila Pa 1976)
    2008;33(4):379-383.
    Twenty-five patients were treated surgically with modern implants for a cervical spine disorder. The authors
    conclude this is a safe and efficacious technique, even in
    young children.

    4.

    Klimo P Jr, Kan P, Rao G, Apfelbaum R, Brockmeyer


    D: Os odontoideum: Presentation, diagnosis, and treatment in a series of 78 patients. J Neurosurg Spine 2008;
    9(4):332-342.
    A retrospective review of 78 patients with os odontoideum included three patients who were asymptomatic at
    the time of diagnosis and were observed. All three patients developed neurologic symptoms, leading the authors to conclude that this disorder requires posterior

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Injury to the thoracic or lumbar spine in children is less


    common than cervical spine injury. The injury tends to
    occur at the thoracolumbar junction, usually as the result of a motor vehicle crash or sports injury.39 The
    three-column classification of spine injuries in adults
    also is applicable to children. The mechanism of injury
    and its stability are determined by the extent of injury
    to the anterior, middle, and posterior columns. The injury is classified as a compression fracture, burst fracture, flexion-distraction injury, or fracture-dislocation.
    Compression fractures involve a failure of the anterior column without injury to the middle or posterior
    column. A compression fracture can occur at multiple
    levels as the result of a flexion mechanism of injury. A
    compression fracture with a less than 50% loss of
    height is considered stable and unlikely to have any associated neurologic injury. The injury will heal with 4
    to 6 weeks of brace immobilization. Vertebral body
    height can partially reconstitute itself if significant
    growth remains. Posterior surgical stabilization may be
    needed if there is significant kyphosis from multiple
    compression fractures.
    Burst fractures involve a failure of the anterior and
    middle columns. A burst fracture is most common in
    adolescents and young adults who sustain an axial
    load, as with a fall from a height. An associated neurologic injury is likely to be caused by the retropulsed
    fragments into the canal or neuroforamina. The evaluation should include an MRI before reduction to rule
    out a dural tear or nerve root entrapment. Stabilization
    with posterior instrumentation is preferred in children
    with significant remaining anterior growth. A pedicle
    screw construct that includes one or two levels above
    and below the fracture site sometimes can restore sufficient sagittal alignment. Anterior column reconstruction may be needed if the vertebral body height is less
    than 60% or for anterior decompression of the canal.

    A flexion-distraction injury, also known as a Chance


    fracture, is a compression fracture of the anterior column with a distraction injury to the middle and posterior columns. In children, the posterior and middle column injury can be osseous or ligamentous. The
    ligamentous injury propagates between the spinous
    processes, and the end plate separates from the vertebral body. This fracture is best appreciated on MRI.40
    Nearly all of these fractures are seat belt injuries, usually in children younger than 10 years. They may be accompanied by major abdominal injuries including aortic dissection.20 Injuries involving bony elements with
    less than 15 of segmental kyphosis can be treated with
    an extension cast or a brace, if adequate reduction is
    achieved. Surgical stabilization with pedicle screws or
    wires is preferable if significant kyphosis or ligamentous injury exists.
    A fracture-dislocation is a rare injury that involves a
    failure of all three columns. The thoracolumbar junction is the most common site of injury. These highly unstable fractures almost always require surgical reduction, decompression, and internal fixation. Neurologic
    injury is likely.

    723

    Section 6: Pediatrics

    cervical arthrodesis. Transarticular screws can be successfully used in the pediatric population.
    5.

    6.

    Thompson GH, Akbarnia BA, Campbell RM Jr: Growing rod techniques in early-onset scoliosis. J Pediatr Orthop 2007;27(3):354-361.
    The use of growing-rod techniques for early-onset scoliosis is reviewed. This technique allows continued
    growth of the spine while controlling curvature. The
    complication rate, while moderate, is acceptable and relates to hook disengagement or rod breakage.

    7.

    Sanders JO, Khoury JG, Kishan S, et al: Predicting scoliosis progression from skeletal maturity: A simplified
    classification during adolescence. J Bone Joint Surg Am
    2008;90(3):540-553.
    The radiographic appearance of the epiphyses of the
    phalanges, metacarpals, and distal radius are correlated
    with the adolescent growth phases. A useful classification system is presented for determining the timing of
    growth in relation to a bone age radiograph. The information is useful for determining the potential for successful bracing in patients with idiopathic scoliosis.

    8.

    6: Pediatrics

    9.

    10.

    724

    Sanders JO, DAstous J, Fitzgerald M, Khoury JG, Kishan S, Sturm PF: Derotational casting for progressive
    infantile scoliosis. J Pediatr Orthop 2009;29(6):581587.
    The authors experience with derotation casting for infantile scoliosis is reviewed. This prospective study
    found that casting is best for patients younger than 20
    months with a Cobb angle of less than 60. Older patients with a larger Cobb angle tended to have a poorer
    outcome with serial casting.

    Lenke LG, Betz RR, Harms J, et al: Adolescent idiopathic scoliosis: A new classification to determine extent
    of spinal arthrodesis. J Bone Joint Surg Am 2001;83(8):
    1169-1181.
    Newton PO, Upasani VV, Lhamby J, Ugrinow VL,
    Pawelek JB, Bastrom TP: Surgical treatment of main
    thoracic scoliosis with thoracoscopic anterior instrumentation: A five-year follow-up study. J Bone Joint
    Surg Am 2008;90(10):2077-2089.
    Forty-one patients were treated with anterior thoracoscopic fusion and instrumentation for adolescent idiopathic scoliosis, with 5-year follow-up. The advantages
    of limited scar and muscle dissection must be weighed
    against the increased risk of pseudarthrosis and implant
    failure, compared with posterior instrumentation techniques.
    Suk SI, Kim JH, Cho KJ, Kim SS, Lee JJ, Han YT: Is anterior release necessary in severe scoliosis treated by
    posterior segmental pedicle screw fixation? Eur Spine J
    2007;16(9):1359-1365.
    Thirty-five patients with curves greater than 70 treated
    with posterior surgery alone were retrospectively reviewed. Satisfactory coronal and sagital correction was
    achieved with segmental pedicle screw fixation.

    Orthopaedic Knowledge Update 10

    11.

    Schwartz DM, Auerbach JD, Dormans JP, et al: Neurophysiological detection of impending spinal cord injury
    during scoliosis surgery. J Bone Joint Surg Am 2007;
    89(11):2440-2449.
    A clinical study of 1,121 patients who underwent instrumented spine fusion for adolescent idiopathic scoliosis found that transcranial monitoring of motor-evoked
    potentials is more specific than monitoring of
    somatosensory-evoked potentials with regard to spinal
    cord insult. Both motor- and somatosensory-evoked potentials should be used for spine deformity surgery.

    12.

    Geck MJ, Macagno A, Ponte A, Shufflebarger HL: The


    Ponte procedure: Posterior only treatment of Scheuermanns kyphosis using segmental posterior shortening
    and pedicle screw instrumentation. J Spinal Disord Tech
    2007;20(8):586-593.
    A prospective study of 17 patients treated with Ponte
    osteotomies and posterior instrumentation for Scheuermann kyphosis found that even for larger degrees of kyphosis, correction is possible with apical osteotomies
    and pedicle screw fixation from a posterior-only approach.

    13.

    Klein G, Mehlman CT, McCarty M: Nonoperative


    treatment of spondylolysis and grade I spondylolisthesis
    in children and young adults: A meta-analysis of observational studies. J Pediatr Orthop 2009;29(2):146-156.
    A meta-analysis of 15 observational studies found
    83.9% of patients treated nonsurgically for spondylolysis had a successful clinical outcome after at least 1 year.

    14.

    Leboeuf-Yde C, Kyvik KO: At what age does low back


    pain become a common problem? A study of 29,424 individuals aged 12-41 years. Spine (Phila Pa 1976) 1998;
    23(2):228-234.

    15.

    Bhatia NN, Chow G, Timon SJ, Watts HG: Diagnostic


    modalities for the evaluation of pediatric back pain: A
    prospective study. J Pediatr Orthop 2008;28(2):230233.
    The authors present level II evidence that exhaustive diagnostic testing for pediatric back pain infrequently
    leads to a definitive diagnosis.

    16.

    Ahlqwist A, Hagman M, Kjellby-Wendt G, Beckung E:


    Physical therapy treatment of back complaints on children and adolescents. Spine (Phila Pa 1976) 2008;
    33(20):E721-E727.
    In a randomized study, 45 children with back complaints demonstrated improvement with both individualized and nonindividualized physical therapy but
    shorter duration of pain with an individualized therapy
    program.

    17.

    Bilston LE, Brown J: Pediatric spinal injury type and severity are age and mechanism dependent. Spine (Phila
    Pa 1976) 2007;32(21):2339-2347.
    A retrospective review of 340 patients with pediatric
    spine trauma found that in older children spine injuries
    are likely to result from sports and recreation, and they
    become more evenly distributed between the cervical
    and thoracolumbar spine.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 56: Spine Trauma and Disorders: Pediatrics

    18.

    Carreon LY, Glassman SD, Campbell MJ: Pediatric


    spine fractures: A review of 137 hospital admissions.
    J Spinal Disord Tech 2004;17(6):477-482.

    19.

    Polk-Williams A, Carr BG, Blinman TA, Masiakos PT,


    Wiebe DJ, Nance ML: Cervical spine injury in young
    children: A National Trauma Data Bank review. J Pediatr Surg 2008;43(9):1718-1721.
    The study reviewed 95,654 blunt traumas in children
    younger than 3 years. The rate and type of spinal column injuries in this population are detailed.

    20.

    21.

    22.

    23.

    Junkins EP Jr, Stotts A, Santiago R, Guenther E: The


    clinical presentation of pediatric thoracolumbar fractures: A prospective study. J Trauma 2008;65(5):10661071.
    This prospective study of children at a level I trauma
    center during a 1-year period found that examination
    was only 81% sensitive and 68% specific for diagnosing
    a thoracolumbar fracture.
    Jimenez RR, Deguzman MA, Shiran S, Karrellas A, Lorenzo RL: CT versus plain radiographs for evaluation of
    c-spine injury in young children: Do benefits outweigh
    risks? Pediatr Radiol 2008;38(6):635-644.
    CT and conventional radiography are compared as a
    primary screening tool for pediatric spine injury. Radiation exposure is as much as 90 times greater with CT,
    but CT often was used as a screening tool regardless of
    injury severity.
    Rana AR, Drongowski R, Breckner G, Ehrlich PF: Traumatic cervical spine injuries: Characteristics of missed
    injuries. J Pediatr Surg 2009;44(1):151-155, discussion
    155.
    This study of 1,307 patients suggested that CT is the optimal primary means of detecting cervical spine injuries.
    Flynn JM, Closkey RF, Mahboubi S, Dormans JP: Role
    of magnetic resonance imaging in the assessment of pediatric cervical spine injuries. J Pediatr Orthop 2002;
    22(5):573-577.
    Junewick JJ, Meesa IR, Luttenton CR, Hinman JM: Occult injury of the pediatric craniocervical junction.
    Emerg Radiol 2009;16(6):483-488.

    25.

    Launay F, Leet AI, Sponseller PD: Pediatric spinal cord


    injury without radiographic abnormality: A metaanalysis. Clin Orthop Relat Res 2005;433:166-170.

    26.

    Bracken MB, Shepard MJ, Collins WF, et al: A randomized controlled trial of methylprednisolone or naloxone
    in the treatment of acute spinal cord injury: Results of
    the second national acute spinal cord injury study. N
    Engl J Med 1990;322:1405-1411.

    27.

    Ito Y, Sugimoto Y, Tomioka M, Kai N, Tanaka M:


    Does high dose methylprednisolone sodium succinate
    really improve neurological status in patient with acute
    cervical cord injury? A prospective study about neurological recovery and early complications. Spine (Phila
    Pa 1976) 2009;34(20):2121-2124.

    2011 American Academy of Orthopaedic Surgeons

    28.

    Pereira JE, Costa LM, Cabrita AM, et al: Methylprednisolone fails to improve functional and histological outcome following spinal cord injury in rats. Exp Neurol
    2009;220(1):71-81.
    The effects of methylprednisolone were compared with
    saline solution in the treatment of rats with a T10 contusion injury. Results indicate that methylprednisolone
    does not lead to improved functional outcome.

    29.

    Hedequist D, Proctor M: Screw fixation to C2 in children: A case series and technical report. J Pediatr Orthop 2009;29(1):21-25.
    This is one of the first reports on the safety and efficacy
    of various screw fixation techniques to C2, even in
    young children.

    30.

    Reilly CW, Choit RL: Transarticular screws in the management of C1-C2 instability in children. J Pediatr Orthop 2006;26(5):582-588.

    31.

    Cil A, Yazici M, Daglioglu K, et al: The effect of pedicle


    screw placement with or without application of compression across the neurocentral cartilage on the morphology of the spinal canal and pedicle in immature
    pigs. Spine (Phila Pa 1976) 2005;30(11):1287-1293.

    32.

    Zhang H, Sucato DJ: Unilateral pedicle screw epiphysiodesis of the neurocentral synchondrosis: Production of
    idiopathic-like scoliosis in an immature animal model.
    J Bone Joint Surg Am 2008;90(11):2460-2469.
    The authors induced scoliosis in young pigs by placing
    unilateral pedicle screws across the neurocentral synchondrosis.

    33.

    AuYong N, Piatt J Jr: Jefferson fractures of the immature spine: Report of 3 cases. J Neurosurg Pediatr 2009;
    3(1):15-19.
    This article describes common findings and possible
    sources for missing Jefferson fractures in young children.

    34.

    Skaggs DL, Lerman LD, Albrektson J, Lerman M, Stewart DG, Tolo VT: Use of a noninvasive halo in children.
    Spine (Phila Pa 1976) 2008;33(15):1650-1654.
    Twenty-nine of 30 children were successfully immobilized with a new pinless halo, including seven with cervical fusion and five with atlantoaxial rotatory instability.

    35.

    Mandabach M, Ruge JR, Hahn YS, McLone DG: Pediatric axis fractures: Early halo immobilization, management and outcome. Pediatr Neurosurg 1993;19(5):225232.

    36.

    Reilly CW: Pediatric spine trauma. J Bone Joint Surg


    Am 2007;89(suppl 1):98-107.

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    24.

    This retrospective comparison of adults treated with or


    without steroids at the time of spinal cord injury failed
    to find any neurologic benefit to steroids while noting a
    higher rate of pulmonary complications in patients who
    received steroids.

    725

    Section 6: Pediatrics

    The authors present a review article on pediatric spine


    trauma.
    Pang D, Li V: Atlantoaxial rotatory fixation: Part III. A
    prospective study of the clinical manifestation, diagnosis, management, and outcome of children with atlantoaxial rotatory fixation. Neurosurgery 2005;57(5):954972, discussion 954-972.

    38.

    Dogan S, Safavi-Abbasi S, Theodore N, Horn E, Rekate


    HL, Sonntag VK: Pediatric subaxial cervical spine injuries: Origins, management, and outcome in 51 patients.
    Neurosurg Focus 2006;20(2):E1.

    Dogan S, Safavi-Abbasi S, Theodore N, et al: Thoracolumbar and sacral spinal injuries in children and adolescents: A review of 89 cases. J Neurosurg 2007;106(6,
    suppl):426-433.
    This large retrospective study of children with thoracolumbar injuries describes the common location, associated injuries, and rates of recovery.

    40.

    de Gauzy JS, Jouve JL, Violas P, et al: Classification of


    Chance fracture in children using magnetic resonance
    imaging. Spine (Phila Pa 1976) 2007;32(2):E89-E92.
    Three types of Chance fracture lesions in children are all
    well visualized on MRI.

    6: Pediatrics

    37.

    39.

    726

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 57

    Pelvis, Hip, and Femur


    Trauma: Pediatrics
    Amy L. McIntosh, MD

    Karl E. Rathjen, MD

    Introduction
    Injury to the pelvis, hip, or femur in a child usually is
    the result of high-energy trauma. The possibility of
    nonaccidental trauma must be remembered if the child
    is younger than 2 years. It is important that the assessment of every child with an injury to the pelvis, hip, or
    femur begins with basic trauma care. When it has been
    determined the patient is stable and all injuries have
    been identified, a treatment plan can be developed that
    takes into consideration the unique characteristics of
    the immature skeleton as well as the patients specific
    injuries.

    Pelvic Fracture

    Characteristics

    Neither Dr. McIntosh nor any immediate family member


    has received anything of value from or owns stock in a
    commercial company or institution related directly or indirectly to the subject of this chapter. Dr. Rathjen or an
    immediate family member serves as an unpaid consultant to Orthopediatrics.

    2011 American Academy of Orthopaedic Surgeons

    Most pelvic fractures in children are stable and can be


    treated nonsurgically with spica casting or protected
    weight bearing. Adolescents are more likely to have an
    unstable injury requiring surgical stabilization. In a review of 166 pediatric patients with a pelvic fracture, all
    patients requiring open reduction and internal fixation
    were found to have a closed triradiate cartilage.7 However, a review of 148 pediatric patients with a pelvic
    fracture found that a third of the 18 patients requiring
    open reduction had an open triradiate cartilage.8 The
    indications for surgical management in children are
    similar to those for adults; they include pelvic ring disruption with more than 2 cm of displacement, acetabular fracture, and triradiate cartilage injury with more
    than 2 mm of displacement.9

    Complications
    Death is uncommon in children with a pelvic fracture,
    and it almost always is the result of a head or visceral
    injury. Pelvic fractureassociated hemorrhage is less
    common in children than in adults. A solid visceral injury is more likely than a pelvic vascular disruption to
    cause massive blood loss in children with a pelvic
    fracture.10-12
    Pelvic ring disruption is unlikely to remodel, and
    healing with more than 1 cm of pelvic asymmetry may
    increase the risk of nonstructural scoliosis, lumbar
    pain, the Trendelenburg sign, or sacroiliac joint tenderness and pain.13 Patients with acetabular fractures generally do well with treatment, but those with triradiate
    cartilage injury may not and conditions can deteriorate
    over time.14 Injury to the triradiate cartilage may produce physeal arrest and subsequent hip dysplasia.15,16 If
    a triradiate physeal bar is identified early, it may be
    possible to excise it and prevent or limit subsequent
    dysplasia.17

    6: Pediatrics

    Pelvic fractures include pelvic ring injuries, acetabular


    fractures, and apophyseal avulsion fractures (also discussed in chapter 61). Pelvic ring and acetabular fractures in children most commonly result from a pedestrianmotor vehicle collision or a motor vehicle crash.
    Pelvic ring injuries are more common than acetabular
    fractures, which were found to account for only 13%
    of pelvic injuries.1,2 Although two studies attempted to
    identify risk factors for pelvic fracture,3,4 it is important
    to remember that 30% of patients had a normal physical examination.2 With all traumatic injuries, the treating personnel must maintain a high degree of suspicion
    as well as a low threshold for obtaining appropriate radiographs. Children can sustain an open pelvic injury,
    although this injury is uncommon. It is important that
    a child with a pelvic fracture receive a thorough rectal
    and genitourinary examination.5,6

    Treatment

    Hip Dislocation

    Characteristics
    Most traumatic hip dislocations are posterior, although
    anterior dislocations do occur. A careful examination
    should be performed to delineate all associated injuries.

    Orthopaedic Knowledge Update 10

    727

    Section 6: Pediatrics

    Figure 1

    Posterior dislocation of a childs left hip. A, Radiograph showing the dislocation. B, AP pelvic radiograph showing
    the hip after attempted closed reduction. The hip is not concentrically reduced (arrow). C, CT showing the noncongruently reduced left hip (arrow). There are no entrapped osteocartilaginous fragments. D, MRI showing an
    enfolded ligamentum teres or capsule (arrow) causing the nonconcentric hip reduction. E, AP pelvic radiograph
    showing mild coxa magna and subtle femoral neck deformity 4 years after open reduction and removal of
    entrapped capsule and ligamentum.

    An associated fracture (particularly fracture of the


    proximal femoral epiphysis), a nerve injury (most commonly to the peroneal branch of the sciatic nerve), or
    an ipsilateral knee injury is reported in 5% to 30% of
    patients.18-21
    6: Pediatrics

    Treatment
    A timely attempt at closed reduction is the first treatment for all traumatic hip dislocations. Closed reduction is successful for most dislocated hips. Because of
    the possibility of displacing the proximal femoral
    epiphysis, it is imperative that closed reduction be done
    with appropriate sedation or anesthesia. To prevent
    proximal femoral physeal separation, the use of fluoroscopy during the reduction has been recommended.22
    Postreduction radiographs should be carefully assessed.
    In children, a nonconcentric reduction may be caused
    by interposed capsule or labrum. Unlike osteocartilagi728

    Orthopaedic Knowledge Update 10

    nous fragments in adults, the interposed soft tissue is


    not evident on postreduction CT. It is important to remember that subtle asymmetry on postreduction radiographs may be the only indication that an open reduction is necessary19,23-26 (Figure 1). If open reduction is
    required, the traditional surgical approach is in the direction of the dislocation (most commonly posteriorly).
    However, the Ganz surgical dislocation technique can
    be used to provide excellent circumferential exposure
    of the labrum.27,28
    Traumatic hip dislocation in children generally has a
    good long-term outcome. In 42 children with a traumatic hip dislocation, 95% had mild pain (usually
    weather related) or no pain, and 78% continued to participate in high-demand activities such as football, soccer, and basketball.20 Traumatic hip dislocations still
    may be neglected in the developing world; these patients may benefit from open reduction.29,30

    2011 American Academy of Orthopaedic Surgeons

    Chapter 57: Pelvis, Hip, and Femur Trauma: Pediatrics

    Complications
    The complications of traumatic hip dislocation in children include nerve injury, redislocation, coxa magna,
    and osteonecrosis. Osteonecrosis in children who have
    traumatic hip dislocation without femoral neck fracture
    is less common than in adults, and it may be related to
    a delay in reduction.20 Coxa magna is a common radiographic finding that is not associated with functional
    limitation. Redislocation is rare and can be treated with
    prolonged immobilization or capsulorrhaphy, depending on the age of the patient and the time elapsed since
    injury.31 In adults, 60% to 70% of nerve injuries associated with hip dislocation spontaneously improve.21

    Femoral Neck Fracture

    Characteristics
    Femoral neck fractures in children are classified using
    the Delbet system. Type I is a transphyseal separation,
    type II is transcervical, type III is basicervical, and type
    IV is intertrochanteric. A femoral neck fracture in the
    absence of a history of high-energy trauma should raise
    suspicion of nonaccidental trauma or pathologic
    bone.32,33

    Treatment

    2011 American Academy of Orthopaedic Surgeons

    Complications
    Osteonecrosis is the most common and significant complication of femoral neck fracture in children. A review
    of 25 femoral neck fractures with a meta-analysis of an
    additional 335 fractures found that the development of
    osteonecrosis was correlated with the age of the patient
    and the type of fracture. For each year of increasing
    age, patients were 1.14 times more likely to develop osteonecrosis. The rate of osteonecrosis was 38% for
    Delbet type I fractures, 28% for type II fractures, 18%
    for type III fractures, and 5% for type IV fractures.40
    Delayed union or nonunion has been reported to occur after 3% to 67% of femoral neck fractures in children.41,42 Delayed union and nonunion can be successfully managed with proximal femoral valgus
    osteotomy43 (Figure 2). Other reported complications
    include coxa vara, coxa valga, coxa magna, premature
    physeal closure, limb-length difference, and infection.41,42,44

    Subtrochanteric Femur Fracture

    Characteristics
    In adults, a subtrochanteric femur fracture is defined as
    a fracture no more than 5 cm below the lesser trochanter. As modified for children, the definition is a
    fracture within 10% of the total femoral length of the
    lesser trochanter.45 A subtrochanteric fracture resulting
    from low-energy trauma should raise suspicion of a
    preexisting pathologic lesion.46

    Treatment and Complications


    Subtrochanteric femur fractures can be treated with
    spica casting, traction followed by spica casting, or surgical stabilization using external fixation or a plateand-screw or intramedullary device.47 These fractures
    tend to develop unacceptable varus and shortening, and
    therefore displaced fractures should be managed with
    some form of stabilization.45,48,49 An incomplete and
    nondisplaced fracture can be managed in an immediate
    spica cast, but it should be followed closely during the
    first 2 to 3 weeks to ensure that deformity does not develop.47 Limb-length discrepancy and angular malalignment are the most commonly reported complications of
    subtrochanteric femur fracture. Careful attention to detail during treatment may limit the risk of these complications. Osteonecrosis of the femoral head, heterotopic
    ossification, and infection also can occur.

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Displaced physeal separation in an infant sometimes


    occurs as a result of obstetric or nonaccidental trauma.
    Because of an infants tremendous remodeling potential, this injury can be successfully treated with immobilization in a Pavlik harness or spica cast. In these children, a nondisplaced, incomplete femoral neck fracture
    resulting from low-energy trauma can be managed with
    spica casting and close follow-up to ensure displacement and deformity do not develop. Because of a
    childs propensity to develop progressive deformity,
    protected weight bearing should be undertaken with
    extreme caution.34
    Almost all other displaced femoral neck fractures in
    children should be managed with urgent anatomic reduction, stable fixation, and external immobilization.
    No conclusive evidence has established the superiority
    of a closed reduction or an open reduction. However,
    the time to reduction and the quality of the reduction
    influence the risk of osteonecrosis.35,36 Thus, it is imperative that the reduction be timely and anatomic, regardless of whether the surgeon chooses closed reduction and percutaneous fixation, an anterior approach
    with percutaneous fixation, or an anterolateral approach for reduction and fixation. Recent studies suggested that decompression of the hip capsule may decrease the incidence of osteonecrosis37,38
    Because of the relatively frequent occurrence of delayed union or nonunion, fracture stability should take
    precedence over physeal viability. Surgeons should
    cross the physis with implants whenever necessary; the
    implants can be removed after the fracture has healed36
    (Figure 2). Adequate fixation is important, and supplemental immobilization with a hip spica cast is effective

    at decreasing the rotational forces produced by the distal fragment. It is wise to recognize that the leg is an exceptionally long moment arm that can produce tremendous rotational forces at the fracture site even when it
    is not bearing weight. Avoidance of weight bearing is
    not always achievable in children, and therefore it is
    not surprising that supplemental spica casting is associated with low rates of delayed union or nonunion.39

    729

    6: Pediatrics

    Section 6: Pediatrics

    Figure 2

    730

    Basicervical femoral neck fracture of the right hip in an adolescent girl. A, AP pelvic radiograph showing the fracture. B, AP pelvic radiograph taken immediately after attempted percutaneous reduction. The reduction is not
    anatomic. To avoid crossing the physis, relatively short screws were used. C, AP (left) and frog-lateral (right) pelvic
    radiographs taken 4 months after injury, showing slight varus collapse, backing out of the screws, and delayed
    fracture union. D, AP (left) and lateral (right) fluoroscopic views showing valgus osteotomy, revision fixation, and
    bone grafting of the femoral neck site through the compression hip screw tract. E, AP pelvic radiograph taken
    2 years after valgus osteotomy, showing the slightly shortened femoral neck.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 57: Pelvis, Hip, and Femur Trauma: Pediatrics

    Femoral Shaft Fracture


    Fractures of the femoral shaft are common, and most
    orthopaedic surgeons treat them on a regular basis.
    Cortical thickness increases throughout childhood; the
    mechanism of injury in femoral shaft fractures therefore is correlated with age. A fall is the most common
    mechanism of injury in toddlers and children younger
    than 10 years. The most common mechanism among
    older children and adolescents is a pedestrianmotor
    vehicle collision or a motor vehicle crash.50
    Repeated fractures or a fracture after minor trauma
    should alert the clinician to the possibility of an underlying pathologic condition. Osteogenesis imperfecta is
    diagnosed based on the presence of multiple fractures
    and other typical signs including dentinogenesis imperfecta, blue sclerae, and hearing loss. The diagnosis can
    be confirmed by analysis of collagen produced by cultured dermal fibroblasts. Generalized osteopenia from
    cerebral palsy, myelomeningocele, and other neuromuscular conditions also leads to a predisposition to fracture.51 Radiographs always should be carefully evaluated for localized pathologic conditions that could
    predispose the patient to fracture. The most common
    benign conditions include a unicameral bone cyst,
    nonossifying fibroma, eosinophilic granuloma, or aneurysmal bone cyst. Malignant conditions are far less
    common; they include osteogenic sarcoma, Ewing sarcoma, and lymphoma.
    Nonaccidental trauma accounts for 50% to 69% of
    all fractures in children younger than 1 year.52 Such
    fractures are the second most common symptom of
    child abuse, after soft-tissue injury such as bruising or
    burn injury. Among child abuserelated long bone injuries, humerus fractures are the most common and femur fractures are the second most common. The age of
    the patient is important in identifying injury patterns
    that may be related to abuse. A rib, tibia-fibula, humerus, or femur fracture is more likely to be the result
    of nonaccidental trauma in a patient younger than 18
    months than in an older patient.53

    Table 1

    Age-Based Treatment Recommendations


    for Femoral Diaphyseal Fractures
    Age: 0-6 months
    Pavlik harness or spica casting
    Age: 7 months-5 years
    Early spica cast if 2cm of initial shortening
    If > 2 cm of shortening or polytrauma/open fracture:
    Flexible Intramedullary fixation
    Bridge versus open plating
    Skeletal traction for 2-3 weeks, followed by spica cast
    External fixator
    Age: 6-11 years
    Flexible intramedullary nails if the fracture pattern is length
    stable
    Length stable fracture patterns are either transverse or
    oblique. An oblique fracture is < 2 times the femoral
    diameter at the level of the fracture.
    Submuscular bridge plating if the fracture pattern is length
    unstable or is a very proximal/distal fracture.
    Length unstable fractures patterns are comminuted and/or
    spiral. A spiral fracture is 2 times the femoral diameter
    at the level of the fracture.
    Age: > 11 years
    Flexible intramedullary nails if length stable, and patient
    weighs 100 lb
    Rigid trochanteric entry nail if length unstable, or patient
    weighs > 100 lb
    Submuscular bridge plate if length unstable or very
    proximal/distal fracture

    helps define stability and is best classified at the time of


    initial evaluation as unacceptable (more than 3 cm of
    shortening) or acceptable (less than 3 cm of shortening).

    Treatment and Complications


    Characteristics

    2011 American Academy of Orthopaedic Surgeons

    The American Academy of Orthopaedic Surgeons has


    published a guideline on the treatment of pediatric diaphyseal femur fractures56 (Table 1). Several methods
    can be used to treat femoral shaft fractures in children.
    The age and size of the child are the most important
    factors in deciding which treatment modality is most
    appropriate. In general, infants and children younger
    than 5 years are treated nonsurgically in a Pavlik harness or hip spica cast. Children older than 5 years may
    be treated with some form of skeletal fixation. Additional factors to consider include the mechanism of injury, the presence of multiple injuries, the condition of
    the soft tissue, the family support environment, and the
    available economic resources. As with any form of orthopaedic treatment, the experience, skill, and preference of the treating physician may be significant in determining the treatment. Guidelines based on the age of
    the patient can be used.

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    The classification of femoral shaft fractures, like that of


    most diaphyseal fractures, is based on the radiographic
    examination and the condition of the soft-tissue envelope (that is, whether the fracture is closed or open).
    Radiographs are evaluated for fracture location (proximal, middle, or distal third), configuration (transverse,
    oblique, or spiral), angulation, the extent of comminution, and the amount of displacement, translation, and
    shortening. Spiral and oblique fractures are differentiated based on the length of the fracture. A fracture is
    classified as spiral if its length is more than twice the
    femoral diameter at the level of the fracture. A fracture
    that is shorter than twice the femoral diameter at the
    level of the fracture is considered oblique.54,55 Femur
    fractures are designated as length stable or unstable.
    Stable fractures are transverse or oblique, and unstable
    fractures are spiral or comminuted.54 Shortening also

    731

    Section 6: Pediatrics

    Birth to Age 6 Months


    The Pavlik harness can be used for treatment of a femur fracture in infants younger than 6 months. The advantages of the Pavlik harness include ease of application without sedation or general anesthesia, ability to
    adjust the harness if fracture manipulation is necessary,
    ease of diapering, and absence of the skin irritation
    commonly associated with casting.57 Excessive hip flexion in the presence of a swollen thigh may compress the
    femoral nerve, and the surgeon should monitor quadriceps function during treatment to detect such an injury.

    6: Pediatrics

    Age 7 Months to 5 Years


    In children age 7 months to 5 years without extenuating circumstances such as polytrauma, neurovascular
    injury, or open injury, nonsurgical treatment is with
    closed reduction and immediate spica cast application.
    Preschool-age children tolerate a spica cast much better
    than school-age children because they can be transported more easily and have shorter healing times. An
    unstable fracture with more than 2 to 3 cm of initial
    shortening may be difficult to manage in a spica cast.
    After conscious sedation or general anesthesia has
    been administered, an appropriately sized protective
    liner is applied. The child should be placed on the spica
    table. Towels are folded and placed under the liner in
    the chest and abdominal areas to create room for
    breathing and abdominal distention after eating. The
    surgeon holds the legs with the childs hips in approximately 60 to 90 of flexion and 30 of abduction. The
    more proximal the fracture, the more the hips should
    be flexed. The knees should be flexed to 90. Some external rotation will correct the rotational deformity of
    the distal fragment. An experienced assistant applies
    the cast, and a good condylar and buttock mold is
    placed into the cast to maintain the reduction. Care
    must be taken to avoid excessive compression or traction through the region of the popliteal fossa.
    Compartment syndrome of the leg is a recognized
    complication of early spica casting.58,59 The risk of this
    serious complication can be minimized by avoiding excessive traction while placing the cast, avoiding knee
    flexion of more than 90, and creating a smoothly contoured popliteal fossa. The patients level of comfort as
    well as neurologic and vascular status should be
    checked and documented before discharge.
    Fluoroscopy is used while the cast hardens to allow
    mild manipulation, and cast wedging also can be used
    as needed in the hardened cast. The acceptable alignment depends on the age of the patient, but in general
    no more than 10 of deformity in the coronal plane and
    20 of deformity in the sagittal plane are considered acceptable. Shortening should not exceed 2.0 cm. Radiographs should be obtained weekly during the first 2 to
    3 weeks to allow any loss of the initial reduction to be
    corrected. The time to healing ranges from 4 to 8
    weeks, depending on the age of the child. Physical therapy is not routinely necessary after cast removal. A special child seat is needed for safe transport in an automobile.
    732

    Orthopaedic Knowledge Update 10

    Children who are age 7 months to 5 years should be


    treated surgically if there are extenuating circumstances
    such as polytrauma, open fracture, or a length-unstable
    fracture pattern. The surgical options include external
    fixation, flexible intramedullary fixation, bridge plating, and skeletal traction. Skeletal traction can be applied after placement of a distal femoral traction pin.
    After early callus has formed in 2 to 3 weeks, a spica
    cast can be placed.
    Age 6 to 11 Years
    Flexible (elastic) intramedullary nails are the preferred
    treatment of a length-stable (transverse or short
    oblique) femoral shaft fracture in children age 6 to 11
    years. The elastic nail provides three-point intramedullary contact and load sharing, thus allowing more rapid
    mobilization (Figure 3). The rate of complications is
    greater in children older than 11 to 12 years and/or
    heavier than 100 lb.60,61 The most common minor complication of flexible intramedullary nail fixation is pain
    at the insertion site in the distal femur, which occurs in
    40% of patients.62 Because the pain is associated with
    the amount of distal nail protrusion, it is recommended
    that no more than 25 mm of the nail should be left protruding from the cortex, with a minimal bend of the
    nail. A patient with a very proximal or distal fracture
    or a length-unstable fracture is at relatively high risk of
    a complication. These patients may be best treated with
    a more rigid surgical device such as a bridge plate or
    rigid intramedullary nails.
    Preoperative planning for the use of flexible intramedullary nails includes measuring the narrowest diameter of the femoral canal and multiplying it by 0.4 to
    determine the nail size that will produce the desired
    80% canal fill. The patient is placed on a radiolucent
    table or fracture table, with the unaffected leg abducted
    out of the way. The nails are inserted retrograde; they
    should enter the femur 2 to 2.5 cm proximal to the distal femoral physis. Care is taken to avoid dissection
    about the distal femoral physis and to avoid entering
    the knee joint. The time to union is 10 to 12 weeks.
    Most surgeons remove the nails within 1 year of insertion.
    Age 12 Years or Older
    Treatment options in children age 12 years or older include flexible intramedullary rodding, bridge plating,
    and rigid locked intramedullary nailing using a lateral
    trochanteric entry site. The preferred option depends
    on the fracture stability and the weight of the patient.
    An adolescent who weighs less than 100 lb and has a
    length-stable (transverse or short oblique) fracture can
    usually be treated using flexible nails. Submuscular
    bridge plating for the treatment of a length-unstable,
    very proximal, or distal femur fracture offers several
    advantages, including stability, early mobility, avoidance of growth plates, preservation of the proximal
    femoral blood supply, and limited surgical exposure
    and soft-tissue dissection. The disadvantages of submuscular bridge plating include the technical demand-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 57: Pelvis, Hip, and Femur Trauma: Pediatrics

    Radiographs of a transverse diaphyseal femur fracture (a length-stable fracture) in an 11-year-old boy weighing less
    than 100 lb. A, AP radiograph showing the fracture. AP (B) and lateral (C) radiographs showing treatment with
    flexible intramedullary nails.

    Figure 4

    AP radiograph showing a proximal femoral fracture in a 14-year-old boy. A, The fracture before treatment. B, The
    fracture after locked bridge plating, which was chosen because of the proximal nature of the fracture.

    6: Pediatrics

    Figure 3

    ing application and the time-consuming removal procedure (Figure 4). Before application of the plate, the
    fracture must be provisionally reduced with the aid of

    2011 American Academy of Orthopaedic Surgeons

    traction or a pillow. A 4.5-mm narrow, low-contact


    dynamic compression plate can be used for most patients. Locking plates can be used if the patient has os-

    Orthopaedic Knowledge Update 10

    733

    Section 6: Pediatrics

    teopenia or a proximal or distal fracture with limited


    room for screw placement. Self-tapping screws facilitate insertion, and absorbable suture can be tied
    around the head to avoid loss of the screw in the soft
    tissues. The plate offers 12 to 16 holes over its length
    and should allow placement of three screws above and
    three screws below the fracture. A tabletop bender is
    used to bend the plate to accommodate the proximal
    femur and distal metaphysis. A small incision is made
    distally to allow for insertion. The plate is tunneled between the femoral periosteum and the vastus lateralis,
    and it is provisionally fixed with Kirschner wires or
    Steinmann pins in the most proximal and distal holes.
    A third wire can be placed in the middle portion of the
    plate to prevent recurvatum. The patient must not bear
    weight until callus formation is visible radiographically,
    at an average of 5 weeks after surgery.63
    Rigid interlocking intramedullary nails have been
    successfully used to treat femoral shaft fractures in adolescents. The rigid fixation imparted by the nail, along
    with the rotational control from the interlocking
    screws, allows this device to be used in highly unstable
    fractures, permits weight bearing immediately after surgery, limits the risk of angular deformity, and can be
    dynamized to promote fracture healing.
    Osteonecrosis of the femoral head is the most severe
    complication of intramedullary nailing of a femoral
    shaft fracture in an adolescent, although it is relatively
    rare. It is believed that injury to the medial circumflex
    artery occurs during insertion of the nail medial to the
    tip of the greater trochanter. Osteonecrosis has occurred in at least 18 children and adolescents after intramedullary nailing with large, adult-sized nails placed
    through the piriformis fossa. At least one incident of
    osteonecrosis was associated with a rigid nail placed
    through the tip of the greater trochanter. Nails placed
    through the tip of the greater trochanter also have been
    associated with premature greater trochanteric epiphysiodesis, coxa valga, and hip subluxation.64 However,
    more recent studies did not find these changes in the
    proximal femur after lateral trochanteric entry.65 When
    using rigid nailing, the surgeon should take great care
    to avoid drifting into the region medial to the tip of the
    trochanter and should consider nail removal only after
    closure of the physis. Osteonecrosis can occur from nail
    placement or from damage of the vessels at nail removal.
    6: Pediatrics

    External Fixation
    The primary current indications for external fixation
    are an open fracture; severe disruption of the soft-tissue
    envelope, including severe burn injury; multiple trauma; an extremity with an arterial injury requiring immediate revascularization of the extremity; an unstable
    fracture pattern; and unsuccessful nonsurgical management. The fixators generally are applied for 10 to 16
    weeks, until solid union has been achieved. Weight
    bearing is permitted as early as tolerated, with consideration of the stability of the fracture and the external
    fixator.
    734

    Orthopaedic Knowledge Update 10

    Pin tract infection accounts for approximately 50%


    of complications of treatment with an external fixator.
    In general, pin tract infection responds to good pin care
    and antibiotics. Rates of nonunion, delayed union, and
    angular deformity are generally reported to be slightly
    higher than with more rigid fixation techniques. Delayed union and refracture also are more common,
    with a reported incidence of 1.5% to 21%.66 These
    complications are most common in short oblique fractures because the use of a rigid external fixator means
    that secondary callus is less likely to form.66 When refracture occurs at the previous fracture site as a consequence of incomplete union, the fixator should be left
    in place until solid union is seen radiographically. To
    avoid this complication, the surgeon may consider leaving the pins for a few days after the fixator is removed,
    so as to allow fixator replacement if a fracture occurs.
    Complete apposition of the fracture fragments should
    be achieved at the time of initial reduction.66

    Annotated References
    1.

    Banerjee S, Barry MJ, Paterson JM: Paediatric pelvic


    fractures: 10 years experience in a trauma centre. Injury
    2009;40(4):410-413.
    In a retrospective review, the authors found that pelvic
    fractures in children have a good long-term outcome
    when treated nonsurgically but are an indicator of other
    serious injuries with a high rate of mortality.

    2.

    Junkins EP Jr, Nelson DS, Carroll KL, Hansen K, Furnival RA: A prospective evaluation of the clinical presentation of pediatric pelvic fractures. J Trauma 2001;
    51(1):64-68.

    3.

    Ramirez DW, Schuette JJ, Knight V, Johnson E, Denise


    J, Walker AR: Necessity of routine pelvic radiograph in
    the pediatric blunt trauma patient. Clin Pediatr (Phila)
    2008;47(9):935-940.
    The authors determined that clinical indicators may be
    needed to determine the necessity of pelvic radiographs
    in awake and alert pediatric patients who have experienced blunt trauma.

    4.

    Nabaweesi R, Arnold MA, Chang DC, et al: Prehospital


    predictors of risk for pelvic fractures in pediatric trauma
    patients. Pediatr Surg Int 2008;24(9):1053-1056.
    The authors found that identification of risk factors in
    pediatric trauma patients may help determine which are
    at highest risk of pelvic fracture and may most benefit
    from pelvic radiography.

    5.

    Mosheiff R, Suchar A, Porat S, Shmushkevich A, Segal


    D, Liebergall M: The crushed open pelvis in children.
    Injury 1999;30(suppl 2):B14-B18.

    6.

    Davidson BS, Simmons GT, Williamson PR, Buerk CA:


    Pelvic fractures associated with open perineal wounds:
    A survivable injury. J Trauma 1993;35(1):36-39.

    7.

    Silber JS, Flynn JM: Changing patterns of pediatric pel-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 57: Pelvis, Hip, and Femur Trauma: Pediatrics

    dislocation of the hip. Clin Orthop Relat Res 2000;377:


    84-91.

    vic fractures with skeletal maturation: Implications for


    classification and management. J Pediatr Orthop 2002;
    22(1):22-26.
    8.

    Karunakar MA, Goulet JA, Mueller KL, Bedi A, Le TT:


    Operative treatment of unstable pediatric pelvis and acetabular fractures. J Pediatr Orthop 2004;25(1):34-38.

    9.

    Holden CP, Holman J, Herman MJ: Pediatric pelvic


    fractures. J Am Acad Orthop Surg 2007;15(3):172-177.
    The authors discuss treatment and complications associated with pelvic fractures in children.

    10.

    Demetriades D, Karaiskakis M, Velmahos GC, Alo K,


    Murray J, Chan L: Pelvic fractures in pediatric and
    adult trauma patients: Are they different injuries?
    J Trauma 2003;54(6):1146-1151, discussion 1151.

    11.

    12.

    Grisoni N, Connor S, Marsh E, Thompson GH, Cooperman DR, Blakemore LC: Pelvic fractures in a pediatric
    level I trauma center. J Orthop Trauma 2002;16(7):458463.
    Ismail N, Bellemare JF, Mollitt DL, DiScala C, Koeppel
    B, Tepas JJ III: Death from pelvic fracture: Children are
    different. J Pediatr Surg 1996;31(1):82-85.

    13.

    Smith W, Shurnas P, Morgan S, et al: Clinical outcomes


    of unstable pelvic fractures in skeletally immature patients. J Bone Joint Surg Am 2005;87(11):2423-2431.

    14.

    Heeg M, de Ridder VA, Tornetta P III, de Lange S, Klasen HJ: Acetabular fractures in children and adolescents. Clin Orthop Relat Res 2000;376:80-86.

    15.

    Trousdale RT, Ganz R: Posttraumatic acetabular dysplasia. Clin Orthop Relat Res 1994;305:124-132.

    16.

    Bucholz RW, Ezaki M, Ogden JA: Injury to the acetabular triradiate physeal cartilage. J Bone Joint Surg Am
    1982;64(4):600-609.

    17.

    Peterson HA, Robertson RC: Premature partial closure


    of the triradiate cartilage treated with excision of a
    physical osseous bar: Case report with a fourteen-year
    follow-up. J Bone Joint Surg Am 1997;79(5):767-770.
    Schmidt GL, Sciulli R, Altman GT: Knee injury in patients experiencing a high-energy traumatic ipsilateral
    hip dislocation. J Bone Joint Surg Am 2005;87(6):12001204.

    19.

    Vialle R, Pannier S, Odent T, Schmit P, Pauthier F, Glorion C: Imaging of traumatic dislocation of the hip in
    childhood. Pediatr Radiol 2004;34(12):970-979.

    20.

    21.

    Mehlman CT, Hubbard GW, Crawford AH, Roy DR,


    Wall EJ: Traumatic hip dislocation in children: Longterm followup of 42 patients. Clin Orthop Relat Res
    2000;376:68-79.
    Cornwall R, Radomisli TE: Nerve injury in traumatic

    2011 American Academy of Orthopaedic Surgeons

    Herrera-Soto JA, Price CT, Reuss BL, Riley P, Kasser


    JR, Beaty JH: Proximal femoral epiphysiolysis during
    reduction of hip dislocation in adolescents. J Pediatr
    Orthop 2006;26(3):371-374.

    23.

    Herrera-Soto JA, Price CT: Traumatic hip dislocations


    in children and adolescents: Pitfalls and complications.
    J Am Acad Orthop Surg 2009;17(1):15-21.
    The authors discuss the treatment of traumatic hip dislocations in children and late complications such as osteonecrosis, coxa magna, and osteoarthritis.

    24.

    Chun KA, Morcuende J, El-Khoury GY: Entrapment of


    the acetabular labrum following reduction of traumatic
    hip dislocation in a child. Skeletal Radiol 2004;33(12):
    728-731.

    25.

    Price CT, Pyevich MT, Knapp DR, Phillips JH, Hawker


    JJ: Traumatic hip dislocation with spontaneous incomplete reduction: A diagnostic trap. J Orthop Trauma
    2002;16(10):730-735.

    26.

    Shea KP, Kalamchi A, Thompson GH: Acetabular


    epiphysis-labrum entrapment following traumatic anterior dislocation of the hip in children. J Pediatr Orthop
    1986;6(2):215-219.

    27.

    Ganz R, Huff TW, Leunig M: Extended retinacular


    soft-tissue flap for intra-articular hip surgery: Surgical
    technique, indications, and results of application. Instr
    Course Lect 2009;58:241-255.
    The authors discuss the implications of using the extended retinacular soft-tissue flap as an intra-articular
    procedure.

    28. Ganz R, Gill TJ, Gautier E, Ganz K, Krgel N, Berlemann U: Surgical dislocation of the adult hip: A technique with full access to the femoral head and acetabulum without the risk of avascular necrosis. J Bone Joint
    Surg Br 2001;83(8):1119-1124.
    29.

    Banskota AK, Spiegel DA, Shrestha S, Shrestha OP, Rajbhandary T: Open reduction for neglected traumatic
    hip dislocation in children and adolescents. J Pediatr
    Orthop 2007;27(2):187-191.
    In a retrospective case series, the authors found that surgical reduction may be preferable to other methods of
    treating neglected traumatic hip dislocation in children
    and adolescents.

    30.

    Kumar S, Jain AK: Open reduction of late unreduced


    traumatic posterior hip dislocation in 12 children. Acta
    Orthop Scand 1999;70(6):599-602.

    31.

    Nirmal Kumar J, Hazra S, Yun HH: Redislocation after


    treatment of traumatic dislocation of hip in children: A
    report of two cases and literature review. Arch Orthop
    Trauma Surg 2009;129(6):823-826.
    The authors treated five patients with traumatic disloca-

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    18.

    22.

    735

    Section 6: Pediatrics

    41.

    Canale ST, Bourland WL: Fracture of the neck and intertrochanteric region of the femur in children. J Bone
    Joint Surg Am 1977;59(4):431-443.

    42.

    Morsy HA: Complications of fracture of the neck of the


    femur in children: A long-term follow-up study. Injury
    2001;32(1):45-51.

    43.

    Magu NK, Singh R, Sharma AK, Ummat V: Modified


    Pauwels intertrochanteric osteotomy in neglected femoral neck fractures in children: A report of 10 cases followed for a minimum of 5 years. J Orthop Trauma
    2007;21(4):237-243.
    The authors studied the role of a modified Pauwels intertrochanteric osteotomy in treating neglected femoral
    fractures in children and determined that this procedure
    creates a biomechanical environment conducive to healing while simultaneously correcting associated coxa
    vara.

    44.

    Togrul E, Bayram H, Gulsen M, Kalaci A, Ozbarlas S:


    Fractures of the femoral neck in children: Long-term
    follow-up in 62 hip fractures. Injury 2005;36(1):123130.

    45.

    Pombo MW, Shilt JS: The definition and treatment of


    pediatric subtrochanteric femur fractures with titanium
    elastic nails. J Pediatr Orthop 2006;26(3):364-370.

    46.

    The authors discuss the factors that contribute to the


    occurrence of femoral head osteonecrosis in skeletally
    immature patients with femoral neck fractures. In 20
    patients studied, 18 had fracture healing with no complications.

    Vigler M, Weigl D, Schwarz M, Ben-Itzhak I, Salai M,


    Bar-On E: Subtrochanteric femoral fractures due to simple bone cysts in children. J Pediatr Orthop B 2006;
    15(6):439-442.

    47.

    Jeng C, Sponseller PD, Yates A, Paletta G: Subtrochanteric femoral fractures in children: Alignment after 90
    degrees-90 degrees traction and cast application. Clin
    Orthop Relat Res 1997;341:170-174.

    Boardman MJ, Herman MJ, Buck B, Pizzutillo PD: Hip


    fractures in children. J Am Acad Orthop Surg 2009;
    17(3):162-173.

    48.

    Jarvis J, Davidson D, Letts M: Management of subtrochanteric fractures in skeletally immature adolescents.


    J Trauma 2006;60(3):613-619.

    49.

    Cheng JC, Tang N: Decompression and stable internal


    fixation of femoral neck fractures in children can affect
    the outcome. J Pediatr Orthop 1999;19(3):338-343.

    Segal LS: Custom 95 degree condylar blade plate for pediatric subtrochanteric femur fractures. Orthopedics
    2000;23(2):103-107.

    50.

    Ng GP, Cole WG: Effect of early hip decompression on


    the frequency of avascular necrosis in children with
    fractures of the neck of the femur. Injury 1996;27(6):
    419-421.

    Loder RT, ODonnell PW, Feinberg JR: Epidemiology


    and mechanisms of femur fractures in children. J Pediatr Orthop 2006;26(5):561-566.

    51. Fry K, Hoffer MM, Brink J: Femoral shaft fractures in


    brain-injured children. J Trauma 1976;16(5):371-373.

    tion of the hip; two patients, age 2 and 3 years, had redislocation. Closed reduction was found to be an effective treatment, but adequate immobilization and
    protected weight bearing are necessary in children
    younger than 10 years to avoid redislocation.
    32.

    Gholve P, Arkader A, Gaugler R, Wells L: Femoral neck


    fracture as an atypical presentation of child abuse. Orthopedics 2008;31(3):271.
    The authors discuss an atypical presentation of nonaccidental injury in a 3-year-old child with femoral neck
    fracture. The diagnostic rationale for the nonaccidental
    injury is discussed.

    33.

    Shrader MW, Schwab JH, Shaughnessy WJ, Jacofsky


    DJ: Pathologic femoral neck fractures in children. Am J
    Orthop (Belle Mead NJ) 2009;38(2):83-86, discussion
    86.
    The authors discuss a large series of pathologic femoral
    neck fractures in a pediatric population and review
    treatment methods and complication rates.

    34.

    35.

    36.

    Forster NA, Ramseier LE, Exner GU: Undisplaced femoral neck fractures in children have a high risk of secondary displacement. J Pediatr Orthop B 2006;15(2):
    131-133.
    Shrader MW, Jacofsky DJ, Stans AA, Shaughnessy WJ,
    Haidukewych GJ: Femoral neck fractures in pediatric
    patients: 30 years experience at a level 1 trauma center.
    Clin Orthop Relat Res 2007;454:169-173.

    The authors discuss hip fractures and review complications and surgical options.
    37.

    6: Pediatrics

    38.

    736

    39.

    Flynn JM, Wong KL, Yeh GL, Meyer JS, Davidson RS:
    Displaced fractures of the hip in children: Management
    by early operation and immobilisation in a hip spica
    cast. J Bone Joint Surg Br 2002;84(1):108-112.

    52.

    Banaszkiewicz PA, Scotland TR, Myerscough EJ: Fractures in children younger than age 1 year: Importance of
    collaboration with child protection services. J Pediatr
    Orthop 2002;22(6):740-744.

    40.

    Moon ES, Mehlman CT: Risk factors for avascular necrosis after femoral neck fractures in children: 25 Cincinnati cases and meta-analysis of 360 cases. J Orthop
    Trauma 2006;20(5):323-329.

    53.

    Pandya NK, Baldwin K, Wolfgruber H, Christian CW,


    Drummond DS, Hosalkar HS: Child abuse and orthopaedic injury patterns: Analysis at a level I pediatric
    trauma center. J Pediatr Orthop 2009;29(6):618-625.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 57: Pelvis, Hip, and Femur Trauma: Pediatrics

    A retrospective review of prospectively collected information from an urban level I pediatric trauma center
    found 500 patients with child abuse (age birth to 48
    months) and compared them with 985 accidental
    trauma control patients from 2000 to 2003. Victims of
    abuse were generally younger. There was no difference
    when comparing the sex of the children. Patients
    younger than 18 months with rib, tibia/fibula, humerus,
    or femur fractures are more likely to be victims of nonaccidental trauma. Long bone fractures (humerus and
    femur) in patients older than 18 months were more
    likely due to accidental trauma than to child abuse.
    Level of evidence: III.
    54.

    Rathjen KE, Riccio AI, De La Garza D: Stainless steel


    flexible intramedullary fixation of unstable femoral
    shaft fractures in children. J Pediatr Orthop 2007;27(4):
    432-441.
    Stainless steel flexible intramedullary fixation of 40 unstable femur fractures (spiral and/or comminuted) were
    compared to 41 stable (transverse or oblique) femur
    fractures treated with stainless steel flexible intramedullary fixation. Stainless steel intramedullary fixation was
    effective treatment for unstable femur fractures if cortical abutment was present. Level of evidence: III.

    55.

    Winquist RA, Hansen ST Jr, Clawson DK: Closed intramedullary nailing of femoral fractures: A report of
    five hundred and twenty cases. J Bone Joint Surg Am
    1984;66(4):529-539.

    56.

    Kocher MS, Sink EL, Blasier RD, et al: Treatment of pediatric diaphyseal femur fractures. J Am Acad Orthop
    Surg 2009;17(11):718-725.
    This article discusses an AAOS-approved clinical practice guideline that reviews the evidence published from
    1966 through October 1, 2008. It reviews the good evidence, shows where evidence is lacking, and pinpoints
    topics that future research must target to improve the
    treatment of children with isolated diaphyseal femur
    fractures.
    Podeszwa DA, Mooney JF III, Cramer KE, Mendelow
    MJ: Comparison of Pavlik harness application and immediate spica casting for femur fractures in infants.
    J Pediatr Orthop 2004;24(5):460-462.

    58.

    Halanski M, Noonan KJ: Cast and splint immobilization: Complications. J Am Acad Orthop Surg 2008;
    16(1):30-40.
    This review article discusses materials and techniques to
    avoid casting and splinting complications.

    2011 American Academy of Orthopaedic Surgeons

    Mubarak SJ, Frick S, Sink E, Rathjen K, Noonan KJ:


    Volkmann contracture and compartment syndromes after femur fractures in children treated with 90/90 spica
    casts. J Pediatr Orthop 2006;26(5):567-572.

    60.

    Ho CA, Skaggs DL, Tang CW, Kay RM: Use of flexible


    intramedullary nails in pediatric femur fractures. J Pediatr Orthop 2006;26(4):497-504.

    61.

    Moroz LA, Launay F, Kocher MS, et al: Titanium elastic nailing of fractures of the femur in children: Predictors of complications and poor outcome. J Bone Joint
    Surg Br 2006;88(10):1361-1366.

    62.

    Luhmann SJ, Schootman M, Schoenecker PL, Dobbs


    MB, Gordon JE: Complications of titanium elastic nails
    for pediatric femoral shaft fractures. J Pediatr Orthop
    2003;23(4):443-447.

    63.

    Sink EL, Hedequist D, Morgan SJ, Hresko T: Results


    and technique of unstable pediatric femoral fractures
    treated with submuscular bridge plating. J Pediatr Orthop 2006;26(2):177-181.

    64.

    Gordon JE, Swenning TA, Burd TA, Szymanski DA,


    Schoenecker PL: Proximal femoral radiographic changes
    after lateral transtrochanteric intramedullary nail placement in children. J Bone Joint Surg Am 2003;85(7):
    1295-1301.

    65.

    Keeler KA, Dart B, Luhmann SJ, et al: Antegrade intramedullary nailing of pediatric femoral fractures using
    an interlocking pediatric femoral nail and a lateral trochanteric entry point. J Pediatr Orthop 2009;29(4):345351.
    In a retrospective review, 78 femoral shaft fractures in
    children and adolescents age 8 to 18 years were treated
    with lateral trochanteric entry rigid intramedullary nail
    fixation. All patients progressed to union at an average
    of 7 weeks, with less than 10 of malalignment in all
    planes. No patient developed osteonecrosis or significant differences in their neck-shaft angle or articulotrochanteric distance. Level of evidence: III.

    66.

    Carmichael KD, Bynum J, Goucher N: Rates of refracture associated with external fixation in pediatric femur
    fractures. Am J Orthop (Belle Mead NJ) 2005;34(9):
    439-444, discussion 444.
    6: Pediatrics

    57.

    59.

    Orthopaedic Knowledge Update 10

    737

    Chapter 58

    Hip, Pelvis, and Femur Disorders:


    Pediatrics
    Pablo Castaeda, MD

    Ira Zaltz, MD

    Developmental Dysplasia of the Hip


    Developmental dysplasia of the hip (DDH) is the most
    common orthopaedic defect in newborns. DDH encompasses the spectrum of abnormalities involving the
    growing hip, including radiographic differences of the
    proximal femur or acetabulum and subluxation or dislocation of the hip joint. The incidence of DDH is estimated to range from 1 to more than 35 per 1,000 live
    births, based on the age at diagnosis or the method
    used for detection. For all newborn infants, a physical
    examination using the Ortolani and Barlow maneuvers
    is the most useful procedure to detect instability.
    A discussion of treatment for adolescents and young
    adults with DDH from the perspective of adult reconstruction surgeons is presented in chapter 32.

    Etiology and Pathogenesis


    All components of the hip develop from the same primitive mesenchymal cells. Around the seventh week of
    intrauterine life, a cleft develops, defining the future
    femoral head and acetabulum. By the 11th intrauterine
    week, the hip joint is fully formed; this is the first time
    a dislocation can occur. The abnormalities resulting
    from an early dislocation are so severe that these dislocations are termed teratologic. Many teratologic dislocations are associated with certain neuromuscular conditions and genetic syndromes, especially those in
    which there is decreased or abnormal fetal movement,
    such as arthrogryposis or spina bifida.
    There is a genetic component to DDH. The risk is
    increased twelvefold if a first-degree relative has DDH.1

    2011 American Academy of Orthopaedic Surgeons

    Diagnosis
    Physical Examination
    In the newborn, the palpable sensation of the hip sliding into or out of the acetabulum is the mainstay of a
    positive diagnosis. The Ortolani test is a gentle maneuver in which the examiner feels the dislocated hip reducing as the flexed hip is abducted while the greater
    trochanter is anteriorly lifted. In the Barlow test, the
    examiner gently presses posterior on the flexed, adducted thigh to detect instability of a located hip that
    subluxates or dislocates (Figure 1). A palpable reduction or dislocation constitutes a positive test. Many infants are referred to an orthopaedic surgeon because
    the referring provider has detected soft-tissue clicks.
    Often the referring provider has ordered an ultrasonogram because of these clicks. An ultrasonogram performed before 6 weeks of age may spuriously indicate
    acetabular dysplasia, however. Infants with normal ultrasonographic findings in the presence of a soft-tissue
    click have normal hip development.2
    The Ortolani and Barlow signs are rarely present after 3 months of age because of soft-tissue contracture.
    A dislocation can become fixed, and limited hip abduction in flexion will be present on the affected side. Detection is relatively easy in unilateral dislocation but
    more difficult in bilateral dislocation, where both hips
    are symmetrically limited. In unilateral dislocation,
    apparent shortening of the thigh (the Galeazzi sign) is

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Dr. Zaltz or an immediate family member serves as a


    board member, owner, officer, or committee member of
    the Michigan Orthopaedic Society and has received nonincome support (such as equipment or services), commercially derived honoraria, or other non-research
    related funding (such as paid travel) from DePuy, a
    Johnson & Johnson Company. Neither Dr. Castaneda nor
    any immediate family member has received anything of
    value from or owns stock in a commercial company or
    institution related directly or indirectly to the subject of
    this chapter.

    The condition is most prevalent among Native Americans and Laplanders and is rarely seen in infants of African descent. Cultural traditions, such as swaddling infants with the hips held in extension, also have been
    implicated as important causative factors. Approximately 80% of affected infants are girls; this pattern is
    believed to be related to the perinatal ligamentous laxity caused by infant and maternal hormones. The left
    hip is affected in 60% of children, the right hip in 20%,
    and both hips in 20%. It is believed that the left side is
    more frequently involved because the left femur is adducted against the mothers lumbosacral spine in the
    most common intrauterine position (left occiput anterior), and instability is likely to develop as less femoral
    epiphysis is contained by the acetabulum. Infants in the
    breech position during the third trimester also are at increased risk for DDH.

    739

    Section 6: Pediatrics

    Figure 1

    Drawings showing the clinical tests for detecting developmental dysplasia of the hip. A, The Ortolani test. B, The
    Barlow test. (Reproduced from Guille JT, Pizzutillo PD, MacEwen GD: Developmental dysplasia of the hip from
    birth to six months. J Am Acad Orthop Surg 2000;8:232-224.)

    detected when the infant is positioned supine with both


    hips and knees flexed and the ankles level on the examination table. A walking child with unilateral dislocation may toe walk to compensate for the relative shortening. After a child reaches walking age, bilateral
    dislocation can cause a hip flexion contracture that is
    compensated for with increased lumbar lordosis. These
    patients may walk with a waddle because of bilateral
    gluteus medius functional insufficiency. Dysplasia without dislocation can be clinically silent in a child but
    may appear with hip pain or degenerative disease in adolescence or adulthood.

    6: Pediatrics

    Imaging
    In the normal newborn with clinical evidence of DDH,
    routine radiography of the hips and pelvis may be confirmatory. A normal radiograph does not exclude the
    presence of instability, however. The most common
    method of imaging the neonatal hip is ultrasonography,
    which offers distinct advantages compared with other
    imaging techniques. Unlike plain radiography, it can
    distinguish the cartilaginous components of the acetabulum and the femoral head, and there is no ionizing radiation. Real-time ultrasonography permits multiplanar
    examination that can clearly determine the position of
    the femoral head with respect to the acetabulum and
    permits observation of changes in hip position with
    movement. Unlike other techniques such as MRI, ultrasonography does not require sedation.
    The pioneering work on ultrasonographic examination emphasized a morphologic approach and was
    740

    Orthopaedic Knowledge Update 10

    based on a static coronal image obtained through a lateral approach, with the infant in the lateral decubitus
    position. A subsequent approach was based on a dynamic multiplanar examination that assessed the hip in
    positions produced by the Ortolani and Barlow
    maneuvers.3-5
    These two approaches complement each other. Most
    clinicians now use the so-called dynamic standard minimum examination, which includes assessment in the
    coronal plane with the hip at rest and assessment in the
    transverse plane with the hip under stress. At rest, two
    angles are measured in the coronal plane. A reference
    line is drawn above the acetabulum along the lateral
    wall of the ilium. The angle is formed between the
    reference line and a line drawn tangential to the bony
    roof of the acetabulum; the angle is formed between
    the reference line and a line drawn tangential to the cartilaginous labrum. In general, a normal mature infant
    hip should have an angle of more than 60 and a
    angle of less than 55. The dynamic assessment monitors the position of the head in relation to the posterior
    bony wall of the acetabulum while a modified Barlow
    test is being performed (Figure 2).
    Universal screening of newborns is neither cost effective nor practical, and it can lead to overdiagnosis, especially if performed before age 6 weeks. The current
    recommendation is that infants with a risk factor or an
    equivocal physical finding be referred for ultrasonographic screening. Recent data suggest that physical examination of all neonates for hip dysplasia and selective ultrasonography for infants at high risk are the

    2011 American Academy of Orthopaedic Surgeons

    Chapter 58: Hip, Pelvis, and Femur Disorders: Pediatrics

    Figure 2

    A, Ultrasonogram of a childs dislocated hip. B, The and angles are shown.

    Treatment
    The fundamental goal of treatment for DDH is to obtain a concentric and stable reduction with a minimal
    risk of aseptic necrosis. The complexity, risk, and rate
    of complications after treatment increase with a delay
    in diagnosis.
    Splinting
    Most affected infants who are younger than 6 months
    have hips that are dysplastic, subluxatable (Barlow pos-

    2011 American Academy of Orthopaedic Surgeons

    Figure 3

    Radiograph of a hip with DDH, showing the Hilgenreiner line (yellow), the Perkin line (red), the
    Shenton line (green), and the acetabular index
    (black and yellow angle). The proximal medial
    metaphysis (star) of a located hip should be in
    the inferior medial quadrant of the grid formed
    by the Hilgenreiner and Perkins lines. The right
    is located and the left is dislocated with a break
    in the Shenton line, with displaced metaphysic
    and a higher acetabular index.

    6: Pediatrics

    best means of decreasing the incidence of arthritic hips


    at age 60 years.6 The ossific nucleus of the femoral
    head usually appears on ultrasonographic images at approximately 12 weeks of age, and it becomes apparent
    on plain radiographs by approximately 4 to 6 months.
    At that time, plain radiography becomes the primary
    imaging modality for DDH. Several lines can be projected on the AP radiograph of the pelvis (Figure 3).
    The acetabular index typically has been used to objectively assess the contour of the acetabulum; the normal
    value is less than 25 in children older than 6 months.
    Arthrography, CT, and MRI have narrow indications and are not used in the primary diagnosis of
    DDH. Although arthrography provides information
    about soft-tissue impediments during closed reduction,
    it is an invasive study that requires anesthesia, and the
    interpretation is partially subjective. CT is the method
    of choice for evaluating the position of the femoral
    head after a closed or open reduction. Sedation is seldom required, as the patient is immobilized in a cast.
    Some centers use MRI after reduction to confirm the
    hip position and define the soft-tissue structures about
    the hip.

    itive), or reducible (Ortolani positive). These children


    can be successfully treated with splinting in flexion and
    abduction. The Pavlik harness is the most commonly
    used splint in the United States (Figure 4). This device is
    a dynamic splint that requires normal muscle function;
    it is not used in children who have spina bifida or spasticity. Success with the Pavlik harness depends on the

    Orthopaedic Knowledge Update 10

    741

    Section 6: Pediatrics

    zone is an arc of stable positioning between redislocation (adduction) and the limit of comfortable abduction. The patient is placed in a spica cast in the socalled human position, with 100 of flexion, 45 of
    abduction, and neutral rotation, for at least 6 weeks.
    The patient should then be placed in a second cast or
    an orthosis to maintain abduction until acetabular remodeling is complete. Even after a successful reduction,
    the hip must be followed to detect late acetabular dysplasia requiring a secondary procedure.

    Figure 4

    Photograph of a child wearing a Pavlik harness.

    age at which it is applied and the time spent in the harness. Although an older child sometimes can be treated
    with the harness, most babies who are older than 6
    months and are crawling should be treated with a different method.
    The infant is placed in the harness with the anterior
    straps holding the hips in flexion and the posterior
    straps gradually stretching the hips out into abduction.
    The harness is typically applied with the hips in 90 to
    100 of flexion. Hyperflexion should be avoided to prevent femoral nerve palsy or inferior hip dislocation,
    and wide abduction (more than 60) should not be
    forced because of the risk of necrosis. The harness is
    worn continuously until the hip is stable. Harness use is
    suspended if the hip is found to be displaced in a posterior position, which can cause a failure of development of the posterior wall of the acetabulum, resulting
    in a severe form of acetabular dysplasia (Pavlik harness
    disease). Ultrasonography is used to help identify hips
    that are not developing adequately and may require another form of treatment.7 Use of the harness should be
    continued until normal hip anatomy develops, typically
    between 6 and 8 weeks after stability is achieved. Other
    abduction splints, such as the Von Rosen and
    Hoffmann-Daimler splints, also have been used successfully. Regardless of the orthosis, extreme abduction
    should be avoided. If concentric reduction is not obtained within 2 to 4 weeks, another method of treatment should be selected.

    6: Pediatrics

    Closed Reduction
    In infants who are older than 6 months or who have
    had unsuccessful abduction splinting, closed reduction
    under general anesthesia with an arthrogram should be
    attempted. Excessive force should be avoided because it
    can cause ischemic necrosis. An arthrogram can provide useful information on the quality of the reduction
    and anatomic elements that could impede the hip reduction (the ligamentum teres, pulvinar, and transverse
    ligament). In the presence of a soft-tissue contracture,
    an adductor and/or psoas tenotomy can be considered
    to minimize force. After reduction has been obtained,
    the safe zone of abduction should be assessed. The safe
    742

    Orthopaedic Knowledge Update 10

    Open Reduction
    Failure to obtain a concentric or stable closed reduction
    is an indication for open reduction in a patient of any
    age. Most children older than 18 months require open
    reduction. The anteromedial and medial surgical approaches have been used in children younger than 2
    years. These approaches involve dividing the adductor
    longus and psoas tendons to allow direct access to the
    anteromedial hip capsule, which is opened to reach the
    intra-articular obstacles to reduction. The opportunity
    to perform a capsulorrhaphy is limited, but the ligamentum teres can be shortened and transferred to the
    medial capsule in an effort to increase hip stability. The
    risks of the medial approach include osteonecrosis and
    upper femoral growth disturbance.
    The most commonly used method for open hip reduction is the anterior Smith-Petersen approach. The anterior approach is suitable for a patient of any age because
    the dissection preserves the medial femoral circumflex
    vessels and allows for a capsulorrhaphy and, if needed,
    a pelvic osteotomy. A separate groin incision allows tenotomy of the adductor longus and facilitates hip abduction. The dissection is deepened between the tensor fascia lata and the rectus femoris through a bikini incision
    parallel to the groin flexion crease. The direct origin of
    the rectus femoris is divided to expose the superior and
    lateral hip capsule. The psoas is found in the inferior
    wound and cut. Once the hip capsule is opened, the
    intra-articular structures obstructing reduction including
    the pulvinar, ligamentum teres, and transverse ligaments
    should be removed or transected as necessary. The
    labrum often is found to be tight before division of the
    transverse ligament. Radial cuts in the labrum should be
    avoided because they are a significant risk factor for
    early osteoarthritis.8 Postoperative immobilization
    should be in a functional position, with the hip in 15 of
    flexion, 15 of abduction, and neutral rotation.
    Femoral shortening during the open reduction has
    replaced preoperative traction for reducing the softtissue tension around the hip. The procedure is routinely performed in children older than 3 or 4 years,
    and it is considered necessary for any child if a gentle
    reduction is not obtained. The femur is shortened in the
    subtrochanteric region. With the hip reduced, the
    amount of femoral overlap is assessed and resected,
    and the femur is internally fixed with a plate and
    screws. Varus and rotation can be treated through this
    osteotomy as needed, but excessive retroversion of the
    femur should be avoided.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 58: Hip, Pelvis, and Femur Disorders: Pediatrics

    Figure 5

    Drawings showing three pelvic osteotomies. A, The Dega osteotomy. B, The Salter innominate osteotomy. C, The
    Ganz periacetabular osteotomy. (Reproduced from Gillingham BL, Sanchez AA, Wenger DR: Pelvic osteotomies for
    the treatment of hip dysplasia in children and young adults. J Am Acad Orthop Surg 1999;7:325-337.)

    Pelvic Osteotomy
    In an older child, the acetabulum may be severely dysplastic with anterolateral insufficiency. If this condition
    is found, a pelvic osteotomy should be considered during the open reduction to maximize stability. The Salter
    innominate osteotomy is a redirectional osteotomy that
    hinges through the pubic symphysis and restores approximately 25 of lateral coverage and 10 of anterior
    coverage. The Pemberton and Dega osteotomies have
    been extensively used, with similar results9 (Figure 5).

    Redislocation
    Redislocation after a closed reduction usually is treated
    with a repeat closed reduction or an open reduction,
    without deleterious effects on the long-term outcome.

    2011 American Academy of Orthopaedic Surgeons

    Ischemic Necrosis
    Ischemic necrosis can result from extrinsic compression
    of the vasculature supplying the capital femoral epiphysis and excessive direct pressure on the cartilaginous
    head; these can be provoked by excessive or forceful
    abduction, multiple attempts at closed reduction, or repeat surgery. The radiographic appearance of ischemic
    necrosis may include failure of the ossific nucleus to develop within 1 year after reduction, broadening of the
    femoral neck, increased density or fragmentation of the
    capital femoral epiphysis, or residual deformity of the
    femoral head and neck after ossification. The most
    common classification of ischemic necrosis distinguishes between epiphyseal and metaphyseal involvement. Treatment depends on the degree of severity as
    well as the presence of symptoms related to deformity
    of the femoral neck or upper femur.

    6: Pediatrics

    Age Limits for Reduction


    The long-term results are best if a patient with DDH is
    diagnosed and treated at a young age. The rate of complications increases proportionally with age, and diminished results can be expected with increasing age. Beyond a certain age, surgical treatment is unlikely to
    produce a stable, mobile, and pain-free joint for the
    long term.10 Despite the obvious gait abnormalities,
    pain-free bilateral dislocations probably should not be
    reduced after the child reaches age 4 to 5 years. Unilateral dislocations can be more problematic because of
    limb-length inequality and pelvic obliquity, but even
    these generally fare better without treatment beyond
    age 6 years.11 An appropriately performed epiphysiodesis can treat the limb-length discrepancy in these patients.

    Redislocation after open reduction often is attributable


    to actions taken during the initial procedure, such as
    insufficient capsular release, inadequate capsulorrhaphy, or combined femoral and pelvic osteotomies resulting in posterior instability. These actions almost always necessitate repeat surgery, and the results may
    deteriorate depending on the duration of the redislocation.

    Late Dysplasia
    Children who are diagnosed with DDH should be followed until skeletal maturity, even after a successful
    closed or open reduction. Serial radiographs should be
    obtained. The acetabulum continues to develop until

    Orthopaedic Knowledge Update 10

    743

    Section 6: Pediatrics

    approximately age 6 years, and failure of the acetabulum to develop normally may be an indication for intervention.
    The presence of asymptomatic dysplasia in an adolescent warrants further follow-up. CT or MRI can
    provide important information in symptomatic patients. Radiographic dysplasia such as a decreased lateral center-edge angle (the angle of Wiberg) or an anterior center-edge angle (the angle of Lequesne) is
    associated with early osteoarthritis, especially in the
    presence of a labral tear. This dysplasia is an indication
    for surgery in a symptomatic patient. In experienced
    hands, the Ganz periacetabular osteotomy is the procedure of choice for the correction of the bony dysplasia
    (Figure 5, C). The labral tear should be repaired
    through an open or arthroscopic approach.12

    Developmental Coxa Vara

    6: Pediatrics

    Developmental coxa vara is relatively uncommon, with


    an incidence of 1 in 25,000 live births. There is bilateral involvement in 30% to 50% of patients. Although
    the etiology is unknown, developmental coxa vara has
    been considered an unusual localized dysplasia that occurs if an unspecified primary ossification defect in the
    inferior femoral neck undergoes fatigue failure when
    bearing weight, resulting in progressive varus displacement. Radiographically, a decreased femoral neck-shaft
    angle is noted with an associated decrease in the articulotrochanteric distance and increased femoral retroversion. The classic radiographic changes include an inverted Y-shaped radiolucency in the inferior femoral
    neck. The position of the physeal plate should be measured using the Hilgenreiner physeal angle, which is determined from an AP radiograph as the angle between
    the Hilgenreiner line and the plane of the proximal
    femoral physis. A normal Hilgenreiner angle should be
    less than 25. With an increasing Hilgenreiner angle,
    there is a greater chance of progression of the coxa
    vara, stress fracture, nonunion of the femoral neck, and
    early degenerative arthritis of the hip.
    Patients typically have a progressive but painless limp
    during early childhood, with the coxa vara creating a
    high-riding position of the greater trochanter and subsequent functional weakening of the abductors. Children
    with bilateral involvement walk with a waddling gait and
    may have increased lumbar lordosis. Unilateral involvement causes a Trendelenburg gait, and the limb-length
    inequality can accentuate the limping.
    Nonsurgical treatment has not proved effective. Surgical correction should address the deformity in both
    the sagittal and coronal planes. A valgus and derotational osteotomy is indicated if the femoral neck-shaft
    angle is less than 90, the Hilgenreiner angle is greater
    than 60, or the physeal angle is greater than 45. Surgical treatment should aim for overcorrection of the
    neck-shaft angle to approximately 160, restoration of
    the Hilgenreiner angle to approximately 25, and normalization of femoral rotation. Supplemental bone
    grafting is generally not necessary. Internal fixation
    744

    Orthopaedic Knowledge Update 10

    with plates allows early mobilization. Percutaneous


    techniques with external fixation have also been used
    successfully.13
    If adequate correction is achieved, the defect in the
    neck closes within approximately 6 months after surgery. The physis closes approximately 24 months after
    surgery, even if it has not been violated. The patient
    must be monitored for limb-length inequality. Recurrence of the varus is unusual if adequate valgus has
    been achieved.

    Legg-Calv-Perthes Disease
    Legg-Calv-Perthes (LCP) disease is widely believed to
    result from an initial interruption of the blood supply
    to a variable portion of the proximal femoral epiphysis,
    possibly extending to the adjacent femoral growth plate
    and metaphysis. The condition is not simply ischemic;
    the consequences of epiphyseal bone resorption, collapse, and repair affect the course of the disease. LCP
    disease has a variable course to final healing of the femoral epiphysis. The symptoms can extend over 2 to 5
    years. Most patients recover satisfactory, minimally
    symptomatic function. There are rare incidences of
    minimal disease with little or no permanent change in
    the contour of the femoral head, but most patients have
    moderately severe disease that results in an aspherical
    femoral head at maturity. Approximately half of patients develop premature osteoarthritis.

    Epidemiology and Etiology


    The disease most commonly occurs in boys age 4 and
    10 years, although it can occur in children as young as
    2 years and occasionally occurs in teenagers. The maleto-female ratio is approximately 5 to 1. LCP disease is
    distinguished from adult osteonecrosis because of the
    greater potential for healing and remodeling. The disease is bilateral in approximately 10% of children, but
    it does not appear at the same stage in both hips. Simultaneous bilateral involvement should alert the clinician to the possibility of a different diagnosis. Conditions that should be ruled out include multiple
    epiphyseal dysplasia, spondyloepiphyseal dysplasia,
    sickle cell disease, Gaucher disease, and hypothyroidism.
    Despite some causal associations, including parental
    smoking, thrombophilic disorders, and cartilage gene
    mutations, no conclusive cause has been identified.
    Children with LCP disease tend to be of short stature
    and have delayed bone maturation compared with normally developing children. There is a significant rate of
    attention deficit disorder among affected children.

    Pathogenesis
    There are numerous experiments in which Perthes-like
    changes are produced without injuring the arterial supply.14,15 There is growing experimental evidence of recurrent injury to the circumflex arteries in animals that
    mimics the appearance of LCP disease, suggesting that

    2011 American Academy of Orthopaedic Surgeons

    Chapter 58: Hip, Pelvis, and Femur Disorders: Pediatrics

    Figure 6

    Drawings showing the lateral pillar classification of LCP disease. (Adapted from Skaggs DL, Tolo VT: Legg-CalvPerthes disease. J Am Acad Orthop Surg 1996;4:9-16.)

    the bone necrosis and repair develop over time after repetitive ischemic insults. A porcine model of LCP disease suggests that the physeal tissue is most often
    spared.16 Iliac crest biopsy specimens from patients
    with LCP disease suggested the presence of cytoplasmic
    granules containing lipid and fibrillar material, but the
    clinical significance is unknown.17 Linkage studies of a
    family with a history of LCP disease and precocious arthritis revealed a mutation in COL2A1 gene that decreases collagen helical mechanical properties.18

    Clinical Evaluation, Imaging, and


    Classification

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    A child with LCP disease typically has a Trendelenburg


    gait or antalgic limp that is intermittently painful. Discomfort may be referred to the thigh, knee, or groin.
    The clinical examination reveals variable hip irritability
    and stiffness; limitation in abduction and internal rotation are most common. In severe LCP disease, a limblength discrepancy may be present later in the course of
    the disease. The differential diagnosis includes septic arthritis, transient synovitis, proximal femoral osteomyelitis, and pyomyositis. Infectious processes are differentiated by the clinical setting and laboratory analysis.
    MRI, CT, and bone scanning have been investigated
    for imaging hips with LCP disease, but their clinical
    value has not yet been clearly established. MRI is well
    established for the diagnosis of labral and articular cartilage anomalies, particularly in skeletally mature patients with healed LCP. Standard radiographs are the
    basis for classification and treatment. The radiographic
    course of LCP is divided into four stages. The initial
    stage, characterized by apparent widening of the joint
    and mild symptoms, is presumed to occur after infarc-

    tion and can extend as long as 6 months. The fragmentation stage can last from 6 months to 2 years. Hiprelated symptoms are most prevalent during this
    period. Fragmentation is thought to begin when a subchondral lucent line (the crescent sign) appears and
    there is progressive radiographic dissolution of the
    epiphysis. A crescent sign may be present, involving less
    or more than half of the epiphysis (Salter-Thompson
    type A or B, respectively). The Catterall classification is
    based on the extent of epiphyseal fragmentation; it has
    poor interobserver and intraobserver reliability and is
    of historical importance only. Currently, the most
    widely used system for the fragmentation stage is the
    lateral pillar classification19 (Figure 6). This system is
    based on the first AP hip radiograph obtained during
    the fragmentation stage. The lateral third of the epiphysis, usually located lateral to the central sequestrum, is
    compared to that of the contralateral hip and is measured for grading. The epiphysis is considered type A if
    its height is equal to that of the contralateral epiphysis,
    type B if there is collapse and the height of the epiphysis is greater than 50%, and type C if there is greater
    collapse and the height is less than 50% of that of the
    contralateral epiphysis. A fourth type, called type B/C
    borderline, was recently added to categorize hips with a
    thin or poorly ossified lateral pillar and loss of exactly
    50% of the original height of the lateral pillar. This
    classification system has good intraobserver and interobserver reliability and is well correlated with the prognosis.20 The lateral pillar classification progresses during fragmentation in approximately 30% of hips, and
    changes are more common in extensively involved
    hips.21 Lateral subluxation and hinge abduction are definitively related to a poor prognosis.22 Hinge abduc745

    Section 6: Pediatrics

    tients with Stulberg types develop degenerative arthritis.20,25

    Natural History and Prognosis


    Patients with LCP disease with significant femoral head
    deformity function relatively well into the fourth and
    fifth decades of life. The long-term prognosis is best
    with a young age at onset; approximately 80% of children with onset before age 6 years have a favorable
    prognosis. Poor results can be predicted for patients
    with type B/C or C hips whose age at onset was 4 or 5
    years.26,27 In an older patient, less residual joint deformity is associated with an improved prognosis.

    Treatment
    Figure 7

    Radiograph of a patient with bilateral LCP disease. The left hip is almost completely healed
    while the right hip is in the early reossification
    stage. Lateral subluxation and deformity of the
    right epiphysis suggests hinge abduction.

    6: Pediatrics

    tion, in which a deformity of the lateral epiphysis prevents abduction and causes hinging on the lateral
    acetabulum, is diagnosed using an AP pelvic radiograph with the hips abducted (Figure 7).
    Reossification, the third radiographic phase of LCP
    disease, occurs when new bone formation is clearly recognizable on radiographs. This phase may last as long
    as 18 months. Healing or remodeling, the fourth stage,
    begins when the epiphyseal bone density normalizes
    and trabecular patterns appear. The common residual
    deformities may be more recognizable at this stage, including femoral neck shortening (coxa breva), head
    widening (coxa magna), and flattening (coxa plana).
    With involvement of the capital femoral growth plate,
    there can be tilting of the femoral neck (coxa valga)
    and relative overgrowth of the greater trochanter. Secondary changes in acetabulum depth and orientation
    occur throughout the course of LCP disease and partially determine joint congruence, hip motion, and the
    long-term durability of the hip.23 The Stulberg classification is used to assess joint congruity at skeletal maturity. Type I is defined as a completely normal hip. A
    type II hip (spherically congruent) has a spherical femoral head that may be larger than normal and has a
    short neck or an abnormal acetabulum. A type III hip
    (aspherically congruent) is nonspherical, with an ovoid,
    mushroom, or umbrella shape that is not flat. A type IV
    hip (also aspherically congruent) is flat and articulates
    with a correspondingly flat acetabulum. A type V hip
    (incongruent) has a flat or deformed femoral head that
    articulates with a differently shaped acetabulum. The
    accuracy of the Stulberg classification system has been
    questioned.24 The interobserver and intraobserver reliability of this system is moderate. Only type I and some
    type II hips seem to function well over the course of a
    lifetime. By the fifth or sixth decade of life, most pa746

    Orthopaedic Knowledge Update 10

    Treatment during the initial symptomatic phase includes rest, activity modification, the use of nonsteroidal anti-inflammatory drugs, and physical therapy to
    maintain hip motion and muscle strength. Bracing and
    casting have no significant benefit. Surgical treatment is
    controversial; a recent landmark study determined that
    patients who are older than 8 years at onset and have a
    hip in the lateral pillar B group or the B/C border group
    have a better outcome with surgical treatment than
    with nonsurgical treatment.25
    Children who are younger than 8 years at onset and
    have a group A or B hip have a very favorable outcome
    unrelated to treatment. Children of any age with a
    group C hip frequently have a poor outcome; the hip is
    unaffected by treatment. The timing of surgery has a
    significant impact on the result; no positive effect has
    been found from containment surgery performed after
    the initial or early fragmentation stage. Surgical options
    to improve containment include femoral varus osteotomy, acetabular enhancement procedures such as periacetabular osteotomy, or shelf arthroplasty. Successful
    treatment of established hinge abduction has been reported using a valgus or abduction-type procedure, intertrochanteric osteotomy, or shelf arthroplasty.28
    Occasionally, a patient with LCP disease develops mechanical symptoms related to loose fragments of cartilage or labral pathology. The diagnosis of internal derangement has been facilitated by magnetic resonance
    arthrography. Management of hip abnormalities related
    to LCP disease is evolving with the increasing understanding of femoroacetabular impingement and patterns
    of labral and chondral injury. Surgical treatment using
    hip arthroscopy and surgical dislocation is emerging for
    the management of disorders related to LCP disease.

    Slipped Capital Femoral Epiphysis


    Slipped capital femoral epiphysis (SCFE) is a disorder
    characterized by posterior and interior displacement of
    the epiphysis on the femoral neck. It is the most common disorder affecting adolescent hips, although
    younger children with hormonal or systemic disorders
    can also be affected. Patients with SCFE may have
    acute or chronic symptoms as a result of varying de-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 58: Hip, Pelvis, and Femur Disorders: Pediatrics

    Figure 8

    A and B, Radiographs showing an unstable SCFE.

    grees of epiphyseal stability that may affect the ability


    of the child to ambulate.

    Etiology
    Mechanical forces acting through a susceptible physis
    are thought to be responsible for the observed translation. Children affected by a hormonal abnormality or
    imbalance may be more susceptible to SCFE at an earlier age. Disorders of vitamin D metabolism, thyroid
    hormone production, renal osteodystrophy, pelvic radiation therapy, and parenteral administration of growth
    hormone are associated with SCFE. Other factors associated with SCFE include femoral retroversion and obesity. A recent study using laser capture techniques to
    examine chondrocytes from the physeal plates of patients with SCFE found downregulation of gene expression for type II collagen and aggrecan.29 It is not known
    whether this finding is a cause of or a response to
    SCFE.

    Incidence

    2011 American Academy of Orthopaedic Surgeons

    The mean age at presentation is 13.4 years for boys and


    12.2 years for girls. The classification of SCFE is based
    on epiphyseal stability.34 A stable slip is defined by the
    ability of the patient to walk or bear weight on the extremity. An unstable slip is defined by the inability to
    bear weight. A patient with unstable SCFE is more
    likely to develop osteonecrosis of the epiphysis; the reported rate of osteonecrosis in unstable SCFE ranges
    from 0 to 54.5%, with an average of 22%.35,36
    In general, patients with an unstable slip show
    guarding on attempted passive examination as well as
    an inability to walk. The slip in these patients is likely
    to be quite unstable, with an externally rotated, shortened limb that is akin to an acute fracture. Most patients have a stable slip. Their symptoms are more indolent and have an average duration of 5.7 months.37
    These patients have pain in the groin, thigh, knee, buttock, or peritrochanteric region. An external rotation
    limp usually is present and is correlated with both the
    severity of the proximal femoral deformity and the stability of the physeal plate. Passive flexion of the involved hip produces obligatory external rotation, and
    attempted passive internal rotation often produces discomfort.
    6: Pediatrics

    SCFE is more prevalent in boys than in girls and, in decreasing frequency, affects children of African, Hispanic, Native American, and Caucasian descent. Recent
    multistate data from the United States suggest an incidence of 10 per 100,000.30 Obesity is the single greatest
    risk factor for the development of SCFE; approximately
    75% of affected children have a weight above the 90th
    percentile. SCFE has not been shown to be linked to
    other obesity-related disorders such as tibia vara or
    type II diabetes.31 Although the historically reported incidence of SCFE is variable, recent reports suggest that
    the overall rate of disease may be increasing, probably
    as a result of the increased prevalence of pediatric obesity.30,32 The severity of SCFE has been shown to be
    proportionate to both body mass index and duration of
    symptoms.33

    Clinical Evaluation and Classification

    Imaging
    Traditional plain radiographs, including pelvic AP and
    true lateral views, are used to establish the diagnosis of
    SCFE (Figure 8). SCFE is most readily seen on lateral
    radiographs. The reliability of the Klein line, a traditional diagnostic sign, has recently been questioned.38
    Depending on the chronicity of the symptoms, a variable amount of femoral metaphyseal remodeling is radiographically visible.
    Two methods are used to estimate the anatomic severity of SCFE. On the lateral radiograph, the slip an-

    Orthopaedic Knowledge Update 10

    747

    Section 6: Pediatrics

    Figure 9

    A and B, Radiographs after initial treatment with in situ pinning in the patient whose radiographs are shown in Figure 8. The patient continued to have symptoms related to impingement.

    gle measures angulation between the femoral epiphysis


    and the femoral neck as mild (less than 30), moderate
    (30 to 60), or severe (more than 60). The slip percentage measures translation between the epiphysis and
    femoral neck on AP or lateral views as mild (less than
    25%), moderate (25% to 50%), or severe (more than
    50%). Recent CT data suggest that a plain radiographic assessment of SCFE may underestimate the anatomic SCFE deformity and, thus, its long-term consequences.39

    Treatment

    6: Pediatrics

    A stable SCFE is treated with stabilization of the epiphysis to prevent further displacement and to promote
    stability and healing of the physis (Figure 9). For this
    purpose, percutaneous in situ fixation is used with a
    cannulated screw inserted into the center of the epiphysis and a minimum of four threads crossing the physis.
    The outcome of the procedure is predictable in most
    patients. The few complications of in situ pinning include insertion site femoral fracture, acetabular screw
    impingement, progressive slip after pin insertion, and
    chondrolysis.40 Patients with stable SCFE are permitted
    to bear full weight with crutches after the first 4 to 6
    weeks after screw insertion.
    The traditional treatment of unstable SCFE is in situ
    fixation using one central cannulated screw; a second
    screw is added if necessary for stability. Forceful closed
    manipulative reduction is not recommended because it
    increases the risk of osteonecrosis. The use of emergency anterior capsulotomy with hematoma or fluid
    evacuation, followed by controlled epiphyseal reduction to the preslip position and smooth Kirschner wire
    fixation, also has been reported for managing unstable
    SCFE.41 The long-term anatomic consequences of a
    slipped epiphysis, the association between femoroacetabular impingement and the development of osteoarthritis, and applied understanding of the vascular anat748

    Orthopaedic Knowledge Update 10

    omy of the upper femoral epiphysis are changing the


    traditional approaches to unstable and some high-grade
    stable SCFEs. Two techniques permit controlled reduction of the epiphysis. Epiphyseal reorientation using a
    surgical dislocation approach and a modified Dunn
    procedure are reported to permit full correction at the
    site of deformity and stabilization of the epiphysis
    while protecting the epiphyseal vascular flap.42
    Recent midterm data on 105 patients with severe
    SCFE treated with in situ fixation found that 49% had
    an excellent result, 26% a good result, and 24% a fair
    or poor result. The mean Iowa hip score was 84.7.43 A
    study of symptomatic femoroacetabular impingement
    after SCFE treatment found that 31% of patients had
    symptomatic hips and 32% had clinical evidence of impingement at a mean 6.1 years after treatment.44
    The presence of symptomatic impingement was not
    correlated with slip severity but with the angle (headneck junction morphology) after healing. The natural
    history of an individual patient with SCFE and the
    ideal hip for acute operative reduction remain undetermined.
    The role of prophylactic contralateral in situ fixation
    remains controversial in both stable and unstable
    SCFE. It is difficult to predict the occurrence of a contralateral slip in patients with a unilateral SCFE, and
    prediction accuracy may vary considerably depending
    on the population. A high percentage of patients who
    develop a contralateral SCFE are not symptomatic.45
    The prevalence of contralateral SCFE ranges from 20%
    to 60% and is higher in patients younger than 10
    years.46,47 The prevalence of simultaneous bilateral
    SCFE is approximately 20%.48 Data accumulated over
    a 10-year period revealed contralateral SCFE in 36% of
    patients. Of these patients, 22% had a severe slip, and
    6% developed osteonecrosis or chondrolysis. Contralateral pinning was determined to be safer than observation until symptoms develop.49 Contralateral pinning is

    2011 American Academy of Orthopaedic Surgeons

    Chapter 58: Hip, Pelvis, and Femur Disorders: Pediatrics

    Figure 10

    A and B, Radiographs after a surgical hip dislocation, head and neck osteochondroplasty, and intertrochanteric
    flexion derotational osteotomy in the patient discussed in Figures 8 and 9.

    commonly recommended for patients who have unstable SCFE, are younger than 10 years, or have a systemic metabolic disorder.

    and head-neck junction may improve the efficacy of


    traditional realignment procedures. The role of headneck junction osteoplasty and subcapital osteotomy remains to be determined52-54 (Figure 10).

    Complications

    2011 American Academy of Orthopaedic Surgeons

    Annotated References
    1.

    Stevenson DA, Mineau G, Kerber RA, Viskochil DH,


    Schaefer C, Roach JW: Familial predisposition to developmental dysplasia of the hip. J Pediatr Orthop 2009;
    29(5):463-466.
    A large database was reviewed to determine the incidence of DDH as well as the relative risk associated
    with a familial history. The finding that there is a significantly increased risk if a first-degree relative is affected
    should lead to future research into the phenotypic characterization of patients with DDH, as well as genetic
    analysis.

    2.

    Kane TP, Harvey JR, Richards RH, Burby NG, Clarke


    NM: Radiological outcome of innocent infant hip
    clicks. J Pediatr Orthop B 2003;12(4):259-263.

    3.

    Grissom LE, Harke HT: Developmental dysplasia of the


    pediatric hip with emphasis on sonographic evaluation.
    Semin Musculoskelet Radiol 1999;3(4):359-370.

    4.

    Graf R: Fundamentals of sonographic diagnosis of infant hip dysplasia. J Pediatr Orthop 1984;4(6):735-740.

    5.

    Harcke HT, Kumar SJ: Current concepts review: The


    role of ultrasound in the diagnosis and management of
    congenital dislocation and dysplasia of the hip. J Bone
    Joint Surg Am 1991;73:622-628.

    6.

    Mahan ST, Katz JN, Kim YJ: To screen or not to


    screen? A decision analysis of the utility of screening for
    developmental dysplasia of the hip. J Bone Joint Surg
    Am 2009;91(7):1705-1719.

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Complications resulting from the treatment of SCFE include osteonecrosis, chondrolysis, slip progression,
    pinning-associated femur fracture, screw impingement,
    and painful or function-limiting upper femoral deformity. The reported incidence of osteonecrosis in stable
    SCFE is approximately 4%, and the incidence in unstable SCFE averages 22%.35,50
    The treatment of established osteonecrosis depends
    on the location of the necrotic segment, healing of the
    physeal plate, extent of epiphyseal involvement, and
    any associated deformity. The evaluation should include plain radiographs, CT with sagittal and coronal
    reformatting, and MRI. Screw removal is often necessary after physeal healing to prevent intra-articular
    penetration and facilitate imaging. Small, nonweightbearing zone lesions are observed. Reconstructive procedures include realignment osteotomies, distraction,
    and vascularized fibular transfers.44 Salvage procedures
    include arthrodesis and total hip arthroplasty. The role
    of bisphosphonates for treating post-SCFE osteonecrosis is under investigation.51
    The indications for treatment and the surgical techniques for reconstructing painful or function-limiting
    upper femoral deformities are evolving. The patients
    most at risk include those with an increased angle
    and/or an associated acetabular retroversion or anterior
    overcoverage.44 If feasible, the preoperative evaluation
    of these patients should include magnetic resonance arthrography to assess labral damage and chondral injury. The traditional treatments include flexion-valgusderotational osteotomies of the femur at the
    intertrochanteric or subtrochanteric level. The use of
    surgical dislocation to reach the labrum, acetabulum,

    749

    Section 6: Pediatrics

    Decision analysis was applied to reach a concise and


    clinically relevant conclusion: the highest probability of
    having a nonarthritic hip at age 60 years results from
    screening all neonates clinically for hip dysplasia and using imaging modalities in selected infants.
    7.

    Lerman JA, Emans JB, Millis MB, Share J, Zurakowski


    D, Kasser JR: Early failure of Pavlik harness treatment
    for developmental hip dysplasia: Clinical and ultrasound predictors. J Pediatr Orthop 2001;21(3):348353.

    8.

    Jessel RH, Zurakowski D, Zilkens C, Burstein D, Gray


    ML, Kim YJ: Radiographic and patient factors associated with pre-radiographic osteoarthritis in hip dysplasia. J Bone Joint Surg Am 2009;91(5):1120-1129.
    An unequivocal relationship is established among DDH,
    osteoarthritis with increasing age, and the severity of the
    dysplasia, as shown by decreased center-edge angles as
    well as the presence of labral tears.

    9.

    10.

    11.

    6: Pediatrics

    Vallamshetla VR, Mughal E, OHara JN: Congenital


    dislocation of the hip: A re-appraisal of the upper age
    limit for treatment. J Bone Joint Surg Br 2006;88(8):
    1076-1081.
    Crawford AH, Mehlman CT, Slovek RW: The fate of
    untreated developmental dislocation of the hip: Longterm follow-up of eleven patients. J Pediatr Orthop
    1999;19(5):641-644.

    17.

    Kitoh H, Kitakoji T, Kawasumi M, Ishiguro N: A histological and ultrastructural study of the iliac crest apophysis in Legg-Calve-Perthes disease. J Pediatr Orthop
    2008;28(4):435-439.
    Eleven iliac crest biopsies from patients with LCP disease were compared with 10 iliac crest biopsies from patients with hip dysplasia. Resting zone chondrocytes
    were found to have cytoplasmic granules thought to be
    lipid material and fibrillar inclusions.

    18.

    Su P, Li R, Liu S, et al: Age at onset-dependent presentations of premature hip osteoarthritis, avascular necrosis of the femoral head, or Legg-Calv-Perthes disease in
    a single family, consequent upon a p.Gly1170Ser mutation of COL2A1. Arthritis Rheum 2008;58(6):17011706.
    A review of 42 members of a five-generation family with
    a history of premature osteoarthritis found that a serineto-glycine mutation of COL2A1 may loosen the helical
    structure of collagen segregated in patients with LCP
    disease.

    19.

    Herring JA, Kim HT, Browne R: Legg-Calve-Perthes


    disease: Part I. Classification of radiographs with use of
    the modified lateral pillar and Stulberg classifications.
    J Bone Joint Surg Am 2004;86(10):2103-2120.

    20.

    Akgun R, Yazici M, Aksoy MC, Cil A, Alpaslan AM,


    Tumer Y: The accuracy and reliability of estimation of
    lateral pillar height in determining the herring grade in
    Legg-CalvePerthes disease. J Pediatr Orthop 2004;
    24(6):651-653.

    21.

    Kuroda T, Mitani S, Sugimoto Y, et al: Changes in the


    lateral pillar classification in Perthes disease. J Pediatr
    Orthop B 2009;18(3):116-119.
    A retrospective review of 102 patients with LCP disease
    found changes in lateral pillar morphology and classification after initial classification. Change was observed
    in 31%, and this finding was more prevalent in patients
    with extensive disease.

    12.

    Trousdale RT: Acetabular osteotomy: Indications and


    results. Clin Orthop Relat Res 2004;429:182-187.

    13.

    Sabharwal S, Mittal R, Cox G: Percutaneous triplanar


    femoral osteotomy correction for developmental coxa
    vara: A new technique. J Pediatr Orthop 2005;25(1):
    28-33.

    22.

    Liu SL, Ho TC: The role of venous hypertension in the


    pathogenesis of Legg-Perthes disease: A clinical and experimental study. J Bone Joint Surg Am 1991;73(2):
    194-200.

    Gigante C, Frizziero P, Turra S: Prognostic value of Catterall and Herring classification in Legg-Calve-Perthes
    disease: Follow-up to skeletal maturity of 32 patients.
    J Pediatr Orthop 2002;22(3):345-349.

    23.

    Sankar WN, Flynn JM: The development of acetabular


    retroversion in children with Legg-Calv-Perthes disease. J Pediatr Orthop 2008;28(4):440-443.
    In 53 patients with axial imaging obtained early in the
    course of LCP disease, there was a 1.8% incidence of
    retroversion. Following skeletal maturation, 5 of 16
    hips had plain radiographic evidence of retroversion,
    suggesting adaptive development during the disease
    course.

    24.

    Neyt JG, Weinstein SL, Spratt KF, et al: Stulberg classification system for evaluation of Legg-Calve-Perthes disease: Intra-rater and inter-rater reliability. J Bone Joint
    Surg Am 1999;81(9):1209-1216.

    14.

    750

    Lpez-Carreo E, Carillo H, Gutirrez M: Dega versus


    Salter osteotomy for the treatment of developmental
    dysplasia of the hip. J Pediatr Orthop B 2008;17(5):
    213-221.
    Patients treated with Dega and Salter osteotomies had
    similar results at midterm follow-up.

    crosis in a porcine model. Most animals with surgically


    induced necrosis had no visible physeal abnormality.

    15.

    Boss JH, Misselevich I: Osteonecrosis of the femoral


    head of laboratory animals: The lessons learned from a
    comparative study of osteonecrosis in man and experimental animals. Vet Pathol 2003;40(4):345-354.

    16.

    Kim HK, Stephenson N, Garces A, Aya-ay J, Bian H: Effects of disruption of epiphyseal vasculature on the
    proximal femoral growth plate. J Bone Joint Surg Am
    2009;91(5):1149-1158.
    The authors evaluated the viability of physeal chondrocytes and the architecture of the proximal femoral
    physis after suture ligatureinduced epiphyseal osteone-

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 58: Hip, Pelvis, and Femur Disorders: Pediatrics

    25.

    26.

    27.

    28.

    Herring JA, Kim HT, Browne R: Legg-Calve-Perthes


    disease: Part II. Prospective multicenter study of the effect of treatment on outcome. J Bone Joint Surg Am
    2004;86(10):2121-2134.
    Canavese F, Dimeglio A: Perthes disease: Prognosis in
    children under six years of age. J Bone Joint Surg Br
    2008;90(7):940-945.
    A retrospective review of 166 patients younger than 6
    years when LCP disease appeared found that mild LCP
    disease had a generally good radiographic outcome and
    that severe disease did not benefit from containment
    treatment using the Salter innominate osteotomy, compared with nonsurgical treatment.
    Rosenfeld SB, Herring JA, Chao JC: Legg-calve-perthes
    disease: A review of cases with onset before six years of
    age. J Bone Joint Surg Am 2007;89(12):2712-2722.
    A retrospective review of 188 patients with LCP disease
    appearing before age 6 years found that all had a Stulberg type I or II radiographic outcome, except for those
    classified into the lateral column B/C or C group and
    those age 5 years or older.
    Freeman RT, Wainwright AM, Theologis TN, Benson
    MK: The outcome of patients with hinge abduction in
    severe Perthes disease treated by shelf acetabuloplasty.
    J Pediatr Orthop 2008;28(6):619-625.
    In a retrospective review of the outcomes of arthrographically proved hinge abduction and subsequent
    treatment with the Staheli shelf arthroplasty, 52% of the
    patients had Stulberg type I or II disease. Decreased medial joint space and improved acetabular coverage were
    reported.

    29.

    Scharschmidt T, Jacquet R, Weiner D, Lowder E,


    Schrickel T, Landis WJ: Gene expression in slipped capital femoral epiphysis: Evaluation with laser capture microdissection and quantitative reverse transcriptionpolymerase chain reaction. J Bone Joint Surg Am 2009;
    91(2):366-377.
    The authors evaluated expression of mRNA for key
    structural molecules in growth plate chondrocytes of patients with SCFE.

    30.

    Benson EC, Miller M, Bosch P, Szalay EA: A new look


    at the incidence of slipped capital femoral epiphysis in
    New Mexico. J Pediatr Orthop 2008;28(5):529-533.
    The current and past reported incidences of SCFE were
    compared to identify factors related to the fivefold increased incidence of SCFE since the 1960s.

    32.

    Bowen JR, Assis M, Sinha K, Hassink S, Littleton A: Associations among slipped capital femoral epiphysis, tibia
    vara, and type 2 juvenile diabetes. J Pediatr Orthop
    2009;29(4):341-344.
    A retrospective review investigated multiple disease occurrence in adolescents with obesity. No disease coexistence was established among tibia vara, SCFE, and type
    II diabetes.
    Murray AW, Wilson NI: Changing incidence of slipped
    capital femoral epiphysis: A relationship with obesity?
    J Bone Joint Surg Br 2008;90(1):92-94.

    2011 American Academy of Orthopaedic Surgeons

    33.

    Loder RT: Correlation of radiographic changes with


    disease severity and demographic variables in children
    with stable slipped capital femoral epiphysis. J Pediatr
    Orthop 2008;28(3):284-290.
    A retrospective review of 97 patients treated for stable
    SCFE correlated slip severity, symptom severity, and
    metaphyseal deformity with the duration of symptoms.

    34.

    Loder RT, Richards BS, Shapiro PS, Reznick LR, Aronson DD: Acute slipped capital femoral epiphysis: The
    importance of physeal stability. J Bone Joint Surg Am
    1993;75(8):1134-1140.

    35.

    Phillips SA, Griffiths WE, Clarke NM: The timing of reduction and stabilisation of the acute, unstable, slipped
    upper femoral epiphysis. J Bone Joint Surg Br 2001;
    83(7):1046-1049.

    36.

    Tokmakova KP, Stanton RP, Mason DE: Factors influencing the development of osteonecrosis in patients
    treated for slipped capital femoral epiphysis. J Bone
    Joint Surg Am 2003;85(5):798-801.

    37.

    Green DW, Reynolds RA, Khan SN, Tolo V: The delay


    in diagnosis of slipped capital femoral epiphysis: A review of 102 patients. HSS J 2005;1(1):103-106.

    38.

    Loder RT: Correlation of radiographic changes with


    disease severity and demographic variables in children
    with stable slipped capital femoral epiphysis. J Pediatr
    Orthop 2008;28(3):284-290.

    39.

    Mamisch TC, Kim YJ, Richolt JA, Millis MB, Kordelle


    J: Femoral morphology due to impingement influences
    the range of motion in slipped capital femoral epiphysis.
    Clin Orthop Relat Res 2009;467(3):692-698.
    Computer reconstruction was used to evaluate the effect
    of metaphyseal morphology on post-SCFE femoral acetabular impingement. The presence of metaphyseal deformity and decreased head-neck offset increases the
    likelihood of impingement with relatively mild slip severity.

    40.

    Goodwin RC, Mahar AT, Oswald TS, Wenger DR:


    Screw head impingement after in situ fixation in moderate and severe slipped capital femoral epiphysis. J Pediatr Orthop 2007;27(3):319-325.
    An in vitro study evaluated arc of motion and screwhead acetabular impingement in a cadaver model. Using
    perpendicular technique, the authors found flexionrelated impingement at 70 in moderate SCFE and 50
    in severe SCFE.

    41.

    Parsch K, Weller S, Parsch D: Open reduction and


    smooth Kirschner wire fixation for unstable slipped
    capital femoral epiphysis. J Pediatr Orthop 2009;29(1):
    1-8.
    At 5-year follow-up after urgent anterior capsulotomy
    with controlled epiphyseal reduction and fixation using
    smooth Kirschner wires, the overall rate of osteonecrosis was 4.7% and the average Iowa hip score was 94.5.

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    31.

    Increasing rates of childhood obesity and SCFE are investigated in the Scottish population.

    751

    Section 6: Pediatrics

    42.

    43.

    44.

    45.

    46.

    6: Pediatrics

    47.

    752

    Ziebarth K, Zilkens C, Spencer S, Leunig M, Ganz R,


    Kim YJ: Capital realignment for moderate and severe
    SCFE using a modified Dunn procedure. Clin Orthop
    Relat Res 2009;467(3):704-716.
    No osteonecrosis was reported in 40 patients at two institutions after moderate or severe SCFE was reduced
    with surgical dislocation and modified Dunn osteotomy.
    Significant intra-articular pathology was reported at the
    time of open reduction.
    Castaeda P, Macas C, Rocha A, Harfush A, Cassis N:
    Functional outcome of stable grade III slipped capital
    femoral epiphysis treated with in situ pinning. J Pediatr
    Orthop 2009;29(5):454-458.
    In 129 severe slips retrospectively analyzed at an average of 5 years after in situ fixation, the lowest Iowa hip
    scores and the highest complication rate were noted in
    patients in whom pin placement was inadequate.
    Dodds MK, McCormack D, Mulhall KJ: Femoroacetabular impingement after slipped capital femoral epiphysis: Does slip severity predict clinical symptoms? J Pediatr Orthop 2009;29(6):535-539.
    Retrospective evaluation of 49 patients at a mean 6
    years after in situ pinning for SCFE found that femoroacetabular impingement is correlated with the angle
    and not with slip severity.
    Koenig KM, Thomson JD, Anderson KL, Carney BT:
    Does skeletal maturity predict sequential contralateral
    involvement after fixation of slipped capital femoral
    epiphysis? J Pediatr Orthop 2007;27(7):796-800.
    In a retrospective review of 71 patients with unilateral
    SCFE, 23% of patients with open triradiate cartilage developed mild contralateral SCFE. No single factor predicted sequential slip.

    Retrospective evaluation of 227 patients treated for unilateral SCFE from 1993 to 2003 found that 36% developed contralateral SCFE within 6.5 months. Based on
    severity and complications related to SCFE, prophylactic pinning was determined to be warranted.
    50.

    Palocaren T, Holmes L, Rogers K, Kumar SJ: Outcome


    of in situ pinning in patients with unstable slipped capital femoral epiphysis: Assessment of risk factors associated with avascular necrosis. J Pediatr Orthop 2010;
    30(1):31-36.
    The authors determined that female sex and slip magnitude are potential predisposing factors for the development of osteonecrosis.

    51.

    Ramachandran M, Ward K, Brown RR, Munns CF,


    Cowell CT, Little DG: Intravenous bisphosphonate
    therapy for traumatic osteonecrosis of the femoral head
    in adolescents. J Bone Joint Surg Am 2007;89(8):17271734.
    A prospective, nonrandomized study of bisphosphonate
    use in patients at risk for developing osteonecrosis was
    based on posttreatment bone scans. At a mean 38month follow-up, all hips were rated good or excellent.

    52.

    A retrospective review of arthrodiastasis in the treatment of osteonecrosis found that patients with SCFEassociated osteonecrosis were least likely to benefit from
    the procedure.
    53.

    Jerre R, Billing L, Hansson G, Karlsson J, Wallin J: Bilaterality in slipped capital femoral epiphysis: Importance of a reliable radiographic method. J Pediatr Orthop B 1996;5(2):80-84.
    Azzopardi T, Sharma S, Bennet GC: Slipped capital
    femoral epiphysis in children aged less than 10 years.
    J Pediatr Orthop B 2010;19(1):13-18.
    The authors studied 10 children younger than 10 years
    with SCFE and found that obesity is closely related to
    the development of the condition in younger children.

    48.

    Kamarulzaman MA, Abdul Halim AR, Ibrahim S.


    Slipped capital femoral epiphysis (SCFE): A 12-year review. Med J Malaysia 2006;61(suppl A):71-87.

    49.

    Yildirim Y, Bautista S, Davidson RS: Chondrolysis, osteonecrosis, and slip severity in patients with subsequent
    contralateral slipped capital femoral epiphysis. J Bone
    Joint Surg Am 2008;90(3):485-492.

    Orthopaedic Knowledge Update 10

    Gomez JA, Matsumoto H, Roye DP Jr, et al: Articulated


    hip distraction: A treatment option for femoral head
    avascular necrosis in adolescence. J Pediatr Orthop
    2009;29(2):163-169.

    Rebello G, Spencer S, Millis MB, Kim YJ: Surgical dislocation in the management of pediatric and adolescent
    hip deformity. Clin Orthop Relat Res 2009;467(3):724731.
    A surgical dislocation approach was used in the management of a variety of pediatric hip disorders. Four of
    58 patients developed osteonecrosis.

    54.

    Mamisch TC, Kim YJ, Richolt J, et al: Range of motion


    after computed tomography-based simulation of intertrochanteric corrective osteotomy in cases of slipped
    capital femoral epiphysis: Comparison of uniplanar
    flexion osteotomy and multiplanar flexion, valgisation,
    and rotational osteotomies. J Pediatr Orthop 2009;29:
    336-340.
    Computer simulation was used to compare corrective
    uniplanar flexion with corrective mulitplanar osteotomies in the management of post-SCFE deformity. Similar improvement was noted in flexion and internal rotation regardless of the procedure. Multiplanar
    osteotomies offered superior restoration of abduction.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 59

    Knee, Leg, Ankle, and Foot


    Trauma: Pediatrics
    Matthew A. Halanski, MD

    Jos A. Herrera-Soto, MD

    Introduction
    Injuries in the lower extremity occur frequently in children and vary in their complexity, treatment, and outcomes. Because most lower extremity growth occurs at
    the physes about the knee, posttraumatic growth arrest
    can lead to significant malalignment or limb-length discrepancies. Injuries such as corner fractures, SalterHarris type I fractures of the distal femur, patellar
    sleeve fractures, and Tillaux fractures may be subtle on
    radiographs, yet significant long-term consequences
    exist if they are not managed appropriately. Pediatric
    polytrauma patients may present with multiple lower
    extremity injuries and the clinician must be vigilant in
    looking for all injuries even in the face of obvious fractures (Figure 1). Thus satisfaction of search1,2 has the
    potential to miss other injuries and complications such
    as compartment syndrome as seen in some tibia fractures.

    a distal-to-proximal direction. Once the wire has


    crossed the fracture and the far cortex, it is gently advanced proximally until out of the skin, where it is bent
    over. In the older patient with limited growth, plating
    may be valuable,3 especially in more proximal fractures
    where there is a lower risk to the physis.
    When a small peripheral metaphyseal fragment of
    bone (corner fracture) is found in the young child, nonaccidental trauma should be suspected. This very subtle
    radiologic finding is the result of violent force and is often seen in the distal femur and the proximal and distal
    tibia (Figure 2). Nonaccidental trauma should always
    be expected when the history is discordant or when
    long bone fractures occur in nonambulatory children.
    A complete skeletal survey and child protective services
    consultation should be obtained in these cases.

    Distal Femoral Metaphyseal Fractures

    Dr. Herrera-Soto or an immediate family member has received royalties from Biomet; is a member of a speakers
    bureau or has made paid presentations on behalf of Bonutti Technologies and Biomet; serves as a paid consultant
    to Biomet; and has received research or institutional support from Biomet. Neither Dr. Halanski nor any immediate
    family member has received anything of value from or
    owns stock in a commercial company or institution related
    directly or indirectly to the subject of this chapter.

    2011 American Academy of Orthopaedic Surgeons

    6: Pediatrics

    Distal metaphyseal fractures occur proximal to the


    growth plate, and most are unstable after reduction unless fixation is obtained with a construct such as
    crossed smooth Kirschner wires (K-wires). The physis
    should be avoided with these wires, but those fractures
    in close proximity to the growth plate mandate crossing the physis to achieve fracture stability. With the use
    of crossed K-wires, the surgeon must recognize the risk
    of joint sepsis from pin tract infection. To avoid this,
    burying the wires or using a retrograde fixation method
    is recommended. In this manner a wire is introduced in

    Figure 1

    AP and lateral radiographs of a 13-year-old boy


    with an obvious femoral shaft fracture from an
    motor vehicle accident. One day later, after
    femoral fixation, the patient kept reporting
    knee pain that led to late diagnosis of a proximal tibia physeal fracture (arrow) that required
    fixation.

    Orthopaedic Knowledge Update 10

    753

    Section 6: Pediatrics

    Distal Femur Physeal Injuries


    The distal femoral growth plate accounts for 70% of the
    growth from the femur and contributes to 40% of the
    whole lower extremity. When a fracture occurs, multiple

    zones of the growth plate can be damaged and result in


    partial or complete premature physeal closure. Thus, the
    younger the patient at the time of injury, the worse the
    angular deformity or limb-length inequality will be. Fortunately, distal femoral physeal injuries are relatively uncommon, as they account for less than 2% of all injuries
    to the physes. A varus or valgus mechanism of injury and
    associated injuries around the knee should alert the physician to the possibility of this injury.
    Nondisplaced injuries (2 mm) are amenable to long
    leg casting. Typically these patients present with pain
    and swelling in the affected extremity and normal radiographs, making confirmation of the presence of injury difficult. The best tool for evaluation is still the
    physical examination, which will alert the examiner to
    tenderness along the physis with an associated effusion.
    In the past, stress radiographs were used to confirm
    this injury; however, MRI or ultrasound is now the diagnostic modality of choice. If MRI is not available, the
    surgeon may place the extremity in a cast and watch
    for callus formation within 2 to 3 weeks after injury.
    Although most authors agree that casting alone is sufficient for these injuries, they may displace even after
    well-molded casting and should be monitored closely. If
    any signs of displacement are present, fixation is warranted. Also, any patients not amenable to casting
    (obese patients or those with a closed head injury) may
    benefit from fixation to avoid loss of reduction.
    Fracture fragments displaced over 50% of the bone
    diameter have a high potential for growth plate arrest
    (Figure 3). Hence, anatomic physeal alignment is of utmost importance. Salter-Harris I injuries and SalterHarris II injuries with a small metaphyseal fragment
    are best managed with crossed K-wires (Figure 4).
    Smooth K-wires that do not cross at the fracture site
    should be used for maximal stability. If these wires are
    placed in a retrograde manner (from the epiphysis into
    the metaphysis), they will traverse the knee joint and

    Radiographs of the knee in a 9-month-old patient


    demonstrates a corner fracture of the proximal
    tibia (white arrow). Corner fractures and multiple fractures at different stages of healing are
    pathognomonic for nonaccidental fractures.
    Fractures at different stages of healing (black
    arrows) can be seen in this example, with periosteal healing of the femur indicating a likely
    older occult injury to the femur as well as a
    corner fracture of the tibia.

    Figure 3

    A, AP and lateral radiographs of the knee of a 14-year-old girl who was hit by a car and sustained a Salter-Harris
    type II fracture. B, Coronal MRI of the femur 9 months after open reduction and internal fixation. The patient has
    asymmetric growth plate closure from the trauma. Yet due to relative skeletal maturity, little effect on limb length
    is expected.

    6: Pediatrics

    Figure 2

    754

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 59: Knee, Leg, Ankle, and Foot Trauma: Pediatrics

    Figure 4

    A, Radiographs showing a proximal fibula greenstick fracture in a patient who injured the lateral aspect of her
    knee when she was hit by a car. On physical examination she presented with swelling and severe pain to manipulation. The femoral growth plate appears wide. B, The patient was obese; therefore, percutaneous fixation was
    recommended. Intraoperative stress films show fracture gap with valgus stress. MRI would be the current modality
    of choice to diagnose this injury. These pins traverse the knee joint and should be buried or pulled through to
    decrease the risk of joint infection.

    Patella Fractures
    Patella fractures are less common in children than in
    adults. Most patella fractures in children occur from either a direct blow or a sudden contraction of the extensor mechanism. Avulsion fractures of the patella, on the
    other hand, are more common in children and may be
    difficult to diagnose.6 The sleeve fracture is unique to
    children and consists of a large articular chondral frag-

    2011 American Academy of Orthopaedic Surgeons

    Figure 5

    Lateral radiograph of the knee demonstrates a


    small fleck of bone at the inferior pole of the
    patella (arrow). Inability to perform a straight
    leg raise indicates extensor mechanism disruption and requires surgical fixation. The treating
    surgeon should be aware of possible articular
    flap consistent with a sleeve fracture.

    6: Pediatrics

    should be buried to prevent pin tractinduced septic arthritis. Placing these wires in an antegrade fashion or
    pulling them through the skin proximally after retrograde placement is an alternative that reduces the risk
    of septic arthritis from pin tract infection. In type II injuries with a large metaphyseal fragment, screw fixation may be used. The screws are usually placed from
    the side of the metaphyseal fragment (Thurston Holland), thus fixing the distal fragment to the intact metaphysis.
    Displaced intra-articular injuries or Salter-Harris
    type III and IV injuries (>2 mm) must be reduced to
    prevent articular step-off and early arthrosis. Open reduction and fixation of intra-articular injuries with
    screws parallel to the growth plate is the recommended
    method. Recently, arthroscopic assessment of reduction
    after fixation has been suggested as an alternative.4
    The most common complications are partial growth
    disturbance with residual angular deformity or shortening. The likelihood of physeal growth disturbance is
    greater when initial displacement is segmented. The
    need for additional surgery can occur in about 40% to
    60% of the cases, and has been reported in up to 50%
    of patients regardless of an anatomic reduction. The
    treating physician should avoid performing multiple attempts at closed manipulation because the risk of
    growth disturbance may increase. Ligament injuries
    have been associated with these injuries.5

    ment with a small bone fragment pulled from the ossification center. Radiographic examination reveals a
    small fleck of bone inferiorly and an associated patella
    alta (Figure 5). A high index of suspicion is needed to
    prevent this pitfall. Physical examination will demonstrate knee effusion and inability to fully extend the
    knee.
    In general, patella fractures in children can be
    treated similarly to those in adults. Nondisplaced fractures with an intact extensor mechanism can be treated
    with long leg or cylinder casting. Progressive weight

    Orthopaedic Knowledge Update 10

    755

    Section 6: Pediatrics

    bearing as tolerated can be started once pain control is


    adequate. In patients with displaced fractures the restoration of knee extension function and articular congruity are the goals of treatment. This requires an anatomic reduction and stabilization of the fracture
    fragments.7 Internal fixation is performed using a
    figure-of-8 tension band of either wire or nonabsorbable sutures or tape, which are tied around either
    smooth K-wires or cannulated screws. A recent study
    concluded that a horizontal figure-of-8 band with two
    twists of wire at contiguous corners provides the greatest compression and stability.8 Sleeve fractures require
    open reduction and internal fixation of the patellar tendon to the distal patella.

    Proximal Tibial Physeal Fractures

    6: Pediatrics

    Proximal tibial fractures are common in the pediatric


    population. Several anatomic regions and fracture patterns correlate with the childs age and the mechanism
    of injury.9 Intra-articular injuries are rare and correlate
    with adultlike injury patterns, whereas metaphyseal
    fractures are seen in the younger patient. Physeal injuries account for less than 1% of all physeal injuries.
    This growth plate has added stability because of the anterior epiphyseal extension of the tibial tubercle. There
    are also significant contributions to fragment stability
    from the collateral ligaments and the fibula. As a result,
    it requires a high-energy injury to incite a fracture of
    the proximal tibia epiphysis.
    Nondisplaced fractures are treated by long leg casting and can be followed closely to assess maintenance
    of reduction. A bivalved long leg cast allows fracture
    stabilization while allowing swelling to occur. Displaced fractures also can be treated by closed manipulation and casting. These patients should be admitted
    for observation in light of the potential development of
    compartment syndrome. When intra-articular injuries
    are treated closed, CT after casting can help in the evaluation of joint congruity. Should internal fixation be
    needed, epiphyseal screws that are parallel to the
    growth plate are the most desirable. This is especially
    true in skeletally immature children with over 2 years
    of growth remaining. However, as in distal femoral injuries, stability must never be sacrificed to avoid a potential growth plate arrest and, if necessary, smooth
    wires across the physis may be needed.
    A feared complication is the potential development
    of vascular injury and/or compartment syndrome as a
    result of the tethering effect of the popliteal artery. It is
    important to recognize that spontaneous reduction may
    occur and all proximal tibial physeal fractures may
    have vascular compromise. In displaced fractures,
    many of these vascular occlusions resolve once reduction is achieved. Nevertheless, careful observation is
    warranted during and after the treatment. Other possible complications are partial or premature growth arrest leading to angular deformity and limb-length inequality.
    756

    Orthopaedic Knowledge Update 10

    Tibial Tubercle Fractures


    Avulsion fractures of the tibial tubercle occur mostly in
    adolescents during a sporting (jumping) activity and
    represent less than 1% of all physeal injuries. The patient often presents with a knee effusion, inability to
    extend the knee, and an anterior knee mass. Minimally
    displaced fractures can be treated with long leg or cylinder casting. Intra-articular fractures and those with
    more than 2 mm of displacement require anatomic reduction; many can be percutaneously stabilized with
    screw fixation after closed manipulation. Open reduction and fixation is warranted if the fracture is displaced despite closed reduction attempts. Anterior compartment syndrome may result from bleeding of the
    recurrent anterior tibial artery after tibial tubercle fractures. For open treatment, a prophylactic fasciotomy of
    the anterior compartment may reduce the risk of compartment syndrome in patients with marked swelling
    and pain in the anterior compartment. Screw prominence is a common complication; once the fracture has
    healed, removal will alleviate the symptoms. Growth
    arrest and recurvatum is possible; however, most patients are adolescents with less risk of progressive deformity.

    Metaphyseal Fractures
    Proximal metaphyseal fractures in young children may
    provoke overgrowth of the medial aspect of the proximal tibia leading to genu valgum (Cozen fracture); this
    deformity peaks around 1 year after injury. Families are
    instructed to watch for progressive deformity. Some
    studies have shown that the associated valgus deformity will resolve spontaneously.10 In a long-term study
    with an average 15-year follow-up, almost 50% of the
    patients with posttraumatic tibial valgus had reports of
    knee and/or ankle pain on the affected side with 6
    more in valgus than the contralateral side.11 The mechanical axis eventually improved in all, giving them an
    S-shape tibia or increase in ankle varus. Careful
    follow-up and little tolerance to valgus progression is
    warranted. Hemiepiphysiodesis with guided growth is
    the recommended treatment of this relatively rare residual deformity.12

    Tibial Shaft Fractures


    Tibial shaft fractures are among the most common pediatric fractures. Treatment is tailored according patient
    age and type of injury. Most can be treated by closed
    methods. Nondisplaced or minimally displaced tibia
    fractures are best managed by long leg casting. The most
    common method of managing displaced tibial shaft fractures is closed reduction and long leg casting. Close
    follow-up is needed to ensure maintenance of alignment.
    Alignment is based on the age of the patient: the younger
    the patient, the more angulation that can be accepted.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 59: Knee, Leg, Ankle, and Foot Trauma: Pediatrics

    Figure 6

    Radiographs showing a comminuted tibial shaft fracture in a 10-year-old girl. A, This unstable fracture is amenable
    to internal fixation. B, Three months after flexible nailing, the patient presented with no pain and a united fracture. Nail removal was performed 6 months after surgery.

    Recent reports reviewed the efficacy of elastic intramedullary nailing for comminuted shaft fractures13,14
    (Figure 6). The average time to healing was longer in
    comparison to the expected 10 weeks in patients with
    casts for less significant fractures. Several complications
    were reported to each group including infection,
    malunion, nonunion (10%), skin irritation, and limblength inequality. Another method of treatment is external fixation, which is primarily reserved for open injuries with severe soft-tissue damage.15 Malunion is the
    most common complication, and nonunion occurs in
    about 2% of the cases.
    Although compartment syndrome is less common in
    children than adults, it may occur with almost any injury to the lower extremity. It has to be suspected in
    both closed and open injuries when a patient presents
    with pain out of proportion to his or her injury. Evaluation of compartment syndrome in children can be difficult. Increased anxiety, agitation, and an increasing
    need for narcotics for pain relief, especially after reduction and immobilization, should alert the clinician to
    this possibility. Immediate evaluation and fasciotomies
    can prevent permanent sequelae.

    Ankle Sprains

    2011 American Academy of Orthopaedic Surgeons

    Distal tibial physeal injuries or separations (Salter Harris type I and II) tend to occur most often in children
    age 11 to 13 years.20 Many of these injuries are treated
    with closed reduction and long leg casting. Occasionally open reduction with or without fixation is required
    to improve reduction and remove interposed periosteum. Despite the fractures overall benign appearance,
    up to 25% of patients with type II injuries may show
    signs of premature growth plate closure.20,21 In addition, symptoms resembling those of compartment syndrome have been reported due to impingement of the
    extensor hallucis longus and deep peroneal nerve in displaced fractures (extensor retinacular syndrome).22,23
    Salter-Harris type III and IV fractures of the distal
    tibial epiphysis are both physeal and intra-articular.
    Nondisplaced fractures can be treated with casting;
    however, intra-articular displacement greater than 2
    mm should be treated with open reduction and internal
    fixation to anatomically align the joint space and the
    physis. It is generally thought that diastasis at the fracture site may be better tolerated than articular step-off;
    however, there is no pediatric literature to support this
    theory. CT to evaluate the amount of displacement can
    guide treatment in borderline cases. Screw fixation of
    these fractures is often used; the screws are placed
    within the epiphyseal fragment and often parallel the
    physis and joint surface. If crossing the physis is necessary, smooth wires are typically used. Recently, transepiphyseal bioabsorbable implants have been shown
    to offer equivalent clinical results without requiring
    later implant removal.24
    Transitional fractures of the adolescent distal tibia
    occur as the distal tibial physis begins to close in a predictable fashion, from anteromedial to posterior to lateral and finally to anterolateral. As the distal tibial
    physis closes, the remaining open portions of the physis
    are susceptible to injury. Because the physis closes in a

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Ankle injuries are common in the pediatric patient. As


    the ligamentous structures about the ankle are often
    stronger than the distal tibial and fibular physis, occult
    physeal injuries may be misdiagnosed as ankle sprains.
    However, isolated soft-tissue injuries do occur in the
    pediatric population and have been seen on postinjury
    MRI.16 High-resolution ultrasound has also helped differentiate ankle sprains and occult fractures.17 Overweight children may be at more risk for ankle injury.18
    There does not appear to be a clear advantage to casting versus symptomatic treatment of children with true
    ankle sprains or occult ankle fractures.19

    Distal Tibial Physeal Fractures

    757

    Section 6: Pediatrics

    Figure 7

    CT in an almost skeletally mature individual with


    a displaced juvenile Tillaux fracture.
    Figure 8

    6: Pediatrics

    sequential manner two main types of transitional fractures occur: the Tillaux fracture and the triplane fracture.
    The Tillaux fracture is only seen during adolescence
    as an intra-articular Salter-Harris type III fracture. It
    occurs when the medial physis has closed and the anterior lateral physis remains open in children age 11 to
    16 years. When the ankle is subjected to an external rotation force, the anterolateral portion of the physis is
    avulsed with the anterior tibiofibular ligament (Figure
    7). Although the potential for premature growth arrest
    is low (the physis has already begun to close), intraarticular displacement greater than 2 mm may lead to
    early joint arthritis and tibiofibular instability. CT
    should be used to assess fracture displacement after
    casting. Clearly displaced fractures or those found to be
    displaced (>2 mm) after reduction on CT should be
    treated with open or closed reduction and internal fixation.25 Arthroscopically assisted reduction and percutaneous fixation have also been described.26,27
    Salter-Harris type IV fractures involving the distal
    tibial epiphysis, the physis, and the tibial metaphysis
    are called triplane fractures. This fracture most often
    occurs in patients age 12 to 15 years. Different variants
    (medial and lateral, intra-malleolar, and three- and
    four-part fractures) exist,28 but most commonly the
    epiphysis is fractured in the sagittal plane, the physis is
    separated in the axial plane, and the metaphysis is fractured posteriorly in the coronal plane (Figure 8). The
    lateral portion of the epiphysis is essentially fractured
    from the medial portion, which has already fused with
    the distal tibia. As with other Salter-Harris type III and
    IV injuries, cast immobilization can be used for nondisplaced fractures, and a closed reduction should be attempted on displaced intra-articular fractures (>2 mm).
    CT should be performed in patients in whom reduction
    was attempted to accurately assess fracture displacement. Any fractures not satisfactorily reduced should
    undergo open reduction and internal fixation. CT can
    help with preoperative planning of such surgery and
    can aid in the detection of occult talar dome injuries.29
    Recently, arthroscopically aided reduction and percutaneous fixation has been used with success in treating
    these fractures.30
    758

    Orthopaedic Knowledge Update 10

    Coronal and sagittal CT demonstrates a triplane


    fracture with a sagittal split of the epiphysis, an
    axial separation of the physis, and a coronal
    splint extending from the metaphysis and
    through the epiphysis. The lateral image demonstrates both anterior displacement of the
    Tillaux fracture and posterior displacement of
    the metaphyseal portion. This would imply that
    the Tillaux fragment is separated and is a threepart fracture.

    Fractures of the Distal Fibula


    Factures of the distal fibula are relatively common, and
    most are Salter-Harris type I or type II fractures. When
    the fibular physis is at the level of the tibiotalar joint,
    the physis is more likely to fracture; when the fibular
    physis is below the tibiotalar joint, a metaphyseal injury is more likely.31 Isolated nondisplaced fractures
    may be treated with immobilization. Functional bracing has been shown to be superior to casting for nondisplaced fractures.32 These injuries may occur in isolation or may be associated with distal tibial fractures; in
    these cases the tibia fracture guides treatment and the
    fibula rarely requires fixation. Pinning or plating of fibular fractures is occasionally necessary, especially when
    an unstable ankle injury exists secondary to an additional medial-sided injury. Complications of these fractures are rare, but nonunions33 and growth arrests leading to fibular shortening34 have been described.

    Talus Fractures
    Fractures of the talar neck are rare in children and are a
    result of forced dorsiflexion. The medial malleolus may
    be involved if supination was a component of the injury. Nondisplaced fractures of the talar neck can be
    managed with immobilization and no weight bearing.
    Displaced fractures (>5 mm of displacement or 5 of
    malalignment) should undergo attempted closed reduction, and, if stable, a cast can be worn. If the reduction
    is unacceptable or cannot be maintained, open reduction is necessary. A limited anterior approach can be
    made to aid in reduction while pin or screw fixation
    can be placed posterior laterally.35 As in adults, os-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 59: Knee, Leg, Ankle, and Foot Trauma: Pediatrics

    teonecrosis is a complication with these fractures. Although most other talus fractures are rare, there has
    been an increase in the number of lateral process fractures seen in snowboarders.36 Nondisplaced fractures
    may be immobilized, whereas small symptomatic fragments may require excision.

    Calcaneal Fractures
    Closed calcaneal fractures are rare injuries in children
    and typically are a result of a fall. Extra-articular fractures can be managed with immobilization and restricted weight bearing. In the past, intra-articular fractures have been treated closed with good results. The
    ability of the talus and calcaneus to remodel at the subtalar joint in the growing child has been thought to lead
    to these results. Recently, surgical treatment of displaced (>2 mm) intra-articular fractures, using a lateral
    buttress plate, has been shown to be safer in children
    than in adults and to provide generally good to excellent outcomes.37

    Fractures of the Midfoot


    Midfoot fractures are relatively benign and may involve
    compression-type fractures or avulsions that require a
    period of immobilization. The nutcracker, cuboid
    fracture is a burst-type fracture that occurs when the
    foot is forcefully abducted and sustains an axial load,38
    a condition that can lead to significant lateral column
    shortening that should be surgically restored. This type
    of injury and other midfoot injuries have been associated with equestrian sports.39

    Metatarsal Fractures

    Toe Injuries
    Toe injuries in children result from direct trauma to the
    toe or from kicking an inanimate object. Similar to the
    Seymour fracture of distal phalanx in the hand, open
    Salter-Harris fractures of the distal phalanx in the toes

    2011 American Academy of Orthopaedic Surgeons

    Radiographs of the great toe of a 10-year-old


    child who presented late with pain and purulence after stubbing her toe and who had
    bleeding from her nail fold. Radiographs of
    the contralateral toe (A), and injured toe (B)
    demonstrate physeal widening and step-off (arrows). The treatment included nail plate removal, dbridement, reduction, and fixation (C).
    This patient had an unrecognized open physeal
    fracture, which became secondarily infected.

    can occur. These innocuous and initially innocentappearing stubbed toes are actually open injuries associated with nail bed lacerations and require a formal
    dbridement with or without fixation and treatment
    with antibiotics (Figure 9). In most patients with simple
    toe fracture, buddy taping and a stiff-soled shoe is all
    that is required. Fractures with significant deformity
    may require closed reduction and/or pinning to maintain their position. Open dislocations of the great toe
    interphalangeal joint have been described in children
    participating in martial arts activities. These injuries are
    typically treated with irrigation, reduction, closure, and
    immobilization.43

    Lawn Mower Injuries and Traumatic


    Amputations
    Lawn mower injuries continue to be a source of significant morbidity, with an incidence of 11 in 100,00 US
    children,44 and result in amputations or significant impairments of the limb. These injuries require early antibiotics, irrigation, and dbridement.45 Early primary
    closure after adequate dbridement and treatment of
    vascular injury and osseous stabilization has been described.46 Frequently however, repetitive dbridements,
    soft-tissue flaps, and skin grafting are necessary to treat
    these injuries. Another source of severe foot injuries has
    been seen with the use of all-terrain vehicles. Often the
    childs limb gets caught in the vehicles chain mechanism, causing either a crushing or degloving injury that
    can result in a midfoot amputation.47

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Stress fractures in adolescent athletes involving the second metatarsal respond to decreased activity and either
    casting or a rigid-soled shoe.40 In children younger than
    5 years the first metatarsal is most likely to be fractured, often as a result of a fall from a height, whereas
    in the older patient the fifth metatarsal is more likely to
    be injured during athletics.41 Most of these fractures
    may be treated symptomatically in a walking cast. Multiple or severely angulated metatarsal fractures may require surgical fixation. For displaced or intra-articular
    fractures of the fifth metatarsal, a nonweight-bearing
    cast should be implemented.42 Surgical treatment of
    proximal fractures of the fifth metatarsal (Jones fracture) may allow a quicker return to activities.42

    Figure 9

    759

    Section 6: Pediatrics

    term follow-up note. J Bone Joint Surg Am 1999;81(6):


    799-810.

    Annotated References
    1.

    Ashman CJ, Yu JS, Wolfman D: Satisfaction of search in


    osteoradiology. AJR Am J Roentgenol 2000;175(2):
    541-544.

    2.

    Berbaum KS, Franken EA Jr, Dorfman DD, et al: Satisfaction of search in diagnostic radiology. Invest Radiol
    1990;25(2):133-140.

    3.

    Vander Have K, Herrera J, Kohen R, Karunakar M: The


    use of locked plating in skeletally immature patients.
    J Am Acad Orthop Surg 2008;16(8):436-441.
    The authors review the current use of locked plates in
    the pediatric population. Level of evidence: IV.

    4.

    Lee YS, Jung YB, Ahn JH, Shim JS, Nam DC: Arthroscopic assisted reduction and internal fixation of
    lateral femoral epiphyseal injury in adolescent soccer
    player: A report of one case. Knee Surg Sports Traumatol Arthrosc 2007;15(6):744-746.
    A case report using arthroscopic-assisted reduction and
    fixation of distal femoral fracture is discussed. Level of
    evidence: IV.

    5.

    Bertin KC, Goble EM: Ligament injuries associated with


    physeal fractures about the knee. Clin Orthop Relat Res
    1983;177 :188-195.

    6.

    Hunt DM, Somashekar N: A review of sleeve fractures


    of the patella in children. Knee 2005;12(1):3-7.

    7.

    Dai LY, Zhang WM: Fractures of the patella in children. Knee Surg Sports Traumatol Arthrosc 1999;7(4):
    243-245.

    8.

    Rabalais RD, Burger E, Lu Y, Mansour A, Baratta RV:


    Comparison of two tension-band fixation materials and
    techniques in transverse patella fractures: A biomechanical study. Orthopedics 2008;31(2):128.
    The authors of a biomechanical cadaver study looked at
    the use of figure-of-8 versus parallel wire arrangement
    and stainless steel wire versus ultra-highmolecularweight polyethylene tape in transverse patellar fractures.
    Type of material made little difference in results; however, the parallel arrangement demonstrated less fracture
    distraction.

    6: Pediatrics

    9.

    760

    Mubarak SJ, Kim JR, Edmonds EW, Pring ME, Bastrom TP: Classification of proximal tibial fractures in
    children. J Child Orthop 2009;3(3):191-197.
    The authors evaluated 135 pediatric proximal tibia fractures and propose a new classification scheme that reflects both the direction of force and a fracture pattern
    that appears to be age dependent. Level of evidence: IV.

    10.

    Zionts LE, MacEwen GD: Spontaneous improvement of


    post-traumatic tibia valga. J Bone Joint Surg Am 1986;
    68(5):680-687.

    11.

    Tuten HR, Keeler KA, Gabos PG, Zionts LE, MacKenzie WG: Posttraumatic tibia valga in children: A long-

    Orthopaedic Knowledge Update 10

    12.

    Stevens PM, Pease F: Hemiepiphysiodesis for posttraumatic tibial valgus. J Pediatr Orthop 2006;26(3):385392.

    13.

    Gordon JE, Gregush RV, Schoenecker PL, Dobbs MB,


    Luhmann SJ: Complications after titanium elastic nailing of pediatric tibial fractures. J Pediatr Orthop 2007;
    27(4):442-446.
    Fifty children with 51 diaphyseal tibial shaft fractures
    were followed until union; five patients had delayed
    healing. Patients with delayed healing were older (mean
    age, 14.1 years) versus the study population as a whole
    (mean age, 11.7 years). Other complications included
    malunion, osteomyelitis at the fracture site, and nail migration through the skin. Level of evidence: IV.

    14.

    Srivastava AK, Mehlman CT, Wall EJ, Do TT: Elastic


    stable intramedullary nailing of tibial shaft fractures in
    children. J Pediatr Orthop 2008;28(2):152-158.
    The authors reviewed 24 tibial shaft fractures in 24 patients treated surgically by elastic-stable intramedullary
    nailing. The average union time for all tibia fractures
    was 20.4 weeks. Complications include two neurovascular (8%), two infections (8%), two malunions (8%),
    and one limb-length discrepancy (4%).

    15.

    Myers SH, Spiegel D, Flynn JM: External fixation of


    high-energy tibia fractures. J Pediatr Orthop 2007;
    27(5):537-539.
    The authors discuss a retrospective review of 31 children treated with external fixation for high-energy tibial
    shaft fractures. The authors show a long union time (6
    months) in those older than 12 years and increased risk
    of limb-length discrepancy in those younger than 11
    years.

    16.

    Launay F, Barrau K, Petit P, Jouve JL, Auquier P, Bollini G: [Ankle injuries without fracture in children: Prospective study with magnetic resonance in 116 patients].
    Rev Chir Orthop Reparatrice Appar Mot 2008;94(5):
    427-433.
    One hundred two MRIs were examined in children with
    ankle injuries without fractures on plain films. Minor
    ligament injury was noted in 20 patients and ligament
    tear in 5; minor bone injury was noted in 42 patients
    and fracture in 7. None of these fractures were visible
    on the plain radiographs. Level of evidence: IV.

    17.

    Simanovsky N, Lamdan R, Hiller N, Simanovsky N:


    Sonographic detection of radiographically occult fractures in pediatric ankle and wrist injuries. J Pediatr Orthop 2009;29(2):142-145.
    Fifty-eight children age 2 to 16 years who sustained an
    acute ankle and wrist injury suggestive of fracture on
    clinical examination, but with negative radiograph,
    were referred for high-resolution ultrasound. All patients with negative ultrasound studies had negative
    follow-up radiographs. In 13 patients with positive ultrasound, the follow-up radiographs demonstrated a
    periosteal reaction. Level of evidence: I.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 59: Knee, Leg, Ankle, and Foot Trauma: Pediatrics

    18.

    Zonfrillo MR, Seiden JA, House EM, et al: The association of overweight and ankle injuries in children. Ambul Pediatr 2008;8(1):66-69.
    The authors used 180 patients and 180 control subjects
    to look for an increased risk of ankle injury in the overweight population and observed a significant association between children being overweight and ankle injury. Level of evidence: III.

    19.

    26.

    Panagopoulos A, van Niekerk L: Arthroscopic assisted


    reduction and fixation of a juvenile Tillaux fracture.
    Knee Surg Sports Traumatol Arthrosc 2007;15(4):415417.
    A case report demonstrating the usefulness of ankle arthroscopy in treating a juvenile Tillaux fracture is presented.

    27.

    Thaunat M, Billot N, Bauer T, Hardy P: Arthroscopic


    treatment of a juvenile tillaux fracture. Knee Surg
    Sports Traumatol Arthrosc 2007;15(3):286-288.
    A case report demonstrating the usefulness of ankle arthroscopy in treating a juvenile Tillaux fracture is presented.

    Kraus R, Kaiser M: Growth disturbances of the distal


    tibia after physeal separation: What do we know, what
    do we believe we know? A review of current literature.
    Eur J Pediatr Surg 2008;18(5):295-299.

    28.

    Schnetzler KA, Hoernschemeyer D: The pediatric triplane ankle fracture. J Am Acad Orthop Surg 2007;
    15(12):738-747.
    The authors present a thorough review of pediatric triplane fractures.

    29.

    Heusch WL, Albers HW: Intramalleolar triplane fracture with osteochondral talar defect. Am J Orthop
    (Belle Mead NJ) 2008;37(5):262-266.
    A case report of a concomitant medial talar osteochondral injury and triplane fracture is presented.

    30.

    Jennings MM, Lagaay P, Schuberth JM: Arthroscopic


    assisted fixation of juvenile intra-articular epiphyseal
    ankle fractures. J Foot Ankle Surg 2007;46(5):376-386.
    The authors present long-term follow-up on six patients
    with arthroscopic-assisted, percutaneous fixation of
    intra-articular juvenile epiphyseal ankle fracture. All of
    the patients returned to full activity within 14 weeks of
    surgery. Level of evidence: IV.

    31.

    Pesl T, Havranek P, Nanka O: Mutual position of the


    distal fibular physis and the tibiotalar joint space: Radiological typology and clinical significance. Eur J Pediatr Surg 2007;17(5):348-353.
    The authors found a correlation between the location of
    the fibular physis in relation to the tibiotalar joint and
    the level of fibular fracture in pediatric ankle injuries.
    Level of evidence: III.

    32.

    Boutis K, Willan AR, Babyn P, Narayanan UG, Alman


    B, Schuh S: A randomized, controlled trial of a removable brace versus casting in children with low-risk ankle
    fractures. Pediatrics 2007;119(6):e1256-e1263.
    Children with low-risk ankle fractures were randomized
    to receive a removable ankle brace or a below-knee
    walking cast. The removable ankle brace was found to
    be more effective than the cast with respect to recovery
    of physical function, was associated with a faster return
    to baseline activities, was superior with respect to pa-

    An in-depth review of the current literature on distal


    tibial epiphyseal injuries is presented.
    21.

    Leary JT, Handling M, Talerico M, Yong L, Bowe JA:


    Physeal fractures of the distal tibia: Predictive factors of
    premature physeal closure and growth arrest. J Pediatr
    Orthop 2009;29(4):356-361.
    Chart review of 124 pediatric patients with distal tibia
    physeal fractures demonstrates a significant correlation
    between premature physeal closure and both the mechanism of injury and the amount of initial fracture displacement. Level of evidence: III.

    22.

    Cox G, Thambapillay S, Templeton PA: Compartment


    syndrome with an isolated Salter Harris II fracture of
    the distal tibia. J Orthop Trauma 2008;22(2):148-150.
    The authors present a case report demonstrating a compartment syndrome after a Salter-Harris type II fracture
    of the distal tibia.

    23.

    Haumont T, Gauchard GC, Zabee L, Arnoux JM,


    Journeau P, Lascombes P: Extensor retinaculum syndrome after distal tibial fractures: Anatomical basis.
    Surg Radiol Anat 2007;29(4):303-311.
    An anatomic study is presented that provides an anatomic explanation for the clinically described extensor
    retinaculum syndrome. Level of evidence: IV.

    24.

    Podeszwa DA, Wilson PL, Holland AR, Copley LA:


    Comparison of bioabsorbable versus metallic implant
    fixation for physeal and epiphyseal fractures of the distal tibia. J Pediatr Orthop 2008;28(8):859-863.
    Comparison between metallic (n = 26) and bioabsorbable (n = 24) implants used in treating distal tibial epiphyseal fractures found no significant difference between implants. Level of evidence: III.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Kaya A, Altay T, Ozturk H, Karapinar L: Open reduction and internal fixation in displaced juvenile Tillaux
    fractures. Injury 2007;38(2):201-205.
    Ten patients with juvenile Tillaux fractures were treated
    by open reduction and internal fixation and had an average 99.3/100 American Orthopaedic Foot and Ankle
    Society score at follow-up. Level of evidence: IV.

    Launay F, Barrau K, Simeoni MC, Jouve JL, Bollini G,


    Auquier P: [Ankle injury without fracture in children:
    Cast immobilization versus symptomatic treatment. Impact on absenteeism and quality of life]. Arch Pediatr
    2008;15(12):1749-1755.
    The authors discuss a prospective, randomized study of
    treating ankle injuries without fracture with either
    symptomatic care or cast immobilization. No differences in clinical progression were found; however, parental and child absenteeism was higher in the casted
    group. Level of evidence: II.

    20.

    25.

    761

    Section 6: Pediatrics

    One hundred sixty-six metatarsal fractures in children


    were reviewed. In patients who were 5 years old or
    younger, the primary mechanism was a fall from a
    height and the first metatarsal was most commonly injured. In patients who were older than 5 years, most accidents occurred at sports facilities, were caused by a
    fall on a level surface, and most commonly affected the
    fifth metatarsal. Level of evidence: IV.

    tient preferences, and was also cost-effective. Level of


    evidence: II.
    33.

    Mirmiran R, Schuberth JM: Non union of an epiphyseal


    fibular fracture in a pediatric patient. J Foot Ankle Surg
    2006;45(6):410-412.

    34.

    Lui TH, Chan KB, Ngai WK: Premature closure of distal fibular growth plate: A case of longitudinal syndesmosis instability. Arch Orthop Trauma Surg 2008;
    128(1):45-48.
    A case report describing fibular physeal closure, which
    resulted in a shortened fibula and syndesmotic instability, is presented.

    35.

    Beaty JH, Kasser JR: Rockwood and Greens Fractures


    in Children, ed 5. Philadelphia, PA, Lippincott Williams
    & Wilkins, 2009, pp 1172-1175.

    36.

    von Knoch F, Reckord U, von Knoch M, Sommer C:


    Fracture of the lateral process of the talus in snowboarders. J Bone Joint Surg Br 2007;89(6):772-777.
    Twenty-three snowboarders with lateral process fractures of the talus were followed. An average American
    Orthopaedic Foot and Ankle Society hindfoot score of
    94 was found, including nonsurgically and surgically
    treated fractures. Level of evidence: IV.

    37.

    38.

    Ceroni D, De Rosa V, De Coulon G, Kaelin A: Cuboid


    nutcracker fracture due to horseback riding in children:
    Case series and review of the literature. J Pediatr Orthop 2007;27(5):557-561.
    The authors discuss a case series of four children with
    cuboid injuries sustained during equestrian accidents.
    Level of evidence: IV.

    39.

    Ceroni D, De Rosa V, De Coulon G, Kaelin A: The importance of proper shoe gear and safety stirrups in the
    prevention of equestrian foot injuries. J Foot Ankle Surg
    2007;46(1):32-39.
    This is a case series of foot injuries which occurred during equestrian accidents and stresses the importance of
    proper safety equipment for young riders. Level of evidence: IV.

    40.

    Niemeyer P, Weinberg A, Schmitt H, Kreuz PC, Ewerbeck V, Kasten P: Stress fractures in adolescent competitive athletes with open physis. Knee Surg Sports Traumatol Arthrosc 2006;14(8):771-777.

    41.

    Singer G, Cichocki M, Schalamon J, Eberl R, Hllwarth


    ME: A study of metatarsal fractures in children. J Bone
    Joint Surg Am 2008;90(4):772-776.

    6: Pediatrics

    762

    Petit CJ, Lee BM, Kasser JR, Kocher MS: Operative


    treatment of intraarticular calcaneal fractures in the pediatric population. J Pediatr Orthop 2007;27(8):856862.
    The authors present 14 closed calcaneal fractures
    treated with open reduction and internal fixation. The
    authors found most children with displaced intraarticular calcaneal fractures treated with open reduction
    and internal fixation had a good clinical outcome with
    few complications. Level of evidence: IV.

    Orthopaedic Knowledge Update 10

    42.

    Herrera-Soto JA, Scherb M, Duffy MF, Albright JC:


    Fractures of the fifth metatarsal in children and adolescents. J Pediatr Orthop 2007;27(4):427-431.
    A total of 103 patients with fifth metatarsal fractures
    were reviewed. Most fractures of the fifth metatarsal did
    well after a course of walking cast, unless the fracture
    was an intra-articular displaced fracture type or the
    fracture occured in the proximal diaphyseal area. The
    authors recommend nonweight-bearing casts for all angulated or displaced intra-articular injuries to avoid delays in healing and angulation. Level of evidence: IV.

    43.

    Shin YW, Choi IH, Rhee NK: Open lateral collateral


    ligament injury of the interphalangeal joint of the great
    toe in adolescents during Taekwondo. Am J Sports Med
    2008;36(1):158-161.
    Seven study subjects all had an open wound on the dorsolateral aspect of the interphalangeal joint of the hallux. All seven patients regained full great toe function
    after surgical repair. Level of evidence: IV.

    44.

    Vollman D, Smith GA: Epidemiology of lawn-mowerrelated injuries to children in the United States, 19902004. Pediatrics 2006;118(2):e273-e278.

    45.

    Nguyen A, Raymond S, Morgan V, Peters J, Macgill K,


    Johnstone B: Lawn mower injuries in children: A 30year experience. ANZ J Surg 2008;78(9):759-763.
    This is a 30-year retrospective review of lawn mower injuries. Admissions for lawn mower injury decreased
    over time but the frequency of admission for ride-on
    lawn mower injuries increased over time. Ride-on lawn
    mowers caused significantly more severe injuries requiring longer periods of recovery in comparison with standard mowers. Level of evidence: IV.

    46.

    Goldsmith JR, Massa EG: Primary closure of lawn


    mower injuries to the foot: A case series. J Foot Ankle
    Surg 2007;46(5):366-371.
    The authors discuss a case series of nine lawn mower injuries in which primary closure was performed. The
    hospital courses for this patient population were remarkably lower than those previously reported in the
    literature. Level of evidence: IV.

    47.

    Thompson TM, Latch R, Parnell D, Dick R, Aitken


    ME, Graham J: Foot injuries associated with all-terrain
    vehicle use in children and adolescents. Pediatr Emerg
    Care 2008;24(7):466-467.
    Ten cases of foot injury were identified in patients with
    a median age of 3 years. Eight had forefoot injuries, including six who had amputation of the great toe, and all
    but one patient had multiple open foot fractures. Level
    of evidence: IV.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 60

    Lower Extremity and Foot


    Disorders: Pediatrics
    J. Eric Gordon, MD

    Matthew B. Dobbs, MD

    Lower Extremity Alignment

    Axial Development and Alignment


    At birth, nearly all infants have physiologic hip and
    knee flexion contractures combined with an external
    rotation contracture of the hips, making the assessment
    of axial alignment difficult. When examined carefully,
    infants are noted to have significant genu varum. The
    hip and knee flexion contractures resolve as children
    approach walking age; this varus becomes more apparent leading to parental concern about this physiologic
    deformity. The genu varum begins to improve toward
    neutral alignment in most children at approximately
    age 8 months, with neutral alignment normally
    achieved between the ages of 18 to 24 months. Beyond
    this age, alignment continues to change toward increasing genu valgum, which peaks at approximately age 5
    years. This physiologic valgus spontaneously corrects
    by approximately age 7 years to neutral adult alignment.1 Whenever children are seen for reports of lower
    extremity malalignment, a detailed family history and
    the age at which the malalignment was first noted is
    important. A careful physical examination noting the
    presence of rotational alignment and abnormalities in
    gait is crucial.

    Rotational Development and Alignment


    At birth, significant femoral anteversion and internal
    tibial torsion are present in almost all infants. Internal
    tibial torsion progressively remodels spontaneously until approximately age 5 to 6 years. After this age, minimal change in tibial torsion occurs. The typical toddlers gait pattern arises when children have some

    2011 American Academy of Orthopaedic Surgeons

    Radiographic Analysis and Planning


    The primary tool for evaluating children and adolescents with suspected lower extremity coronal plane deformities is the standing long cassette radiograph,2,3 obtained with the child or adolescent standing with the
    knee facing directly anteriorly; the patella is centered
    over the femoral condyles and the distal femur should
    be symmetric with a true anteroposterior appearance.
    The position of the foot should be ignored, as rotational abnormalities of the tibia can lead to malpositioning of the radiograph and greatly lower its diagnostic value. Ideally, the patient should be able to bear
    weight on both extremities, and both extremities from
    the hip to the ankle should be seen on the same radiograph. Severe genu varum or valgum deformities may
    prohibit both extremities from being seen on the same
    radiograph; if so, the extremities may be imaged separately.
    Once the radiograph is inspected for adequacy, the
    malalignment test is performed by drawing the mechanical axis, a line from the center of the femoral head
    to the center of the ankle. The distance from the center
    of the knee to the line is measured and the direction
    noted. Normal values and ranges for the mechanical

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Dr. Gordon or an immediate family member has received royalties from Orthopediatrics and serves as a
    paid consultant to Orthopediatrics. Dr. Dobbs or an immediate family member serves as a board member,
    owner, officer, or committee member of the Association
    of Bone and Joint Surgeons, the Orthopaedic Research
    and Education Foundation, the Pediatric Orthopaedic
    Society of North America, and Scoliosis Research; has received royalties from D-Bar Enterprises; and serves as a
    paid consultant to D-Bar Enterprises.

    persistence of the external rotation hip contracture as


    they begin walking, and outtoeing occurs as a physiologic mechanism to aid in balance. As the child continues to grow, the external hip contractures decrease and
    the femoral anteversion becomes more obvious with an
    intoed gait pattern that can be exacerbated by persistent tibial torsion. Nearly all children correct the excessive femoral anteversion that is often present at age 5
    years by age 8 to 9 years. Avoiding W-sitting (the
    childs bottom is planted between the feet), walking
    with the feet turned outward, heel wedges, and twister
    cables have all been recommended to promote remodeling and improvement, but there is no evidence that
    any of these interventions changes the natural history
    of femoral anteversion. Symmetric intoeing or outtoeing is not a pathologic condition, but hip dysplasia
    should be suspected in children with asymmetric excessive femoral anteversion. Children with excessive unilateral external femoral rotation and a positive
    Galeazzi sign should also be evaluated carefully for evidence of congenital coxa vara.

    763

    Section 6: Pediatrics

    drawn from the center of the knee to the center of the


    ankle representing the mechanical axis of the tibia. A
    line is then drawn across the proximal tibial condyles
    and the intersection with the mechanical axis of the
    tibia is measured medially as the medial proximal tibial
    angle (normal average is 87). Distally, a line is drawn
    along the distal tibial articular surface and the lateral
    intersection with the tibial mechanical axis is measured
    as the lateral distal tibial angle (normal average is 90).
    Finally, the intersection of the lines created across the
    distal femoral condyles and the proximal tibial condyles can be measured as the joint line congruity angle
    (normal average is 0) to assess intrarticular pathology
    (Figure 1, A).
    The site of bony malalignment can be identified in
    simple or uniapical deformities by reconstructing normal proximal and distal axes of the involved bone and
    resolving these axes into a center of rotation angulation
    (CORA). The CORA identifies the site within the bone
    where the deformity resides. Correction of the deformity should be around the CORA (Figure 2). Lateral
    axes at the distal femur, proximal tibia, and distal tibia
    also exist and should be taken into account when correcting lower extremity deformities (Figure 1, B).
    Figure 1

    A, Illustration showing the measurement of the


    mechanical axis deviation (MAD), lateral proximal femoral angle (LPFA), lateral distal femoral
    angle (LDFA), medial proximal tibial angle
    (MPTA), and lateral distal tibial angle (LDTA) and
    their normal values and ranges. JLCA = joint line
    congruity angle. B, The measurement of the
    posterior distal femoral angle (PDFA), posterior
    proximal tibial angle (PPTA), and anterior distal
    tibial angle (ADTA) and their normal values.

    6: Pediatrics

    axis deviation (MAD) and other measurements are


    noted in Figure 1. If the MAD is outside the normal
    range, further analysis must be performed to determine
    the source of the malalignment.
    The source of the malalignment may be due to bony
    deformity in the femur, tibia, or joint or due to ligamentous laxity within the knee joint or some combination of these conditions. To determine the source of the
    malalignment, either mechanical axis planning or anatomic axis planning may be performed. With either
    method, comparison to the normal side allows one to
    determine the amount of deformity present. Should
    both sides be affected, population-based averages can
    be used.
    In mechanical axis planning, a line is drawn from
    the center of the femoral head to the center of the knee
    representing the mechanical axis of the femur. A second
    line is then constructed across the distal femoral condyles. The lateral angle measured by the intersection of
    these lines is the lateral distal femoral angle (normal average is 87). A third line is then drawn from the tip of
    the greater trochanter to the center of the femoral head
    and the lateral angle formed with the femoral mechanical axis is measured as the lateral proximal femoral
    angle (normal average spine is 90). Next, a line is
    764

    Orthopaedic Knowledge Update 10

    Principles of Deformity Correction:


    Osteotomy and Physeal Modification
    Axial lower extremity deformities can be corrected by
    osteotomy combined with either internal or external
    fixation. Skeletally immature individuals can also be
    treated by physeal modification using either permanent
    or temporary hemiepiphysiodesis. When an osteotomy
    is selected, the correction should be about the previously measured CORA. The position of the osteotomy
    should be chosen based on the CORA as well as physiologic and biologic factors.

    Conditions Causing Malalignment


    Metabolic Bone Disease
    Metabolic bone disease often results in deformity by
    causing weakness within the physis, allowing worsening of existing deformity, or preventing the normal progression of alignment changes as outlined in the previous section. The deformity that is produced can be
    predicted based on the age of onset of the metabolic
    bone disease. Rickets, either from dietary causes or as
    X-linked hypophosphatemic rickets, produces very
    early changes in the physis that lead to an inability to
    remodel early physiologic genu varum with a persistent
    and worsening varus deformity, with characteristic
    physeal widening, and trumpeting of the metaphysis
    (Figure 3). Chronic renal failure produces a somewhat
    later onset metabolic bone disease with similar physeal
    widening but a characteristic valgus deformity due to
    failure to remodel the later physiologic genu valgum
    deformity (Figure 4). Deformities caused by metabolic
    bone disease can be successfully corrected by either
    hemiepiphysiodesis or osteotomy. If the deformity is
    corrected using temporary hemiepiphysiodesis, improvement in the radiographic appearance of the physis

    2011 American Academy of Orthopaedic Surgeons

    Chapter 60: Lower Extremity and Foot Disorders: Pediatrics

    Figure 2

    A, Standing AP radiograph of both lower extremities showing the normal LPFA and LDFA (right). A valgus deformity
    is demonstrated by lateral deviation of the MAD due to a lateral physeal arrest of the distal femur after a physeal
    fracture (left). The normal LPFA and LDFA have been reconstructed to identify the CORA (green dot) with an 8
    deformity. B, An AP view of the right knee 2 weeks after an 8 varus distal femoral opening wedge osteotomy
    stabilized with a blade plate. C, Standing AP radiograph of both lower extremities showing a normal MAD 1 year
    after osteotomy.

    Tibia Vara
    Tibia vara or Blount disease is a complex deformity of
    the lower extremity characterized by progressive varus
    of the lower extremity centered at the tibia. Secondary
    deformities include femoral deformity, internal tibial
    torsion, procurvatum of the proximal tibia, and distal
    tibial valgus. Tibia vara can occur as early-onset or infantile disease, in which bowing is first noted between

    2011 American Academy of Orthopaedic Surgeons

    birth and 3 years of age, and late-onset disease, in


    which bowing is first noted at age 4 years or older. The
    late-onset group can be subdivided into a juvenile form,
    with bowing noted at age 4 to 10 years, and an adolescent form, in which bowing is noted at age 11 years or
    older.6
    Infantile tibia vara can often be difficult to differentiate from physiologic bowing of the lower extremity.
    Most commonly, the metaphyseal-diaphyseal angle is
    used to diagnose tibia vara in the population younger
    than 3 years. Metaphyseal-diaphyseal angles less than
    9 almost universally indicate the presence of physio-

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    is noted as alignment improves.4 Alternatively, correction can be performed successfully using circular external fixation.5

    765

    Section 6: Pediatrics

    Figure 3

    A standing AP radiograph of an 18-month-old boy


    with partially treated X-linked hypophosphatemic rickets showing widening of all of the physes
    and mild trumpeting of the distal femoral
    metaphyses.

    6: Pediatrics

    logic bowing. Angles of 9 to 15 are intermediate, and


    angles of 16 or more nearly always indicate the presence of tibia vara.7,8 The reliability of this measurement
    was recently confirmed on digital radiographs.9 Earlyonset tibia vara can be classified according to the classification system developed by Langenskild as stages I
    through VI.10 Physeal bar formation is present in stages
    V and VI (Figure 5). Older patients with early-onset
    tibia vara frequently develop severe varus deformities
    that can be associated with medial joint depression. In
    severe neglected cases, mild compensatory distal femoral valgus can infrequently occur. After the initial diagnosis in children 21 months to 4 years, it is believed
    that early-onset tibia vara can be successfully treated
    with daytime bracing. Instrumented hemiepiphysiodesis
    may also be an option in this younger age group. If
    varus is present after age 4 years, proximal tibial osteotomy is indicated to correct the deformity. If a physeal bar has formed medially, epiphyseolysis should be
    considered in conjunction with the tibial osteotomy to
    allow growth. When diagnosis is delayed and the patient has developed joint line depression, plateau eleva766

    Orthopaedic Knowledge Update 10

    Figure 4

    A standing AP radiograph of both lower extremities in a 10-year-old boy with chronic renal failure showing a valgus deformity with severe widening of the physes.

    tion can also be performed either as an initial procedure in a staged reconstruction or as a single-stage
    procedure with tibial osteotomy (Figure 6).
    Late-Onset Tibia Vara
    Late-onset tibia vara does not have classic Langenskild changes and is characterized by more mild deformities than are found in early-onset disease. Although
    the name would suggest that the deformity is solely in
    the tibia, varus deformity in the femur is commonly
    present and can account for half of the deformity in
    many patients.11 Approximately 60% of patients with
    growth remaining can be treated with hemiepiphysiodesis.12 Authors of a 2009 study suggested younger patients with less deformity were somewhat more likely
    to correct after epiphysiodesis but were unable to identify strong prognostic factors.13 Patients in whom full
    correction fails with hemiepiphysiodesis, who are skeletally mature, or who have significant pain with ambulation can be treated with definitive correction in a

    2011 American Academy of Orthopaedic Surgeons

    Chapter 60: Lower Extremity and Foot Disorders: Pediatrics

    The Langenskild classification of early-onset tibia vara, showing stages I through VI. (Adapted from Langenskild, A:
    Tibia vara. J Pediatr Orthop 1994;14[2]:141-142.)

    Figure 6

    A, AP view of the knee in a 10-year-old girl with early-onset tibia vara and medial joint depression. B, AP view of
    the knee after medial plateau elevation and simultaneous proximal tibial metaphyseal osteotomy with fixation by a
    circular external fixator. C, AP radiograph of the proximal tibia 2 months after surgery showing progressive healing
    of the plateau elevation and regenerate bone after gradual correction and lengthening of the metaphyseal
    osteotomy.

    single-stage procedure with distal femoral and proximal tibial osteotomies, if needed.14-18 The proximal tibial osteotomy can be performed with either acute or
    gradual correction using a variety of different plates or
    monolateral, circular, or computer-driven external fixation systems. Fibular osteotomy does not seem to be
    necessary when a computer-driven external fixation
    system is used with gradual correction.18 Gradual correction can also allow distal transport of the proximal

    2011 American Academy of Orthopaedic Surgeons

    6: Pediatrics

    Figure 5

    fibula to tighten the lateral collateral ligament in patients who have developed joint laxity.17
    Genu Valgum
    Idiopathic genu valgum can occur in patients with incomplete remodeling after physiologic valgus. Minimal
    correction of frontal plane alignment occurs after age
    10 years. After this age, when the deformity is significant and the patient is symptomatic with either knee

    Orthopaedic Knowledge Update 10

    767

    Section 6: Pediatrics

    obtaining healing of the pseudarthrosis.19 Unfortunately, without intramedullary fixation, a high rate of
    refracture with pseudarthrosis development has been
    observed.20 This has led some to recommend placement
    of intramedullary stabilization at the time of external
    fixator removal. Others have recommended vascularized fibula transfer from the contralateral limb. Although it leads to a high rate of healing, vascularized
    fibula transfer has been associated with donor-site morbidity including ankle valgus and ipsilateral fracture
    with pseudarthrosis reformation at either the proximal
    or distal end of the vascularized graft. Finally, several
    authors have advocated open reduction with resection
    of the pseudarthrosis, iliac crest bone grafting, and intramedullary fixation using a Williams rod.20 This
    treatment has been complicated by persistence of the
    pseudarthrosis and problems with late calcaneus foot
    deformities and long-term weakness of the
    gastrocnemius-soleus complex. Other approaches have
    included creation of a one-bone lower leg by synostosis
    to the fibula and the use of an allograft fibula to bypass
    a dysplastic tibia and prevent fracture.21,22 Most recently, success has been reported with the use of bone
    morphogenetic protein to increase the healing rate.23-25

    Rotational Malalignment

    Figure 7

    AP (A) and lateral (B) radiographs of the tibia


    in a 2-year-old girl with anterolateral bowing
    without a fracture.

    pain or difficulty performing athletic activities, hemiepiphysiodesis is the preferred technique to correct the
    deformity while growth remains. After skeletal maturity, in severe cases, corrective osteotomy can be performed to correct the deformity in the involved bone.

    6: Pediatrics

    Congenital Pseudarthrosis of the Tibia


    Congenital pseudarthrosis of the tibia is associated
    with anterolateral bowing of the tibia, which can lead
    to dysplastic changes in the tibia and fibula and in most
    cases to fracture with persistent pseudarthrosis of the
    tibia. The initial fracture can occur at any time from
    the neonatal period into late childhood. Neurofibromatosis type I is found in approximately 50% of patients
    with congenital pseudarthrosis of the tibia. Prior to
    fracture (Figure 7), protective bracing with a clamshelltype brace is indicated and should be maintained until
    the end of growth or beyond. After fracture, long leg
    casting can sometimes result in bony union but should
    be attempted. When the fragments are extremely dystrophic or if nonsurgical treatment leads to no evidence
    of healing after 3 to 4 months, surgical treatment is indicated. Treatment with open reduction, iliac crest
    bone grafting, and circular external fixation with or
    without proximal lengthening has been successful in
    768

    Orthopaedic Knowledge Update 10

    Increased Femoral Anteversion


    After age 8 years, minimal changes in femoral anteversion occur, and some children have persistent intoeing
    due to the residual excessive femoral anteversion. Several studies have failed to show any association of persistent anteversion into adulthood with degenerative
    changes of the hip or knee. Although this intoeing is
    usually asymptomatic, children older than 8 years with
    external hip rotation less than 20 in extension can
    have functional limitations in sports and activities of
    daily living (such as tripping during walking or running) that in selected cases make treatment indicated.
    Nonsurgical treatment of femoral anteversion in both
    older and younger children is not effective. Derotational osteotomies can be performed proximally, or distally with an open technique and Kirschner wire fixation with a cast or plate fixation. Derotational
    osteotomies can also be performed percutaneously in
    the diaphysis and stabilized with a transtrochanteric
    femoral nail.26,27
    Tibial Torsion
    Although less common than increased femoral anteversion, persistent internal tibial torsion can be a cause of
    persistent intoeing that can produce functional problems during sports or activities of daily living. Children
    older than 6 years with more than 10 of internal rotation that produces functional problems can be treated
    by derotational osteotomy.
    External tibial torsion can occasionally produce
    knee or ankle pain when a thigh-foot angle over 20
    exists in conjunction with hindfoot valgus. Most commonly this condition is seen in patients older than 8
    years in conjunction with a tight Achilles tendon. Sur-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 60: Lower Extremity and Foot Disorders: Pediatrics

    gical correction is indicated when pain persists despite


    an adequate physical therapy program emphasizing
    Achilles tendon stretching. Surgical correction of either
    internal or external tibial torsion is most commonly
    performed in the distal metaphysis and can be stabilized by Kirschner wires or staples and a cast or a small
    plate with or without fibular osteotomy.28,29
    Miserable or Malignant Malalignment
    Combined excessive or increased femoral anteversion
    with external tibial torsion often produces knee pain
    through shear at the joint surface during ambulation or
    by producing anterior knee pain leading to a condition
    identified as miserable or malignant malalignment. Patients will ambulate with the foot facing forward but
    with the anterior knee pointing medially. Patients with
    mild amounts of femoral anteversion and tibial torsion
    can sometimes be treated successfully by a physical
    therapy program emphasizing vastus medialis obliquus
    strengthening and hamstring stretching. Significant
    combined increased femoral anteversion and external
    tibial torsion can be effectively treated surgically with
    combined femoral and tibial derotational osteotomies
    in a single or staged fashion.

    Limb-Length Discrepancy

    2011 American Academy of Orthopaedic Surgeons

    Figure 8

    AP radiograph of both lower extremities in a patient with left proximal femoral focal deficiency,
    showing proximal femoral varus and significant
    shortening of the femur.

    Congenital Femoral Deficiency


    Congenital femoral deficiency includes congenital short
    femur, proximal femoral focal deficiency, and femoral
    hypoplasia. Shortening of the femur is associated with
    varying degrees of proximal femoral varus, distal femoral valgus, femoral retroversion, acetabular dysplasia,
    and congenital absence or incompetence of the cruciate
    ligaments of the knee (Figure 8). Approximately half of
    these patients will have associated fibular hemimelia.
    Several different classification schemes have been developed to guide treatment. These classification systems
    focus on stability of the hip and the amount of shortening noted in the femur.
    The projected limb-length discrepancy and the stability of the associated joints as well as the severity of
    the associated deformities determine treatment options.
    Patients with a projected limb-length discrepancy of
    less than 15 to 20 cm with relatively stable or surgically
    stable joints and a functional, plantigrade foot are often candidates for limb lengthening. The presence of
    projected limb-length discrepancies of more than 20
    cm, very unstable joints, or a nonfunctional foot are
    relative indications for ablation. This most often takes
    the form of a Syme amputation with or without a knee
    arthrodesis. Selected patients with severe femoral deficiency and a functional ankle and foot can be treated
    by knee arthrodesis combined with Van Ness rotationplasty. This allows the rotated foot to serve as a knee
    joint allowing active flexion of the knee.

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Epiphysiodesis, Closed Femoral Shortening,


    Limb Lengthening
    Limb-length discrepancy can occur because of either
    traumatic or congenital etiologies. Mild discrepancies
    less than 2 cm are common and require no treatment. A
    lift is almost always an option to help equalize limb
    lengths and should be used by children with discrepancies more than 2 cm.
    Evaluation of patients with limb-length discrepancy
    who are still growing should include a projection of the
    discrepancy at maturity. The growth-remaining
    method, Mosley straight-line graph method, or multiplier method can all lead to accurate predictions when
    combined with accurate bone ages. For patients with a
    projected discrepancy of 2 to 4 cm, contralateral epiphysiodesis is most commonly used. Larger discrepancies can be addressed in individual patients using this
    technique. Percutaneous epiphysiodesis, after careful
    planning and evaluation, has proved safe and has a low
    complication rate.30 Skeletally mature patients who
    have discrepancies of 2 to 5 cm can also be treated by
    open shortening with blade plate fixation or closed
    femoral shortening using an intramedullary saw and intramedullary fixation.
    Discrepancies greater than 4 cm are amenable to
    limb lengthening using distraction osteogenesis as described by Ilizarov. This can be accomplished using several available circular, computer-driven, or monolateral
    devices with typical lengthening rates of 1 mm per day.
    Very long discrepancies of up to 15 to 20 cm can be addressed using a combination of multiple lengthenings
    and epiphyseodeses. Larger discrepancies can be treated
    with amputation and prosthetic fitting to equalize limb
    lengths.

    769

    Section 6: Pediatrics

    Figure 9

    A, Photograph of the left lower extremity of a 14month-old patient with fibular hemimelia showing significant anterior bowing with an apical
    dimple, shortening of the limb, a foot with four
    toes, and an equinus contracture. B, A standing
    AP radiograph of a 2-year-old girl with fibular
    hemimelia showing an absent fibula and significant limb-length discrepancy as a result of a
    shortened tibia.

    6: Pediatrics

    Fibular Hemimelia
    Fibular hemimelia is the most common of the congenital long bone deficiencies and is characterized by shortening or complete absence of the fibula, genu valgum,
    mild femoral shortening, and absence of one to three
    rays in the foot. Half of children with fibular hemimelia have tarsal coalitions, often severe coalitions involving the talus and calcaneus that may not be noted on
    initial radiographs due to the cartilaginous nature of
    the bones in early development. This severe coalition
    can lead to ball-and-socket changes in the ankle. Fibular hemimelia is often associated with anterior bowing
    of the tibia with a skin dimple noted anteriorly and an
    equinovalgus contracture of the ankle (Figure 9). Classification depends on the amount of fibular shortening
    or complete absence of the fibula. Treatment of fibular
    hemimelia is determined primarily by the stability and
    function of the foot and ankle and to a lesser extent by
    the projected limb-length discrepancy. Patients with
    mild projected limb-length discrepancy (less than 5 cm)
    and a stable foot can be managed with contralateral
    epiphysiodesis. Limb lengthening should be considered
    for patients with a stable plantigrade foot regardless of
    the number of rays present. Even patients with a threetoe foot, when associated with a stable ankle and a
    plantigrade functional foot, may be good candidates
    for limb lengthening. Patients with unstable valgus foot
    deformities often function better with Syme amputation
    at approximately 1 year of age with subsequent prosthetic fitting.
    770

    Orthopaedic Knowledge Update 10

    Tibial Hemimelia
    Tibial hemimelia is a very rare condition associated
    with absence of part or the entire tibia. Deficiency of either the proximal or distal tibia can occur. This is a genetically linked syndrome31,32 that is associated with ulnar aplasia and other musculoskeletal conditions and
    can be passed down to descendents. Patients often present with shortening of the lower leg and severe clubfoot
    deformities. Treatment is primarily based on the stability of the knee joint. Patients with an ossified proximal
    tibia can be treated by synostosis of the tibia and proximal fibula and a modified Syme amputation, leaving a
    stump ending in the fibula. Patients without a proximal
    tibia have been historically treated by the Brown procedure, with centralization of the proximal tibia beneath
    the femur to reconstruct the knee. This has been universally unsuccessful, leading to flexion contracture of the
    knee and very limited function. These patients are best
    treated with knee disarticulation and prosthetic fitting.
    Patients with distal tibial deficiency can be treated with
    limb lengthening after stabilization of the foot.
    Posteromedial Bowing
    Posteromedial bowing of the tibia is differentiated from
    anterolateral bowing seen in patients with congenital
    pseudarthrosis of the tibia. Posteromedial bowing of
    the tibia is associated frequently with a calcaneovalgus
    foot deformity (Figure 10). Although the etiology is unknown, a mechanism of mechanical trauma associated
    with in utero rupture of the amnion has been suggested.33 Most frequently the bowing deformity will
    gradually improve with age, with some children having
    persistent bowing after age 4 years.8 Some children will
    be left with mild ankle and knee valgus in spite of remodeling. Most children will have mild shortening of
    the limb at birth of approximately 1 to 2 cm. This will
    progress to an average shortening of 4 cm at maturity
    with occasional children developing more severe length
    discrepancies. Treatment of the limb-length discrepancy
    can be accomplished by wearing a lift, or surgically via
    limb lengthening or contralateral epiphysiodesis.
    Hemiatrophy
    Anisomelia with the shorter limb appearing to be abnormally small is known as hemiatrophy. Children with
    this condition are usually otherwise normal and the
    limb-length discrepancy between the two limbs is usually small. Most often this condition is treated with
    shoe lifts in younger children with subsequent definitive
    contralateral epiphysiodesis or limb lengthening in patients with greater ultimate limb-length discrepancy.
    Hemihypertrophy
    Anisomelia with the larger limb appearing to be abnormally large is known as hemihypertrophy. The difference in limb diameter often has little relationship to the
    projected or existing limb-length discrepancy. Hemihypertrophy is sometimes associated with the development of abdominal or retroperitoneal tumors such as
    hepatoblastoma, Wilms tumor, or neuroblastoma. The

    2011 American Academy of Orthopaedic Surgeons

    Chapter 60: Lower Extremity and Foot Disorders: Pediatrics

    Figure 10

    A, Photograph of posteromedial bowing in a 3-month old girl showing a calcaneovalgus foot and a tibia with an
    obvious bowing deformity. B, An AP radiograph of both lower extremities in a 1-year-old girl with posteromedial
    bowing, showing a significant limb-length discrepancy and tibial deformity. C, Lateral radiograph of the tibia in
    the patient in B, showing significant unresolved tibial bowing.

    hemihypertrophy is not caused by the tumor, which


    is often identified years after the diagnosis of hemihypertrophy. Because of the risk of malignant tumor
    development, some recommendations include serum
    -fetoprotein levels every 6 weeks from the time of diagnosis until age 4 years and abdominal ultrasound examinations every 3 months until age 6 to 9 years. Orthopaedic management includes appropriate lifts under
    the normal limb and following the patient for serial determinations of limb-length discrepancy until definitive
    epiphysiodesis at an appropriate age. Limb lengthening
    should rarely be considered, as the normal limb is the
    short limb.

    Other Conditions

    2011 American Academy of Orthopaedic Surgeons

    Congenital Knee Dislocation


    Congenital knee dislocation encompasses a spectrum of
    disorders ranging from simple hyperextension of the
    knee in which the tibia dislocates anterior to the femur
    but can be reduced by simple flexion of the knee, to
    rigid disorders in which the dislocation is fixed with the
    tibia translated anteriorly and proximally. Approximately 50% of patients with congenital dislocation of
    the knee will have hip dysplasia affecting either or both
    hips. Flexing the knee and applying a long leg splint
    with the knee in a flexed position can treat simple hyperextension. Patients with both hip dysplasia and congenital knee dislocation can frequently be treated for
    both disorders with a Pavlik harness. Rigid dislocations
    often require initial serial casting or splinting and either
    percutaneous quadriceps tendon lengthening or open
    quadricepsplasty.

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Congenital Dislocation of the Patella


    Children with congenital dislocation of the patella are
    frequently diagnosed with an irreducible laterally dislocated patella before age 5 years. This condition should
    be differentiated from the much more common situation in which the patella is unstable or dislocates with
    activity in teens or young adults. Congenital dislocation
    of the patella is frequently associated with genu valgum
    flexion contracture of the knee and external tibial torsion. Although most often asymptomatic in younger
    children, the knee frequently becomes symptomatic
    with reports of pain and difficulty running as children

    approach adolescence. Surgical correction involves a


    comprehensive approach with proximal and distal realignment and careful balancing of the soft tissues to
    avoid redislocation because of the shallow trochlear
    groove. Surgery can be successful even in very young
    children by transfer of the entire distal insertion of the
    patellar tendon from its pathologic lateral position to a
    more normal anteromedial position.20

    771

    Section 6: Pediatrics

    Figure 11

    Clinical photographs demonstrating the features of congenital vertical talus. A, Unilateral congenital vertical talus
    deformity in a 6-week-old infant demonstrating the convex plantar surface of the foot. B, Plantar aspect of the
    foot showing forefoot abduction deformity.

    Foot Disorders

    Congenital Vertical Talus

    6: Pediatrics

    Congenital vertical talus is a rare foot deformity that is


    present at birth and has an estimated incidence of 1 in
    10,000. The hallmark of the deformity is a fixed dorsal
    dislocation of the navicular on the head of the talus resulting in a rigid flatfoot deformity. It occurs as an isolated deformity (idiopathic) in approximately half of all
    cases and is associated with neuromuscular and genetic
    disorders in the remaining cases. A careful neurologic
    examination should be performed in all vertical talus
    patients, and MRI evaluation of the neural axis should
    be considered to rule out spinal cord anomalies. Half of
    the children have bilateral involvement and there is
    male predominance over females by a ratio of 2:1. The
    etiology of idiopathic vertical talus has a genetic basis.
    This is supported by a positive family history in up to
    20% of patients and the recent findings that mutations
    in the HOXD10 gene, a member of a large family of
    highly conserved transcription factors that regulate
    limb development, are responsible for vertical talus in
    several familial cases.34
    Congenital vertical talus is characterized by hindfoot
    equinus and valgus due to contractures of the Achilles
    and peroneal tendons and forefoot abduction and dorsiflexion due to contractures of the extensor digitorum
    longus, extensor hallucis longus, and anterior tibialis
    tendons (Figure 11). It is usually recognizable in the
    newborn by the rigidity of the deformities, but it must
    be differentiated from the more common calcaneovalgus foot, posterior medial bowing of the tibia, flexible
    flatfoot, and the oblique talus. Forced plantar flexion
    and dorsiflexion lateral radiographs can confirm the diagnosis of vertical talus. The forced plantar flexion lateral radiograph in a true vertical talus demonstrates
    persistent dorsal dislocation of the first metatarsal axis
    772

    Orthopaedic Knowledge Update 10

    to the longitudinal axis of the talus, while the forced


    dorsiflexion lateral radiograph demonstrates a persistently decreased tibiocalcaneal angle indicating fixed
    hindfoot equinus (Figure 12).
    The goals of treatment are to restore the normal anatomic relationship between the talus, the navicular,
    and the calcaneus to provide a normal weight distribution through the foot. Many short- and long-term complications associated with extensive soft-tissue release
    surgeries for vertical talus have been noted. As such, efforts have been made recently to identify a less invasive
    approach for correcting this deformity.34,35 This new
    approach uses serial casting to stretch the contracted
    dorsal and lateral soft tissues and gradually reduce the
    talonavicular joint. The principles used for casting are
    similar to those used in the Ponseti method of clubfoot
    correction. Once reduction is achieved with casting, the
    talonavicular joint is reduced (open or closed) and
    pinned in the operating room. Percutaneous tenotomy
    of the Achilles tendon is performed to correct the residual equinus contracture. Excellent early results have
    been reported from multiple centers.34-36 Longer
    follow-up will be necessary to ensure maintenance of
    correction.

    Clubfoot
    Clubfoot is one of the most common birth defects involving the musculoskeletal system, with a worldwide
    incidence of about 1 in 1,000 live births. Approximately 80% of clubfeet are isolated birth defects and
    are considered idiopathic. The remaining 20% of clubfeet are associated with neuromuscular conditions and
    genetic syndromes. Although the exact etiology of idiopathic clubfoot is not known, a genetic component is
    suggested by the 33% concordance of identical twins
    and familial occurrence in 25% of cases. Additional evidence for a genetic etiology is provided by differences
    in clubfoot prevalence across ethnic populations, with

    2011 American Academy of Orthopaedic Surgeons

    Chapter 60: Lower Extremity and Foot Disorders: Pediatrics

    Figure 12

    A, Plantar flexion lateral radiograph of the right foot of the patient in Figure 11 with congenital vertical talus,
    showing persistent dorsal translation of the forefoot on the hindfoot. B, Lateral dorsiflexion radiograph of the
    same foot, showing persistent plantar flexion of the talus and calcaneus.

    2011 American Academy of Orthopaedic Surgeons

    Figure 13

    Photograph showing bilateral clubfoot in a


    2-week-old boy, demonstrating hindfoot varus,
    hindfoot equinus, midfoot adduction, and midfoot cavus.

    the need for extensive surgery in most patients with idiopathic clubfeet and has become the gold standard of
    treatment in North American and many parts of the
    world. The upper age limit of a child with clubfoot
    who can be treated with the Ponseti method is yet to be
    defined, with reports of correction obtained in children
    as old as 10 years at the initiation of treatment. In addition, there are recent reports of success using the Ponseti method to treat nonidiopathic clubfeet, including
    clubfeet in patients with distal arthrogryposis, myelomeningocele, and a variety of genetic syndromes.38-40
    The Ponseti method has also been applied successfully

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    the lowest prevalence in the Chinese population and


    the highest in Hawaiians and Maoris. Idiopathic clubfoot is not a single gene disorder. Instead, clubfoot is
    heterogeneous and likely due to multiple genes and epigenetic factors most of which are not yet understood.37
    A recent study has identified PITX1, a transcription
    factor critical for limb development, as the gene responsible for clubfoot in a five-generation family.31 This
    is the first gene identified to date for idiopathic clubfoot. A common genetic pathway for vertical talus and
    clubfoot is likely because many families have been reported in which both disorders are seen, as well as individuals with clubfoot on one side and vertical talus
    on the other.
    Clubfoot is a complex congenital foot deformity that
    can be difficult to treat. It is recognizable at birth and is
    characterized by hindfoot equinus, hindfoot varus,
    midfoot adduction, and midfoot cavus (Figure 13).
    Clubfoot can be differentiated from the more common
    positional foot anomalies on the basis of the rigid equinus deformity seen in clubfoot and its resistance to gentle passive correction. Several classification systems exist but their clinical utility is questionable. In the future
    a genetic classification for clubfoot may be available
    that would allow patients to be categorized in a manner that would help physicians predict response to
    treatment.
    Historically, treatment of clubfoot has consisted of
    serial casting followed by extensive soft-tissue release
    surgery. In addition to the many reported short-term
    complications associated with this procedure, longterm studies have shown many patients treated with extensive soft-tissue releases for clubfoot develop pain, arthritis, and difficulty ambulating as adults. The Ponseti
    method of serial casting, a percutaneous tenotomy of
    the Achilles tendon, and foot abduction bracing avoids

    773

    Section 6: Pediatrics

    ents must be taught how to perform the exercises correctly by abducting the forefoot using a thumb on the
    cuboid as a fulcrum. The stretch is held for a few seconds and repeated 20 times per session. If the forefoot
    is abducted without applying pressure on the cuboid,
    heel valgus may result without correction of the adductus, possibly leading to a skewfoot.
    If the parents are still bothered by the appearance of
    the childs foot at 7 months of age, serial casting can be
    performed with two to three casts changed at 2-week
    intervals. The foot is manipulated as just described followed by application of a long leg plaster cast with the
    knee bent 90 and the plaster well molded with the
    forefoot in abduction. Most feet that are stiff enough to
    warrant casting should be placed into a nighttime foot
    abduction brace for up to 1 year to maintain correction. In the rare 4- to 5-year-old child with severe deformity, midfoot osteotomies can be considered.
    Figure 14

    Photograph showing bilateral skewfeet in an


    8-year-old boy, characterized by forefoot adduction, midfoot abduction, and hindfoot valgus.

    in children previously treated with extensive soft-tissue


    release who later suffered a relapse.41 As a result, there
    is no type of clubfoot or situation for which the Ponseti
    method should not be initially applied. Even in the
    most difficult feet, the method allows partial correction
    that then limits the amount of surgery needed. The goal
    in treatment of all clubfeet should be to obtain plantigrade, mobile feet with the least invasive method possible.

    Metatarsus Adductus

    6: Pediatrics

    Metatarsus adductus is a common foot deformity characterized by adduction of the forefoot with respect to
    the hindfoot. The lateral border of the foot has a convex contour, with the actual curvature occurring at the
    tarsometatarsal joints. There is no deformity in the
    hindfoot, with full range of motion present in the ankle
    and subtalar joints. The incidence is approximately 1 in
    1,000 births with equal frequency in boys and girls and
    bilaterality occurring 50% of the time. Metatarsus adductus is a molding deformity that occurs due to fetal
    crowding as seen in late pregnancy, first pregnancies,
    twin pregnancies, and oligohydramnios.
    Most cases (90%) of metatarsus adductus are mild
    and spontaneously resolve in the first year of life or
    with gentle stretching exercises. An additional 5% of
    cases resolve in the early walking years (1 to 4 years of
    age). In the remaining 5% of cases, the foot is stiffer at
    the outset and the deformity is likely to persist. However, long-term studies have shown that residual metatarsus adductus causes no problems in terms of pain or
    foot function. Given the benign natural history of
    metatarsus adductus, aggressive treatment is generally
    not warranted. Those parents distressed about the position of the foot can be taught stretching exercises to
    perform at diaper changes several times a day. The par774

    Orthopaedic Knowledge Update 10

    Positional Calcaneovalgus
    This common foot deformity is recognizable at birth
    due to the characteristic appearance of the forefoot
    resting on the anterior surface of the lower leg. The deformity is thought to be positional in nature, is more
    common in firstborn children, and has a predilection
    for females. It is important to differentiate this condition from more serious disorders that can have similar
    presentations, such as congenital vertical talus, posteromedial bow of the tiba, and paralytic calcaneus foot deformity. When there is confusion between a calcaneovalgus foot deformity and a true vertical talus, a
    plantar-flexion lateral radiograph is indicated. Treatment of a positional calcaneovalgus foot is not necessary, as spontaneous improvement is the norm.

    Skewfoot
    Skewfoot (also termed Z-foot and serpentine foot) is a
    rare, complex deformity characterized by forefoot adduction, midfoot abduction, and hindfoot valgus (Figure 14). The pathogenesis and natural history of this
    deformity remain unknown. Some cases may result
    from improper casting of metatarsus adductus and/or
    clubfoot. It is difficult to differentiate skewfoot from
    metatarsus adductus radiographically in the infant because of a lack of ossification of the navicular and medial cuneiform. The diagnosis can often be made clinically based on the presence of significant hindfoot
    valgus in combination with the forefoot adduction. In
    the older child and adolescent, radiographs demonstrate the deformities in the hindfoot, midfoot, and
    forefoot (Figure 15). Nonsurgical management in childhood consists of stretching a tight Achilles tendon as
    well as custom soft orthotics to support the talar head
    with weight bearing. Surgery is rarely indicated if nonsurgical treatment fails to relieve pain, and usually involves osteotomies to correct both hindfoot and forefoot deformities as well as lengthening of the heel cord
    and medial reefing of the talonavicular joint.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 60: Lower Extremity and Foot Disorders: Pediatrics

    Flexible Flatfoot
    The incidence of flatfoot is unknown, but the condition
    is most common in infants and decreases with age. Approximately 20% of adults have flatfoot. All flatfeet
    are characterized by a decrease in the medial longitudinal arch with sagging of the midfoot combined with
    hindfoot valgus, and abduction of the forefoot. There
    are three main types of flatfoot: hypermobile flexible
    flatfoot, flexible flatfoot with a short Achilles tendon,
    and rigid flatfoot. The hypermobile flexible flatfoot accounts for most types of flatfeet in children and is
    rarely a clinical problem. This type of flatfoot has excellent mobility of the subtalar joint demonstrated by
    the heel correcting to a varus position with the patient
    standing on toes. The loss of arch is only seen with
    weight bearing. A rigid flatfoot does not correct into
    hindfoot varus with toe rise, indicating limitation of
    motion in the subtalar joint. This is the least common
    type of flatfoot in children, and tarsal coalitions should
    be ruled out in these cases, as they often require surgical treatment. Those patients with a flexible flatfoot
    and tight heel cord should be treated with heel cord
    stretching because this deformity has the potential to
    cause pain. Surgery is indicated when heel cord stretching fails to relieve symptoms. If the flatfoot is mild, a
    lengthening of the gastrocnemius fascia or the heel cord
    (if the soleus is also tight) may be all that is necessary.
    For a more severe deformity, heel cord lengthening
    should be combined with osteotomies to correct the deformity. Patients with hypermobile flatfeet, if symptomatic, can be treated with soft orthotics to change the
    shoe wear pattern and decrease symptoms. Surgery is
    rarely indicated for the flexible flatfoot.

    Tarsal Coalition

    2011 American Academy of Orthopaedic Surgeons

    AP radiographs of the patient in Figure 14 with


    bilateral skewfeet, demonstrating lateral translation of the midfoot on the hindfoot.

    The calcaneonavicular coalition can be diagnosed


    with an internal oblique radiograph of the foot, which
    demonstrates the bony bridge. A standing lateral radiograph may demonstrate a long anterior process of the
    calcaneus, called the anteater sign. Talocalcaneal coalitions are more difficult to diagnose on plain radiographs, and a CT or MRI is usually necessary. Only
    symptomatic coalitions should be treated because up to
    75% of coalitions do not cause pain or disability. The
    initial treatment of a symptomatic coalition includes a
    below-the-knee walking cast for 4 weeks. If the pain is
    not relieved immediately during cast wear, then the coalition may be only an incidental finding. A soft insert
    is used after cast removal, and approximately one third
    of patients will remain symptom free. If symptoms recur, surgery is warranted. Resection of the coalition
    and interposition of fat or the extensor digitorum brevis muscle is successful in most cases of calcaneonavicular coalitions. Overall, the results of talocalcaneal coalition resections and fat interposition are less
    favorable. In particular, if more than 50% of the subtalar joint is affected by the coalition, then resection
    alone is less likely to relieve symptoms. In addition, if
    there is excessive hindfoot valgus, a valgus-correcting
    osteotomy should be considered at the time of resection. Arthrodesis of the subtalar joint is reserved for
    patients with subtalar arthritis.

    6: Pediatrics

    A tarsal coalition refers to a fibrous, cartilaginous, or


    bony union between two or more bones of the midfoot
    or hindfoot. The incidence is not well known but is
    thought to be between 3% to 6% of the general population, with a 2:1 male-to-female distribution. The
    most common coalitions are the calcaneonavicular and
    the talocalcaneal (middle facet). Together these account
    for 90% of all coalitions. Bilaterality occurs in 50% to
    60% of cases, and there is a genetic predisposition evidenced by positive family histories and an autosomal
    dominant pattern of inheritance.42
    Symptoms of activity-related pain may develop as a
    coalition changes from a cartilaginous to a bony union.
    This change occurs commonly between age 8 and 12
    years for calcaneonavicular coalitions and between age
    12 and 16 years for talocalcaneal coalitions. The pain
    in the talocalcaneal coalitions is often poorly localized
    in the hindfoot, whereas a calcaneonavicular coalition
    usually causes pain dorsolaterally in the area of the coalition. A common presentation with a coalition is a
    history of repeated ankle sprains due to limitation of
    subtalar motion. On physical examination there is a
    rigid flatfoot deformity with minimal subtalar motion,
    such that the hindfoot does not invert into varus with
    toe standing.

    Figure 15

    Juvenile Hallux Valgus


    Hallux valgus or bunion deformity is an abnormal
    prominence on the medial side of the first metatarsal
    head with its accompanying bursa (Figure 16). A juve-

    Orthopaedic Knowledge Update 10

    775

    Section 6: Pediatrics

    present but usually consists of a combination of bony


    osteotomies and/or soft-tissue rebalancing.43 One of the
    most important considerations to make preoperatively
    is whether the MTP joint is subluxated. If so, treatment
    must include a distal soft-tissue realignment. Lateral
    hemiepiphysiodesis of the great toe metatarsal has been
    recently proposed as an alternative treatment in the juvenile patient that allows correction to be achieved
    slowly with continued growth of the child.44 Additional
    studies are needed to confirm the efficacy of the procedure and establish treatment guidelines.

    Cavus Foot Deformity

    Figure 16

    Photograph of the foot of an adolescent boy


    with significant hallux valgus deformity. The
    first toe is laterally deviated at the metatarsophalangeal joint causing overlap of the
    second toe onto the first.

    6: Pediatrics

    nile bunion has its onset in the preteen or teenage years,


    when the growth plates of the metatarsals and phalanges are still open. The incidence is unknown but there is
    a female predilection with 80% of surgically treated
    cases. Although the cause is unknown, there is a strong
    genetic component with reports of X-linked, autosomal
    dominant, and polygenic modes of transmission. Standing AP and lateral radiographs of the foot can help determine the site of the deformities. Typical measurements recorded are the first-second intermetatarsal
    angle, the first metatarsalproximal phalanx angle, the
    distal metatarsal articular angle, and metatarsophalangeal (MTP) joint congruity. The natural history of juvenile hallux valgus is not known. Most experts concur
    that a congruous MTP joint is stable and less likely to
    progress than those with subluxation.
    Most adolescents with hallux valgus are asymptomatic and should not undergo any form of treatment.
    Children with pain related to their bunion should first
    have nonsurgical management, including the use of
    shoes with an adequate toe box and a low heel. Splinting can relieve pressure over the deformity but does not
    provide correction long term. Surgery is indicated only
    when prolonged attempts at nonsurgical management
    have failed. The ideal time for surgery is when the physes are closed because open physes contribute to an increased incidence of recurrent deformity. The exact
    procedure chosen is based on the type of deformity
    776

    Orthopaedic Knowledge Update 10

    A cavus foot is characterized by a rigid plantar flexion


    of the forefoot in relation to the hindfoot, resulting in
    an abnormally high arch. The high arch may be due to
    plantar flexion of the first ray alone or may involve
    plantar flexion of all of the metatarsals. The heel in the
    cavus foot may be in neutral, valgus, varus (cavovarus
    foot) (Figure 17, A), calcaneus (calcaneocavus foot), or
    equinus position. A careful physical examination is required in all patients with a cavus foot deformity because most cases are due to an underlying neuromuscular disorder. Unilateral deformities can be associated
    with syringomyelia, lipomeningocele, spinal cord tumor, diastematomyelia, or tethered cord diagnosed on
    MRI of the spine. Genetic testing and a consultation
    with a pediatric neurologist are appropriate; an electromyogram and nerve conduction velocity studies may be
    ordered. Bilateral cases are often due to hereditary sensorimotor neuropathies such as Charcot-Marie-Tooth
    disease and Friedreich ataxia. Because of the familial
    nature of these conditions, examining the feet of the
    parents and other family members should be done if
    possible.
    Patients typically present to the orthopaedic surgeon
    because of difficulty with shoe fitting, pain under the
    metatarsal heads, clawing of the toes, and a history of
    repeated ankle sprains. The deformities seen in the foot
    are caused by muscle imbalance. Relative weakness of
    the anterior tibialis compared to the peroneus longus
    results in plantar flexion of the first ray and the cavus
    deformity. Atrophy of the intrinsic muscles of the foot
    leads to hyperextension of the MTP joints and resulting
    tightening of the plantar fascia. The hindfoot deformities seen with the cavus foot develop last. In the most
    common examples of the cavovarus foot, the hindfoot
    varus develops as a direct result of the plantar-flexed
    first ray. If the first ray is in plantar flexion, the only
    way to maintain the tripod of the foot and get the heel
    on the ground is for the heel to go into varus. This position is reinforced by the relative strength of the posterior tibialis compared to the peroneus brevis.
    Radiographic evaluation of the patient with pes cavus should include AP and lateral radiographs of the
    spine to look for interpedicular distance widening, congenital malformations, or atypical pattern scoliosis.
    Foot radiographs should include standing AP and lateral views. A cavus foot is characterized by plantar
    flexion of the axis of the first metatarsal in relation to

    2011 American Academy of Orthopaedic Surgeons

    Chapter 60: Lower Extremity and Foot Disorders: Pediatrics

    Figure 17

    A, Photograph of a cavus foot deformity in a 14-year-old girl with a peripheral neuropathy. B, Unilateral cavovarus
    foot deformity due to Charcot-Marie-Tooth disease is shown in a 16-year-old boy. Although patients with hereditary sensory motor neuropathy typically have bilateral deformity, unilateral deformity can still occur.

    the axis of the talus on the lateral view. The hindfoot


    can be in varus, valgus, or equinus, although varus is
    most common (Figure 17, B).
    Arch supports and stretching may be appropriate in
    the earliest stages of a developing cavus foot deformity.
    Surgery is indicated for patients with painful calluses
    under the metatarsal heads or on the dorsum of the
    MTP joints, difficulty with shoe wear, and progressive
    deformity with ankle instability. The principles of surgery are to correct the deformities and to balance the
    soft tissues to maintain correction and prevent recurrences. Correction of the deformities involves release of
    the soft-tissue contractures combined with appropriate
    osteotomies.45 The Coleman block test can be used to
    assess the flexibility of the hindfoot varus and help predict whether hindfoot correction can be maintained
    with forefoot procedures alone, or whether additional
    osteotomies of the hindfoot may be necessary. The
    block test is performed by placing a block under the
    lateral border of the foot while the patient is bearing
    weight. The block allows the forefoot to pronate; if the
    hindfoot is flexible, the subtalar joint will correct to
    neutral. Correction of the rigid subtalar joint will not
    occur with this maneuver, indicating that osteotomy of
    the hindfoot will be necessary.

    Kohler disease is an osteochondrosis that affects the


    tarsal navicular. It is a self-limited condition characterized by pain or swelling in the area of the tarsal navicular in association with distinct radiographic findings.
    It occurs in patients 4 to 7 years of age, with 80% of
    cases occurring in boys. The cause is unknown, but it is
    thought to be related to repetitive trauma. On physical
    examination there is typically soft-tissue swelling, erythema, and tenderness to palpation over the tarsal navicular. Active and passive range of motion is normal.

    2011 American Academy of Orthopaedic Surgeons

    Lateral radiograph of the foot in a patient with


    Kohler disease, demonstrating the sclerotic and
    flattened appearance of the navicular.

    The classic radiographic findings include flattening and


    patchy ossification of the navicular bone with preservation of its joint surfaces (Figure 18). The goal of treatment should be relief of symptoms, which can usually
    be accomplished with a short leg weight-bearing cast
    worn for 3 to 4 weeks. Without treatment, most patients have intermittent activity-related symptoms for 1
    to 3 years. Radiographic improvement is noted over a
    1-year period from onset of symptoms, and no longterm disabilities have been reported.
    Freiberg infraction is an osteochondrosis characterized by osteonecrosis of the metatarsal head, the second
    metatarsal being most often affected. This condition is
    most commonly seen in patients age 13 to 18 years and
    is more common in girls than boys. Patients present
    with pain and tenderness around the second MTP joint.
    The second metatarsal head has a flattened appearance
    on radiographs, with areas of increased sclerosis and
    fragmentation. The natural history is variable. Many
    cases are self-limited, with revascularization of the

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Osteochondroses of the Foot

    Figure 18

    777

    Section 6: Pediatrics

    surgical resection of the bony prominence is warranted,


    with reattachment of any posterior tibialis tendon that
    was removed during the bone resection. It is important
    to remove enough bone so the navicular is flush with
    the medial cuneiform on an AP radiograph of the foot.
    Most surgical failures are the result of inadequate removal of bone.

    Lesser Toe Deformities

    Figure 19

    Postaxial polydactyly in a 6-month-old child.

    metatarsal head. Some cases, however, result in significant deformity and secondary degenerative changes at
    the MTP joint. Initial treatment should be nonsurgical
    and includes activity modification and the use of metatarsal pads in the shoes. In some acute cases, casting
    may be beneficial. Surgery is rarely indicated and
    should be reserved for chronic cases unresponsive to
    nonsurgical treatment. Surgery can range from metatarsal neck osteotomy and joint dbridement to resection
    of the metatarsal head.

    Accessory Navicular

    6: Pediatrics

    Approximately 10% of the population older than 5


    years of age has an accessory navicular, with symptoms
    more commonly developing in girls. Pain and tenderness are localized to the prominent accessory navicular
    on the plantar medial aspect of the foot at the insertion
    of the posterior tibialis tendon. Accessory navicular can
    be classified as type I, a small sesamoid bone in the substance of the posterior tibialis tendon; type II, a large
    wedge-shaped bone fragment that appears to be congruous with the navicular through a synchondrosis; or
    type III, a large horn-shaped navicular, likely resulting
    from an earlier fusion of a type II deformity. Evaluation
    of the symptomatic patient should include an external
    oblique radiograph of the foot to better visualize the
    accessory ossification center.
    Nonsurgical management includes activity modifications, foot orthotics, or a short leg walking cast for 3 to
    4 weeks. The goal with nonsurgical management is to
    decrease pressure over the bony prominence and reduce
    strain on the posterior tibialis tendon. If pain persists,
    778

    Orthopaedic Knowledge Update 10

    A curly toe is a common deformity in which the proximal interphalangeal joint is flexed and medially deviated so it underlaps the adjacent toe. The third and
    fourth toes are most commonly involved and the deformities are often bilateral and familial. The etiology is
    congenital tightness and shortening of the toe flexors.
    Most patients are asymptomatic, and approximately
    25% of cases will resolve spontaneously. Treatment
    with stretching and taping can be used but has not been
    shown to provide long-term correction. Surgery is indicated for patients with pain and difficulty with shoe
    wear. Release of the long toe flexor at the level of the
    distal interphalangeal joint is effective in most cases.
    Congenital overriding fifth toe is a familial disorder
    in which the fifth toe is dorsiflexed, adducted, and
    overrides the fourth toe. It is often bilateral and there is
    no sex predilection. Unlike the curly toe, which is flexible, the overriding fifth toe is a rigid deformity that often requires treatment in half of all patients. Treatment
    is indicated for persistent symptoms despite shoe wear
    modifications. Nonsurgical measures such as taping,
    stretching, and splinting are ineffective. Surgical treatment involves releasing the contracted MTP joint capsule, lengthening the extensor tendon, and pinning the
    toe in the corrected position. A dorsal incision is usually avoided because contracture of the scar can lead to
    recurrent deformity.
    Polydactyly is the duplication of a digit and is the
    most common congenital toe deformity. It is often familial and is bilateral in 50% of cases. The fifth toe is
    the most commonly duplicated digit; this condition is
    called postaxial polydactyly (Figure 19). Duplication of
    the great toe is called preaxial polydactyly and occurs
    frequently with tibial hemimelia. PITX1 is the first
    gene identified for the combination of preaxial polydactyly, clubfoot, and tibial hemimelia.31 Treatment is
    generally surgical because of difficulties with shoe wear
    due to the widened forefoot. The procedure is usually
    performed between 9 and 12 months of age. Radiographs are required to assess the extent of the duplication and decide which digit to excise.
    Bunionette deformity is a painful osseous prominence on the lateral aspect of the head of the fifth metatarsal (Figure 20) that is less common than hallux valgus deformity. It is more common in females and the
    exact prevalence of the deformity is unknown. Patients
    usually present because of a painful bursa that develops
    over the prominent fifth metatarsal head. Initial treatment, as with hallux valgus deformities, is shoe wear
    modification, to which most patients respond favorably. For persistent symptoms, surgery may be indi-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 60: Lower Extremity and Foot Disorders: Pediatrics

    begins with instructions to parents on stretching exercises and dorsiflexion strengthening exercises. This
    treatment is most effective in the young patient, age 3
    or 4 years. If improvement is not seen with several
    months of aggressive therapy done by parents and/or
    outside physical therapy, then serial casting can be
    used. A series of two or three short leg casts changed
    every 2 weeks is recommended. At each cast change
    further stretching of the Achilles tendon is attempted.
    For those patients who do not respond to casting or
    those who are older than 7 years, Vulpius lengthening
    of the gastrocnemius or heel cord lengthening (if both
    the soleus and gastrocnemius are tight) should be considered. The heel cord can be lengthened percutaneously in a stepwise manner by starting 1 cm proximal
    to the heel cord and releasing the medial half of the tendon. The lateral half is released 1 cm proximal to the
    first cut, and the medial half is released 1 cm proximal
    to the last cut. This allows the tendon to be lengthened
    but still maintain fiber continuity. The patient is placed
    in a short leg walking cast for 4 weeks followed by a
    walking boot for another 2 weeks. Physical therapy is
    initiated when the patient gets out of the cast. The emphasis is on maintaining ankle dorsiflexion and improving strength in the gastrocnemius. Results are very
    satisfactory with this procedure.

    Figure 20

    AP radiograph of the foot demonstrating bunionette deformity in an adolescent girl.

    Annotated References
    Sabharwal S, Zhao C, Edgar M: Lower limb alignment
    in children: Reference values based on a full-length
    standing radiograph. J Pediatr Orthop 2008;28(7):740746.
    The authors analyzed 354 normal lower extremity long
    cassette radiographs in children of various ages. Initial
    varus alignment corrected to valgus by age 3 years. After age 7 years, the mechanical axis deviation, lateral
    distal tibial angle, and medial proximal tibial angle had
    normalized to values considered normal for adults.

    2.

    Inan M, Jeong C, Chan G, Mackenzie WG, Glutting J:


    Analysis of lower extremity alignment in achondroplasia: Interobserver reliability and intraobserver reproducibility. J Pediatr Orthop 2006;26(1):75-78.

    3.

    Gordon JE, Chen RC, Dobbs MB, Luhmann SJ, Rich


    MM, Schoenecker PL: Interobserver and intraobserver
    reliability in the evaluation of mechanical axis deviation. J Pediatr Orthop 2009;29(3):281-284.
    The authors evaluated interobserver and intraobserver
    reliabilities for mechanical axis deviation, lateral distal
    femoral angle, and medial proximal tibial angle in 35
    pediatric radiographs with a variety of deformities.
    Measurements demonstrated excellent intraobserver
    and interobserver reliabilities regardless of the experience of the observer.

    4.

    Stevens PM, Klatt JB: Guided growth for pathological


    physes: Radiographic improvement during realignment.
    J Pediatr Orthop 2008;28(6):632-639.

    cated. The most common procedure is a fifth metatarsal sliding osteotomy, which has been shown to be safe
    and effective.

    Idiopathic Toe Walking


    Idiopathic toe walking is usually easy to recognize, but
    it is a diagnosis of exclusion. Patients walk on their toes
    and the condition is usually bilateral. It is more common in males and there is a genetic etiology seen with
    many patients having a positive family history. Patients
    typically present for evaluation at age 3 or 4 years. Toe
    walking is normal and is often seen in children who are
    beginning to walk. However, by the age of 3 years, children should walk with a heel strike gait. Persistent toe
    walking beyond this age is abnormal and should be further evaluated. It is important in early-onset toe walking to rule out neuromuscular etiologies such as spastic
    diplegia. If toe walking develops in a child with a previously normal gait then it is necessary to rule out primary muscle diseases such as muscular dystrophy, myotonic dystrophy, dystonia, tethered cord, and central
    nervous system disorders. Unilateral toe walking
    should also be a red flag for an underlying neurologic
    etiology.
    Physical examination of the child with idiopathic toe
    walking demonstrates a loss of passive ankle dorsiflexion. Neurologic examination will be normal. Treatment

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    1.

    779

    Section 6: Pediatrics

    The authors treated 14 patients with rickets using


    guided growth with either staples or 8-plates. When using staples, migration was common and rebound occurred in 41% of physes. No 8-plate migration occurred. As the deformities corrected, the appearance and
    width of the physis improved.
    5.

    6.

    Thompson GH, Carter JR, Smith CW: Late-onset tibia


    vara: A comparative analysis. J Pediatr Orthop 1984;
    4(2):185-194.

    7.

    Feldman MD, Schoenecker PL: Use of the metaphysealdiaphyseal angle in the evaluation of bowed legs. J Bone
    Joint Surg Am 1993;75(11):1602-1609.

    8.

    Shah HH, Doddabasappa SN, Joseph B: Congenital


    posteromedial bowing of the tibia: A retrospective analysis of growth abnormalities in the leg. J Pediatr Orthop B 2009;18(3):120-128.
    Serial radiographs of 20 patients with posteromedial
    bowing of the tibia were reviewed. The angulatory deformity improved rapidly during the first year of life
    and much more slowly after that. Remodeling appeared
    to come from a combination of diaphyseal remodeling
    and physeal realignment. Shortening of 40% was noted
    in one patient.

    6: Pediatrics

    9.

    10.

    780

    Bar-On E, Horesh Z, Katz K, et al: Correction of lower


    limb deformities in children with renal osteodystrophy
    by the Ilizarov method. J Pediatr Orthop 2008;28(7):
    747-751.
    Five patients with eight affected limb segments with coronal angulation were treated with osteotomy and circular external fixation. There were no major complications,
    and pin tract infections responded to oral antibiotics.
    Four of the five patients maintained the alignment
    achieved at the time of external fixator removal.

    Lavelle WF, Shovlin J, Drvaric DM: Reliability of the


    metaphyseal-diaphyseal angle in tibia vara as measured
    on digital images by pediatric orthopaedic surgeons.
    J Pediatr Orthop 2008;28(6):695-698.
    Digital radiographs of 21 patients including 42 lower
    extremities were reviewed by 27 pediatric orthopaedic
    surgeons to determine the intraobserver and interobserver reliability of the metaphyseal-diaphyseal angle.
    Alternative methods of drawing the angle using either
    the lateral border of the tibia or the center of the tibial
    shaft were used. There was excellent reliability of the
    method and no significant variability was seen using either method of drawing the angle.
    Langenskild A: Tibia vara. J Pediatr Orthop 1994;
    14(2):141-142.

    11.

    Gordon JE, King DJ, Luhmann SJ, Dobbs MB, Schoenecker PL: Femoral deformity in tibia vara. J Bone Joint
    Surg Am 2006;88(2):380-386.

    12.

    Park SS, Gordon JE, Luhmann SJ, Dobbs MB, Schoenecker PL: Outcome of hemiepiphyseal stapling for lateonset tibia vara. J Bone Joint Surg Am 2005;87(10):
    2259-2266.

    Orthopaedic Knowledge Update 10

    13.

    Bushnell BD, May R, Campion ER, Schmale GA, Henderson RC: Hemiepiphyseodesis for late-onset tibia
    vara. J Pediatr Orthop 2009;29(3):285-289.
    The authors treated 53 patients with 67 limbs with adolescent tibia vara by hemiepiphysiodesis using staples
    at either the distal femur, proximal tibia or both. This
    procedure was successful in restoring the mechanical
    axis in 38 patients. Although younger age and lesser deformity were weakly predictive of correction, neither
    weight or any other factor was a statistically significant
    predictor of correction.

    14.

    Gilbody J, Thomas G, Ho K: Acute versus gradual correction of idiopathic tibia vara in children: A systematic
    review. J Pediatr Orthop 2009;29(2):110-114.
    A systematic review of the literature revealed only one
    comparative study that provided weak evidence that
    correction with computerized ring fixation resulted in
    improved outcomes. Other series failed to provide evidence of any advantage of either acute or gradual correction of the deformity.

    15.

    Clarke SE, McCarthy JJ, Davidson RS: Treatment of


    Blount disease: a comparison between the multiaxial
    correction system and other external fixators. J Pediatr
    Orthop 2009;29(2):103-109.
    The multiaxial correction external fixator was compared to correction using traditional circular fixation
    and monolateral fixation in 58 extremities with tibia
    vara. There was no difference in accuracy of correction
    or complications with any of the methods.

    16.

    Feldman DS, Madan SS, Ruchelsman DE, Sala DA, Lehman WB: Accuracy of correction of tibia vara: Acute
    versus gradual correction. J Pediatr Orthop 2006;26(6):
    794-798.

    17.

    Gordon JE, Heidenreich FP, Carpenter CJ, Kelly-Hahn


    J, Schoenecker PL: Comprehensive treatment of lateonset tibia vara. J Bone Joint Surg Am 2005;87(7):
    1561-1570.

    18.

    Eidelman M, Bialik V, Katzman A: The use of the Taylor spatial frame in adolescent Blounts disease: Is fibular osteotomy necessary? J Child Orthop 2008;2(3):
    199-204.
    The authors reviewed 10 extremities in patients with
    tibia vara corrected with computer-driven circular fixation without fibular osteotomy. They concluded that
    placement of the origin at the level of the proximal
    tibial-fibular joint obviates the need for fibular osteotomy in patients with mild to moderate tibia vara.

    19.

    Cho TJ, Choi IH, Lee KS, et al: Proximal tibial lengthening by distraction osteogenesis in congenital pseudarthrosis of the tibia. J Pediatr Orthop 2007;27(8):915920.
    The authors review 27 cases of distraction osteogenesis
    in 22 patients with congenital pseudarthrosis of the
    tibia. Patients who had dysplastic proximal tibiae or
    who were being lengthened for the second time were
    much more likely to require bone grafting or other procedures to achieve union of the lengthened segment.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 60: Lower Extremity and Foot Disorders: Pediatrics

    20.

    21.

    22.

    Wada A, Fujii T, Takamura K, Yanagida H, Surijamorn


    P: Congenital dislocation of the patella. J Child Orthop
    2008;2(2):119-123.
    The authors treated seven knees in six patients with
    congenital dislocation of the patella at ages ranging
    from 0.6 years to 3.9 years. Genu valgus and external
    tibial torsion improved after medial transfer of the patellar tendon with posterior knee release and V-Y quadricepsplasty.
    Peterson HA: The treatment of congenital pseudarthrosis of the tibia with ipsilateral fibular transfer to make a
    one-bone lower leg: A review of the literature and case
    report with a 23-year follow-up. J Pediatr Orthop
    2008;28(4):478-482.
    The author reports a single case with 23-year follow-up
    and a review of the literature on nonvascularized ipsilateral fibular transfer to repair a congenital pseudarthrosis of the tibia.
    Ofluoglu O, Davidson RS, Dormans JP: Prophylactic
    bypass grafting and long-term bracing in the management of anterolateral bowing of the tibia and
    neurofibromatosis-1. J Bone Joint Surg Am 2008;
    90(10):2126-2134.
    The authors report a series of 10 patients with dysplastic but intact tibiae treated with allograft fibular grafting. Although several complications occurred, no patient developed a fracture of the dysplastic tibia
    following allograft placement.

    23.

    Anticevic D, Jelic M, Vukicevic S: Treatment of a congenital pseudarthrosis of the tibia by osteogenic


    protein-1 (bone morphogenetic protein-7): A case report. J Pediatr Orthop B 2006;15(3):220-221.

    24.

    Johnston CE, Birch JG: A tale of two tibias: A review of


    treatment options for congenital pseudarthrosis of the
    tibia. J Child Orthop 2008;2(2):133-149.
    The authors compare two common treatment options
    for congenital pseudarthrosis of the tibia and emphasize
    the importance of careful surgical technique in carrying
    out intramedullary fixation of the tibia. The use of bone
    morphogenetic protein2 is described as an aid to obtain union in a single patient.

    25.

    27.

    Gordon JE, Pappademos PC, Schoenecker PL, Dobbs


    MB, Luhmann SJ: Diaphyseal derotational osteotomy
    with intramedullary fixation for correction of excessive
    femoral anteversion in children. J Pediatr Orthop 2005;
    25(4):548-553.
    Stevens PM, Anderson D: Correction of anteversion in
    skeletally immature patients: Percutaneous osteotomy
    and transtrochanteric intramedullary rod. J Pediatr Orthop 2008;28(3):277-283.
    Forty percutaneous diaphyseal derotational femoral os-

    2011 American Academy of Orthopaedic Surgeons

    28.

    Ryan DD, Rethlefsen SA, Skaggs DL, Kay RM: Results


    of tibial rotational osteotomy without concomitant fibular osteotomy in children with cerebral palsy. J Pediatr
    Orthop 2005;25(1):84-88.

    29.

    Savva N, Ramesh R, Richards RH: Supramalleolar osteotomy for unilateral tibial torsion. J Pediatr Orthop B
    2006;15(3):190-193.

    30.

    Inan M, Chan G, Littleton AG, Kubiak P, Bowen JR:


    Efficacy and safety of percutaneous epiphysiodesis. J Pediatr Orthop 2008;28(6):648-651.
    The authors report 97 cases of percutaneous epiphysiodesis followed until skeletal maturity. Complications
    included two knee effusions, one superficial wound infection, and three instances of exostosis formation. Failure of the epiphysiodesis to stop physeal growth occurred in three patients. Complications are infrequent
    and correction is accurate when the straight-line Mosley
    graph is used to plan surgical intervention.

    31.

    Gurnett CA, Alaee F, Kruse LM, et al: Asymmetric


    lower-limb malformations in individuals with homeobox PITX1 gene mutation. Am J Hum Genet 2008;
    83(5):616-622.

    32.

    Babbs C, Heller R, Everman DB, et al: A new locus for


    split hand/foot malformation with long bone deficiency
    (SHFLD) at 2q14.2 identified from a chromosome
    translocation. Hum Genet 2007;122(2):191-199.
    The authors report a sporadic patient with tibial aplasia
    and a chromosome 2;18 translocation.

    33.

    De Maio F, Corsi A, Roggini M, Riminucci M, Bianco


    P, Ippolito E: Congenital unilateral posteromedial bowing of the tibia and fibula: Insights regarding pathogenesis from prenatal pathology. A case report. J Bone Joint
    Surg Am 2005;87(7):1601-1605.

    34.

    Dobbs MB, Purcell DB, Nunley R, Morcuende JA: Early


    results of a new method of treatment for idiopathic congenital vertical talus. J Bone Joint Surg Am 2006;88(6):
    1192-1200.

    35.

    Alaee F, Boehm S, Dobbs MB: A new approach to the


    treatment of congenital vertical talus. J Child Orthop
    2007;1(3):165-174.
    The authors describe a minimally invasive approach to
    congenital vertical talus that has shown good shortterms results while avoiding the need for more extensive
    soft-tissue release surgery.

    36.

    Bhaskar A: Congenital vertical talus: Treatment by reverse Ponseti technique. Indian J Orthop 2008;42(3):
    347-350.
    The authors report on four patients (eight vertical talus
    feet) treated with the new minimally invasive approach
    with excellent short-term results and no patient requiring more extensive surgery.

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    26.

    Lee FY, Sinicropi SM, Lee FS, Vitale MG, Roye DP Jr,
    Choi IH: Treatment of congenital pseudarthrosis of the
    tibia with recombinant human bone morphogenetic
    protein-7 (rhBMP-7). A report of five cases. J Bone
    Joint Surg Am 2006;88(3):627-633.

    teotomies were performed for anteversion. No immobilization was used. All healed without evidence of femoral growth disturbance or osteonecrosis.

    781

    Section 6: Pediatrics

    37.

    38.

    39.

    40.

    Boehm S, Limpaphayom N, Alaee F, Sinclair MF,


    Dobbs MB: Early results of the Ponseti method for the
    treatment of clubfoot in distal arthrogryposis. J Bone
    Joint Surg Am 2008;90(7):1501-1507.
    The authors report the successful correction of 12 consecutive clubfoot patients (24 clubfeet) with the diagnosis of distal arthrogryposis using the Ponseti method.
    The minimum follow-up was 2 years.
    Gerlach DJ, Gurnett CA, Limpaphayom N, et al: Early
    results of the Ponseti method for the treatment of clubfoot associated with myelomeningocele. J Bone Joint
    Surg Am 2009;91(6):1350-1359.
    The authors report the successful use of the Ponseti
    method of clubfoot correction in 16 consecutive patients
    with clubfoot and myelomeningocele and 20 patients
    with idiopathic clubfoot.
    Gurnett CA, Boehm S, Connolly A, Reimschisel T,
    Dobbs MB: Impact of congenital talipes equinovarus
    etiology on treatment outcomes. Dev Med Child Neurol
    2008;50(7):498-502.
    The authors evaluated 357 consecutive clubfoot patients
    treated by one physician and found 24% of patients had
    nonidiopathic clubfoot. Most patients with nonidiopathic clubfoot had disorders affecting the nervous system.
    Garg S, Dobbs MB: Use of the Ponseti method for recurrent clubfoot following posteromedial release. Indian J
    Orthop 2008;42(1):68-72.
    The authors report 11 consecutive clubfoot patients (17
    clubfeet) that had been previously treated with extensive
    soft-tissue release operations for idiopathic clubfoot and

    presented with full relapses. The patients were all


    treated successfully using the Ponseti method of casting
    followed by tibialis anterior tendon transfer and percutaneous heel cord lengthening.
    42.

    Migues A, Slullitel GA, Surez E, Galn HL: Case reports: Symptomatic bilateral talonavicular coalition.
    Clin Orthop Relat Res 2009;467(1):288-292.
    The authors report results in a 24-year-old woman with
    symptomatic talonavicular coalitions bilaterally who
    underwent successful resections.

    43.

    George HL, Casaletto J, Unnikrishnan PN, et al: Outcome of the scarf osteotomy in adolescent hallux valgus.
    J Child Orthop 2009;3(3):185-190.
    The authors report 13 adolescent patients (19 feet)
    treated with the scarf osteotomy for symptomatic hallux
    valgus deformities. Patients were followed for a mean of
    37.6 months and had good radiographic and clinical
    outcomes.

    44.

    Davids JR, McBrayer D, Blackhurst DW: Juvenile hallux valgus deformity: Surgical management by lateral
    hemiepiphyseodesis of the great toe metatarsal. J Pediatr Orthop 2007;27(7):826-830.
    Authors present a series of 7 patients (11 feet) treated
    with lateral hemiepiphysiodesis of the great toe metatarsal of juvenile hallux valgus. The procedure was effective in halting progression of the deformity in all cases
    and allowed significant correction of the deformity in
    50% of cases. This procedure provides an alternative to
    osteotomy procedures in this patient population.

    45.

    Weiner DS, Morscher M, Junko JT, Jacoby J, Weiner B:


    The Akron dome midfoot osteotomy as a salvage procedure for the treatment of rigid pes cavus: A retrospective
    review. J Pediatr Orthop 2008;28(1):68-80.
    A retrospective review of 89 patients (139 feet) treated
    with a salvage procedure for significant pes cavus deformity is presented. A satisfactory result was reported in
    76% of cases.

    6: Pediatrics

    41.

    Kruse LM, Dobbs MB, Gurnett CA: Polygenic threshold


    model with sex dimorphism in clubfoot inheritance: The
    Carter effect. J Bone Joint Surg Am 2008;90(12):26882694.
    The authors demonstrate that idiopathic clubfoot is a
    polygenic disorder, with females as the less affected sex,
    requiring a higher genetic load to be affected.

    782

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 61

    Injuries and Conditions of the


    Pediatric and Adolescent Athlete
    Kevin Shea, MD

    Theodore J. Ganley, MD

    Introduction
    The popularity of youth sports continues to grow, with
    increasing participation of children at younger ages.
    The benefits of sports participation at a young age are
    numerous, including the potential for the development
    of a lifetime of fitness habits, exposure to healthy competition, and psychosocial integration with peers and
    coaches. The risk of injury increases as children mature
    and participate in collision sports. This is due in part to
    increased speed, strength, and contact in older athletes.
    Medical personnel charged with providing care to these
    young athletes must be familiar with the unique, agerelated anatomy and the injuries specific to this population.

    Epidemiology of Athletic Injuries in Youth Sports


    The numbers of young athletes participating in sports
    continues to increase, and recent estimates suggest that
    30 million preadolescents and adolescents are involved
    in organized sports. As society faces increasing numbers of children with obesity, participation in sports
    should be encouraged to improve overall health. This
    participation is beneficial to the overall health of these
    children but is not without risk. In a survey of children
    and adolescents age 5 to 17 years, the estimated annual
    number of injuries resulting from participation in
    sports and recreational activities was 4,379,000, with
    1,363,000 classified as serious (requiring hospitaliza-

    2011 American Academy of Orthopaedic Surgeons

    Training in the Pediatric Population


    Historically, strength training in young athletes was discouraged, although investigations have shown that
    these training programs can be implemented safely.4
    Strength training in young athletes has become more
    common in the past 10 years. The American Academy
    of Pediatrics has endorsed resistance/exercise strengthening programs in children. The National Strength and
    Conditioning Association (NSCA) supports strength
    training in children, provided that appropriate training
    and safety guidelines are met. The NSCA published
    guidelines on proper resistance training in children in
    1985, 1996, and 2009 (http://www.nsca-lift.org/youth
    positionpaper/Youth_Pos_Paper_200902.pdf). With supervision, the implementation of youth strengthening/
    resistance programs can improve conditioning, power,
    motor skills, and habits of lifetime fitness. Similar to injury prevention programs advocated for older athletes,
    injury prevention programs may also play a role in reducing injury risk in pediatric athletes. These injury prevention programs may reduce both traumatic and overuse injuries.5

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Dr. Shea or an immediate family member serves as a


    board member, owner, officer, or committee member of
    the American Academy of Orthopaedic Surgeons, the
    Pediatric Orthopaedic Society of North America, and Intermountain Orthopedics. Neither Dr. Shea nor any immediate family member has received anything of value
    from or owns stock in a commercial company or institution related directly or indirectly to the subject of this
    chapter. Neither Dr. Ganley nor any immediate family
    member has received anything of value from or owns
    stock in a commercial company or institution related directly or indirectly to the subject of this chapter.

    tion, surgical treatment, missed school, or a half day or


    more in bed). Up to 36% of injuries may be directly related to sports participation in patients in these age
    groups.1 As sports participation continues to increase,
    the number of young athletes sustaining injury will
    probably increase. Title IX legislation, enacted in 1972,
    has dramatically increased the number of female athletes participating in youth sports. For adult patients,
    females appear to have higher rates of knee injuries
    than male athletes for sports that involve running,
    jumping, and pivoting activities. A study by the American Academy of Pediatrics suggested that female athletes have higher rates of injury when compared with
    male athletes.2 In a recent study of injury claims from
    an insurance company providing coverage for youth
    soccer leagues, knee and anterior cruciate ligament
    (ACL) injuries in female youth soccer players age 12
    through 15 years were more common than ACL injuries in males of the same age.3

    783

    Section 6: Pediatrics

    Rehabilitation
    As a general rule, young athletes seem to recover from
    injuries faster than older patients. Prolonged stiffness
    and weakness are unusual in younger athletes. Because
    of these differences in healing, younger children seem
    to return to sports earlier and require less physical therapy supervision in many types of injuries. Arthrofibrosis is less common in younger athletes. Return to recreational play may be one of the best forms of therapy
    for many young athletes. Even though injury recovery
    is faster in younger athletes, some injuries, including
    ankle sprain or distal tibia/fibula fractures, require significant recovery time. Return to throwing programs
    may be beneficial for those who have undergone surgical or nonsurgical treatment of osteochondritis dissecans (OCD) of the elbow. A close working relationship
    with a physical therapist who specializes in sports medicine and has experience with young athletes can be
    very helpful for returning these athletes to sports as
    soon as possible.

    Anatomic Considerations in the Young Athlete


    The physis is composed of cartilage, which is less durable than bone; therefore, it is considered a weak link
    in the pediatric skeleton. These regions are more prone
    to injury in traumatic or overuse environments. The
    physeal cartilage is more viscoelastic than bone, adding
    unique biomechanical features to the pediatric skeleton.
    In many types of pediatric injuries, the physeal cartilage
    will fail before the surrounding ligaments or osseous
    tissues, especially under conditions of high-energy
    transfer. As the child becomes older, the physis becomes
    stiffer and may make the incidence of ligament injury
    more likely than a physeal injury. The weakest area of
    the physis is believed to be the zone of hypertrophy, although fractures can occur in other regions. Growth
    plate fractures are complicated by the susceptibility to
    growth disturbance after injury. In addition to acute
    traumatic injuries of the physis, overuse injuries of the
    physeal areas also can occur. This includes overloading
    conditions of the proximal humerus, olecranon, and
    medial epicondyle in throwers and distal radius physis
    in gymnasts.

    6: Pediatrics

    Acute Injuries

    Patellar Dislocation
    Acute patellar dislocation is one of the most common
    causes of acute hemarthrosis in young athletes. When
    comparing patellar dislocation in male and female patients, some studies have suggested similar rates,6 and
    others have demonstrated the highest rates of dislocation in females younger than 18 years.7
    Patellar dislocations occur in otherwise normal individuals, although soft-tissue laxity may be a significant
    risk factor. Other risk factors for patella dislocation,
    784

    Orthopaedic Knowledge Update 10

    both chronic and acute, include increased genu valgum,


    patella alta, lower extremity version abnormalities such
    as femoral anteversion and external tibial torsion,
    trochlear dysplasia, increased quadriceps angle, foot
    pronation, and patellar tilt.6 Recent studies of trochlear
    dysplasia have attempted to define the relationship between trochlear morphology and patellar dislocation.
    Some of these studies have suggested that trochlear dysplasia may have a genetic basis,8 and other studies have
    suggested that the risk of dislocation may be higher in
    some families.7
    Both the medial retinaculum and medial patellofemoral ligament (MPFL) are primary restraints to patellar
    dislocation. Injury to both of these structures can occur
    during dislocation. The MPFL originates from the adductor tubercle and attaches to the upper two thirds of
    the medial patellar border.9 The MPFL is a primary
    soft-tissue structure preventing lateral dislocations of
    the patella. Osteochondral fractures and contusion occur during patellar dislocation, and these contusions
    are seen in up to 40% to 50% of patients. These injuries most commonly occur on the medial facet of the
    patella and the distal lateral trochlea of the lateral femoral condyle (Figure 1).
    Many patients with patellar dislocation will not
    have another dislocation, but some groups of athletes
    appear to have a higher probability of repeat dislocation or subluxation symptoms. In a well-designed prospective cohort study, 189 patients were followed for
    2 to 5 years.7 The group with the highest risk of dislocations was females age 10 to 17 years; 61% of dislocations occurred during sports, and 9% during dancing. The risk of recurrent patellar instability/dislocation
    appeared to be significantly higher in females. Young
    age at the time of the first dislocation was also a significant risk factor for future dislocation/subluxation
    events. Soft-tissue laxity, which may be more common
    in female patients, may increase the risk of primary and
    recurrent patello-femoral subluxation or dislocation
    events.7 Genu recurvatum, hyperextension of the elbows, and soft-tissue laxity of the wrist, thumbs, and
    fingers are findings associated with increased laxity,
    which suggest a higher risk of secondary dislocation.
    Standard three- or four-view knee series that include
    AP, lateral, Merchant, and notch views allow for the
    evaluation of injuries, including osteochondral fragments, avulsion of the soft-tissue attachments and bone
    from the medial aspect of the patella, as well as other
    factors such as patella alta, patella tilt, or trochlea dysplasia.8 MRI may also play a role in the evaluation of
    these injuries because it may provide significant information about soft-tissue injuries, which are more difficult or impossible to identify with plain radiographs.
    The initial treatment option for dislocations may
    consist of brief periods of immobilization followed by
    early rehabilitation with range of motion and strengthening activities.8 The indications for surgical treatment
    continue to evolve. A recent prospective, randomized
    study of surgical treatment (repair of the medial retinacular structures) for first-time dislocation of the patella in children/adolescents did not demonstrate better

    2011 American Academy of Orthopaedic Surgeons

    Chapter 61: Injuries and Conditions of the Pediatric and Adolescent Athlete

    Figure 1

    MRI findings demonstrating increased signal intensity on T2-weighted images of the lateral femoral condyle consistent with contusion after patella dislocation. (Copyright Intermountain Orthopaedics, Boise, ID.)

    outcomes compared with nonsurgical management.10


    For patients with recurrent symptomatic instability episodes, surgical intervention may be beneficial. The
    main indications for surgery in young athletes have
    been outlined in the literature, and it is believed that
    these surgical indications are appropriate for most patients.6 The relative indications for surgery include failure to improve with nonsurgical care, concurrent osteochondral injury, continued gross instability, palpable
    disruption of the MPFL and the vastus medialis
    obliquus, and high-level athletic demands coupled with
    mechanical risk factors. The optimal surgical regimen
    for recurrent patellar dislocation is still evolving; however, soft-tissue procedures that do not involve surgery
    at the level of the physis are preferred in younger patients to reduce the risk of physeal growth complications.

    Meniscal Injuries in Children

    2011 American Academy of Orthopaedic Surgeons

    Tibial Eminence Fractures


    Tibial eminence fractures, also known as tibial spine
    fractures or avulsions, occur predominantly in skeletally immature patients. The mechanism of injury may
    be similar to that seen in adult ACL injury. These injuries have been classified into three types: type I, minimal displacement of the tibial eminence; type II, displacement of the anterior third to one half of the tibial
    eminence, producing a beaklike deformity on the lateral radiograph; and type III, the avulsed tibial eminence is completely lifted from the underlying bone14
    (Figure 2). A rare fourth type of tibial eminence fracture is characterized by complete rotation of the fragment, such that the articular cartilage surface faces the
    donor-site bone. Entrapment of the intermeniscal ligament or anterior meniscus tissue is possible, which may
    be an impediment to reduction of these fractures15 (Figure 3). These fractures may also be associated with
    other soft- tissue injury, including bone contusions, ligament injury, and meniscus tears.16 Treatment options
    include cast immobilization for nondisplaced fractures,
    closed reduction for minimally displaced fractures, and
    surgical treatment of displaced fractures. Both open
    and arthroscopic techniques have been described for
    these injuries. Arthroscopic techniques using sutures,
    wires, and screws have been studied.17-19 Because arthrofibrosis is a significant complication that has been
    associated with the treatment of more severe forms of
    tibial eminence fractures, secure fixation and early motion are recommended for patients treated with surgery.

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Injuries to the meniscus are less common in children


    than adults. In younger patients, they are more likely to
    occur in the setting of ACL or other significant knee injuries. Interpretation of MRI meniscal signals can be
    challenging in children. The MRI signal may suggest a
    meniscus tear in a young patient, but no tear will be
    found at arthroscopy. It has been shown that the meniscal signals on MRI in younger patients can appear to be
    meniscal tears, and these signal variations in young patients are frequently seen during the normal development of the meniscus.11 MRI meniscal signals that do
    not clearly show a tear that communicates with the surface of the meniscus, or that do not show a displaced
    flap, should be interpreted with caution. Because of
    concerns about meniscectomy and the development of
    osteoarthritis, many physicians have advocated that
    meniscal repair be attempted in young patients. Menis-

    cus repairs in young patients may have better potential


    for healing. Some studies show high healing rates in
    young patients,12 whereas others show lower healing
    rates.13

    785

    Section 6: Pediatrics

    Figure 3

    Figure 2

    Lateral radiograph of a type III tibial spine fracture. (Copyright Intermountain Orthopaedics,
    Boise, ID.)

    ACL Injury

    6: Pediatrics

    Treatment of ACL injury in the skeletally immature


    athlete remains controversial, although clinical studies
    continue to provide more guidance about the treatment
    options and avoidance of complications. Recent studies
    suggest that the incidence of this injury may be increasing, and young female athletes start sustaining these injuries in significant numbers at approximately age 12
    to 13 years. These patients may also have a higher risk
    of ACL injury when compared with age-matched male
    athletes. Nonsurgical treatment produces poor outcomes in patients with complete tears because of instability and the potential for additional injury, including
    meniscal tears and chondral damage.20,21
    Surgical treatment carries the risk of physeal injury,
    leading to growth disturbance in some cases.22 A comprehensive understanding of the physeal anatomy
    about the knee, as well as the impact of fixation and
    drilling, should be considered before attempting ACL
    reconstruction in patients with an open physis.23 Techniques have been described to reduce the risks of physeal injury from ACL reconstruction. A physeal sparing
    technique using an autogenous iliotibial band graft has
    been described for patients with significant remaining
    growth. This procedure has demonstrated excellent results, without growth plate arrest.24 For older patients,
    different techniques have been described, although the
    risk of physeal arrest may still be a concern in those
    with significant growth remaining. A recent study of
    786

    Orthopaedic Knowledge Update 10

    Arthroscopic imaging of entrapped anterior horn


    of the medial meniscus after a displaced tibial
    spine fracture. (Copyright Intermountain Orthopaedics, Boise, ID.)

    patients at Tanner stage 3 or 4, who underwent ACL


    reconstruction using a transphyseal technique demonstrated no physeal complications, with excellent clinical
    outcomes.25 In these patients, several technical aspects
    were of importance: metaphyseal fixation was used
    without injury to the physis; autogenous hamstrings
    were used, rather than patellar bone-tendon-bone
    grafts; and Tanner/skeletal maturity staging was used as
    an important part of the decision process to match the
    appropriate surgical procedure for each patient.
    Another technique for the skeletally immature patient is transepiphyseal ACL reconstruction, which
    avoids the femoral and tibial physis. Although this is a
    technically demanding procedure with a small margin
    of error, results in a small population were excellent
    and physeal growth disturbance was absent26 (Figure
    4).
    The risk of physeal complications is still present, and
    a survey demonstrated significant physeal complications in some surgically treated patients with open physes.22 The risks, benefits, and alternatives to surgery
    should be thoroughly discussed with patients and their
    families.

    Quadriceps Contusion
    These injuries are relatively common in young athletes,
    especially in those involved in contact and collision
    sports. Most of these injuries respond well to rest and
    activity modifications, followed by a progressive return
    to sports activities. Physical therapy, including stretching, early motion, and lower impact exercise initially,
    may be of benefit to these patients. In some cases, a
    thigh contusion may lead to heterotopic ossification or
    myositis ossificans. In rare instances, a thigh compartment syndrome can occur.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 61: Injuries and Conditions of the Pediatric and Adolescent Athlete

    Figure 4

    A and B, CT scans of a skeletally immature knee after ACL reconstruction using the transepiphyseal reconstruction
    technique. The black arrow denotes the tibia tunnel and the yellow arrow indicates the femoral tunnel. (Copyright
    Intermountain Orthopaedics, Boise, ID.)

    Figure 5

    A and B, Radiographs of posterior elbow dislocation with medial epicondyle avulsion. Postreduction radiographs
    demonstrate a displaced fragment (arrow). (Copyright Intermountain Orthopaedics, Boise, ID.)

    Ankle Sprains

    2011 American Academy of Orthopaedic Surgeons

    and secondary sprains in athletes involved in higherrisk sports.27

    Medial Epicondyle Avulsion


    Fractures of the medial epicondyle are more common
    than dislocations and account for about 10% of elbow
    fractures in children. The ulnar collateral ligament may
    avulse the medial epicondyle during elbow trauma (Figure 5). Nearly 50% of medial epicondyle fractures are
    associated with dislocation of the elbow; the displaced
    fragment can become incarcerated in the joint, preventing a concentric reduction.
    Acute medial epicondyle fractures and dislocations
    of the elbow can occur in young gymnasts28 and isolated medial epicondyle fractures are occasionally seen
    in adolescent pitchers. Treatment of medial epicondyle

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Ankle sprains remain one of the most common injuries


    in skeletally immature athletes. In patients presenting
    with an ankle sprain, the clinician should strongly consider the possibility of a physeal injury of the distal fibula or tibia. The physis in these patients may be more
    likely to be injured than the ligaments. If examination
    demonstrates localized pain over the physis, treatment
    with several weeks of immobilization may be warranted. The indications for therapy after these injuries
    are not fully defined. Further study will be necessary to
    determine which injuries in skeletally immature patients derive benefit from formal physical therapy. A recent evidence-based medicine review from the Cochrane group demonstrated that the use of ankle braces
    may be effective in reducing the risk of both primary

    787

    Section 6: Pediatrics

    Figure 7

    Figure 6

    Intraoperative fluoroscopic view of the arm of a


    14-year-old girl involved in gymnastics who had
    a displaced medial epicondyle fracture. Because
    of the high demands placed on her arm, open
    reduction and internal fixation was recommended and performed. (Copyright Intermountain Orthopaedics, Boise, ID.)

    fractures is controversial, especially for minimally displaced fractures. Nondisplaced fractures are typically
    treated with casting, but displaced fractures may require surgery. In athletes such as throwers, gymnasts,
    and wrestlers who place high physical demands on the
    elbow, anatomic reduction of medial epicondyle fractures may be important for future athletic performance
    (Figure 6).

    Shoulder Dislocations

    6: Pediatrics

    Traumatic shoulder dislocations primarily occur in


    collision/contact sports in young athletes. It has been
    estimated that 40% of shoulder dislocations occur in
    patients younger than 22 years. Athletes with a history
    of a pediatric dislocation had more than a 90% chance
    of recurrent dislocation.29-31 Pediatric dislocations are
    believed to stretch the capsule more than adult dislocations and diminish the capsules ability to provide the
    support needed for proper function. Surgical treatment
    of instability is generally successful in young patients.32
    Physical examination and diagnostic testing may
    demonstrate the concomitant injuries of anterior bony
    labrum or labral lesions (Bankart injury, superior labral
    anterior and posterior tear, Hill-Sachs lesions [posterolateral humeral head compression fracture]) rotator
    cuff muscle tears, and subscapularis or lesser tubercle
    avulsions. Three-view radiograph series that include
    AP, lateral, and axillary views can detect bone injuries
    of the labrum or Hill-Sachs lesions of the proximal hu788

    Orthopaedic Knowledge Update 10

    AP pelvis radiograph in a 16-year-old male athlete demonstrates avulsion fractures in the pelvis anterior inferior iliac spine region. (Copyright Intermountain Orthopaedics, Boise, ID.)

    merus. MRI arthrograms provide detailed information


    about the capsule and labral tissues.
    In the acute setting, dislocated shoulders should be
    treated with closed reduction. Initial treatment may
    consist of a supervised physical therapy program to recover strength and range of motion. Several recent
    studies have suggested an advantage to immobilization
    in external rotation in adult patients, because this may
    provide better alignment of the labrum injury during
    healing.33,34 Other studies have suggested that immobilization in this position does not improve the outcome
    for shoulder dislocations.35 Treatment of first-time dislocation in high-risk athletes remains controversial,33
    and there is some evidence that early surgery may play
    a role in reducing the risk of secondary dislocation.
    Families should be counseled about the high risk of recurrent instability episodes and associated symptoms. If
    nonsurgical treatment is unsuccessful, surgery (open or
    arthroscopic) will be required to treat the capsular and
    glenoid injuries to create a stable glenohumeral joint.
    Historically, open methods may have provided lower
    redislocation rates, but recent studies in adult patients
    suggest excellent outcomes with arthroscopic stabilization procedures.36 With improving surgical experience
    and technology, some recent literature suggests that arthroscopic surgery can have at least equal outcomes.36

    Apophyseal Avulsions of the Pelvis


    Among the acute injuries of the pelvic region, apophyseal avulsions are the most common and are usually
    caused by sudden muscle contractions. These injuries
    can occur at the ischial tuberosity (hamstring), anterior
    superior iliac spine (tensor fascia lata), lesser trochanter
    (iliopsoas), pubis (adductors), anterior inferior iliac
    spine (rectus femoris), and iliac crest (gluteus medius)
    (Figure 7). The athlete may report a sudden pop, followed immediately by weakness and pain. These symptoms may mimic acute muscle strain. Walking with a

    2011 American Academy of Orthopaedic Surgeons

    Chapter 61: Injuries and Conditions of the Pediatric and Adolescent Athlete

    Figure 8

    AP radiograph of both shoulders in an adolescent baseball pitcher demonstrates right proximal humeral
    epiphyseolysis. (Copyright Intermountain Orthopaedics, Boise, ID.)

    limp indicates a more severe injury. Radiographic evaluation confirms the diagnosis; however, this injury can
    be difficult to detect because of the small size and location of the bony fragment. Initial treatment consists of
    rest, ice, and therapy emphasizing range of motion and
    gentle strengthening. Surgical intervention is infrequently required because most injuries involve minimal
    displacement of the avulsed fragment.37 However, recent literature suggests that surgery may be necessary
    to ensure the best outcomes for some of these injuries,
    especially for large, displaced fragments.38

    Overuse Injuries

    Little Leaguers Shoulder

    2011 American Academy of Orthopaedic Surgeons

    Elbow Conditions in the Throwing Athlete


    Throwers elbow is a generic term used to describe a
    variety of overuse syndromes. The common etiology of
    these injuries is repetitive microtrauma of the immature
    elbow.39 Pain at the medial side of the elbow may occur
    in conjunction with medial epicondyle apophysitis or
    an avulsion fracture. Radiographs will usually demonstrate physeal widening in an apophysis, but may also
    demonstrate fragmentation of the ossification center. It
    may appear to have a growth disturbance represented
    by a delayed ossification, or conversely, an accelerated
    growth marked by premature physeal closure. In older
    adolescents, there may be an injury to the ulnar collateral ligament; the incidence of this injury may be increasing.40 Differentiating between ulnar collateral ligament tear versus medial epicondyle apophysitis,
    fragmentation, or avulsion is important (Figure 9).

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Patients with little leaguers shoulder usually present


    with vague reports of shoulder and proximal arm pain
    that is usually aggravated by throwing and improved
    with rest. The condition is common in pitchers, especially those who are throwing on a regular basis or who
    participate in extended-season baseball programs. The
    examination findings may be very subtle and in many
    cases unremarkable. Radiographs may show subtle
    widening of the physis or changes in the metaphyseal
    bone (Figure 8). This syndrome represents an overuse
    condition of the proximal humeral physis. Treatment
    consists of rest until symptoms resolve, followed by a
    graded return to a throwing program. Treatment is individualized; however, primary areas for improvement
    include stretches for the posterior shoulder capsule, as
    well as rotator cuff strengthening, capsular stabilizing,
    and core strengthening exercises. These exercises as
    well as lower extremity flexibility training, hip
    strengthening, and proprioceptive balance training may
    also provide these young athletes with the added benefit of improved performance.
    These patients may benefit from working with a therapist experienced with treating throwing athletes. Pitching coaches may also evaluate the throwing mechanics
    of these young athletes. Counseling for the family and

    coaches about this condition, and its relationship to excessive throwing is important. Information about appropriate pitch counts is available from the Little League
    Baseball and the American Orthopaedic Society for
    Sports Medicine Websites (http//:www.sportsmed.org/
    tabs/resources/youthbaseballdetails.aspx?DID=231).
    Shoulder injuries in the adolescent athlete are often
    caused by subtle, atraumatic instability, especially in
    sports with overhead movements, such as swimming,
    volleyball, gymnastics, tennis, and baseball. These conditions are more common in female athletes. Repeated
    overhead motions can stress the joint capsule and allow
    excessive motion of the humeral head, and these symptoms may be more likely in those with evidence of increased soft-tissue laxity. A comprehensive shoulder
    therapy program is essential. Many patients will improve significantly, but 6 to 9 months of therapy may
    be necessary. Only in very rare instances is surgical
    treatment required for patients with persistent multidirectional instability. This surgery is reserved for patients with persistent instability with activities of daily
    living despite a prolonged period of intensive nonsurgical treatment.

    789

    Section 6: Pediatrics

    Wrist and Hand Injuries


    Wrist pain in gymnasts is believed to be caused by the
    repetitive tension and compressive loads, well beyond
    those seen in most other sports.43 The wrist pain can be
    vague and poorly localized. These loads may lead to increased or decreased growth of the physis. Radiographic findings include physeal widening, changes in
    metaphyseal bone density, and distortion of the epiphysis.44 Premature physeal closure of the distal radius
    has been reported.
    Treatment includes activity modification. Many
    gymnasts can continue to compete, but may need to decrease training in the routines that aggravate symptoms. Ice and the use of protective wrist braces may
    also play a role in recovery from these overuse injuries.
    In more severe cases, surgery may be necessary to address symptoms, and continued competition at a high
    level may be difficult.
    Other stress injuries can occur about the wrist in
    young athletes, including repetitive stress and acute injuries of the scaphoid and the triangular fibrocartilage
    complex.45,46

    Anterior Knee Pain

    Figure 9

    Radiograph of the arm of an adolescent pitcher


    showing a medial epicondyle partial avulsion.
    (Copyright Intermountain Orthopaedics,
    Boise, ID.)

    6: Pediatrics

    The lateral aspect of the elbow is subject to repetitive compression loading, which can lead to OCD of
    the capitellum, or more rarely, in the radial head. In
    some cases, MRI may be necessary to make the diagnosis if no radiolucencies or osteochondral fragments are
    noted on plain radiographs.
    Posterior elbow pain may represent an injury to the
    olecranon apophysis, an avulsion fracture, or delay of
    apophyseal closure.41 Comparison of contralateral radiographs and possibly a bone scan might be required
    to confirm the diagnosis. With valgus extension overload, the compression stress on the posteromedial olecranon can create osteophytes, which may lead to bony
    extension contracture. It is important to realize that the
    osteophytes are a secondary process or a by-product of
    the pathology and not the primary pathologic process.
    Loose bodies inside the joint may also require surgical
    removal and evaluation of the chondral pathology that
    leads to this condition.42 For most young athletes, nonsurgical treatment is the appropriate first step. In athletes involved in high-demand sports and who do not
    respond to therapy, surgical reconstruction may be indicated.
    Prevention of injury is important; pitchers, coaches,
    and families should be aware of the recommendations
    about limitations involving the number and types of
    pitches thrown.
    790

    Orthopaedic Knowledge Update 10

    Anterior knee pain is common in adolescents but can


    be challenging to evaluate and treat. Symptoms are
    usually aggravated by activities, and patients may report pain with sports, ascending or descending stairs,
    kneeling, or placing the knee in a bent position for an
    extended period of time. In most cases, the symptoms
    will be present bilaterally, although one side may be
    less symptomatic than the other. Patients will localize
    pain to the anterior aspect of the patella.
    The physical examination should evaluate gait, rotation alignment, patellar tracking, foot alignment, and
    hip motion. It is important that symmetric hip motion
    is documented, because a loss of internal rotation may
    signify hip pathology presenting with referred knee
    pain (slipped capital femoral epiphysis). The knee
    should be evaluated for warmth and effusion, the presence of symptomatic plica, atrophy, patellar tracking/
    alignment, and patellar mobility. These patients will localize discomfort to the inferior pole of the patella, the
    patellar tendon, and perhaps the medial and/or lateral
    patellar retinacular tissues. Focal tenderness over the
    femoral condyle or joint line may suggest osteochondritis, plica, or meniscal pathology. If pain is localized to
    other areas (such as the hip), plain radiographs or MRI
    may be necessary to rule out other causes of anterior
    knee pain. If muscle atrophy, skin abnormalities, or allodynia are present, a diagnosis of reflex sympathetic
    dystrophy should be considered. In most cases, the radiographic evaluation will be normal.
    In many patients, the natural history of this condition will demonstrate significant improvement over
    time, and many will have resolution of symptoms. Referral to a physical therapist with expertise in this area
    may be beneficial to these patients.47 The role of patellofemoral rehabilitation has been studied in terms of
    expanding the activities that can be performed in a

    2011 American Academy of Orthopaedic Surgeons

    Chapter 61: Injuries and Conditions of the Pediatric and Adolescent Athlete

    pain-free manner, normalizing the envelope of function of the patellofemoral joint.48 Although adult patients have been the focus of studies, the rehabilitation
    principles also apply to pediatric and adolescent patients. Therapeutic modalities include activity modifications; flexibility and stretching exercises of the thigh
    and leg; progressive strengthening programs that do
    not irritate the patellofemoral joint; intermittent use of
    ice, massage, and heat; ultrasound; and patellar mobilization exercises.

    Osteochondritis Dissecans of the Knee

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    OCD is an acquired idiopathic lesion of the subchondral bone that affects the overlying cartilage secondarily. Although this condition is potentially reversible,
    progression may result in articular cartilage instability.
    In the knee, the most common location is within the
    lateral aspect of the medial femoral condyle. Juvenile
    OCD lesions are defined in patients with widely open
    growth plates and have a better prognosis in terms of
    healing than in older adolescents with OCD.
    Males are more commonly affected than females,
    with a ratio between 2:1 and 3:1. As females and
    younger children participate in sports in greater numbers there has been an increased prevalence among girls
    and a younger mean age of onset for this condition. In
    the largest study to date, the prevalence was 18 in
    100,000 in females and 29 in 100,000 in males.49
    Although repetitive trauma, inflammation, accessory
    centers of ossification, ischemia, and genetic factors
    have all been implicated as causative factors in OCD,
    no body of evidence exists that is sufficient to currently
    support any single theory. Although some familial tendencies exist, it is commonly believed that the most
    prevalent form of OCD is not a familial condition. It
    has been theorized that acute trauma was the causative
    factor and that the tibial spine violently impacted the
    inner condyle of the femur.50 This theory does not account for the multitude of OCD lesions noted at other
    sites. Chronic repetitive microtrauma has been suggested to lead to a stress reaction within the subchondral bone, and in more advanced forms it may lead to
    subchondral bone necrosis. Fragment dissection and
    separation may ensue. Contributing factors to these repetitive stresses in young athletes may include yearround sports, early sports specialization, multiple
    sports in a single season, or multiple teams in a single
    sport, as well as increased training intensity.
    Patients with OCD of the knee initially have nonspecific symptoms, with anterior knee pain and variable
    amounts of intermittent swelling. With progression of
    the disease, patients may report more persistent swelling or effusion, catching, locking, and/or giving way.
    Unfortunately, pain and swelling are not good indicators of dissection. Physical findings may include a positive Wilson test, which reproduces the pain by internally rotating the tibia during extension of the knee
    between 90 and 30, then relieving the pain with tibial
    external rotation. The sensitivity of this test has been
    questioned.

    Standard weight-bearing radiographs of both knees


    are helpful for initially characterizing the lesion type
    and status of the growth plate. The lateral view helps
    identify anteroposterior lesion location and normal, benign accessory ossification centers in the skeletally immature knee. An axial view is helpful if a lesion of the
    patella or trochlea is suspected, and a notch view in 30
    to 50 of knee flexion may help identify the lesions of
    the posterior femoral condyle.
    MRI findings may define the ability of OCD lesions
    to heal following nonsurgical treatment. One study described MRI criteria and noted that a high signal line
    on T2-weighted images behind the fragment was most
    predictive and was found in 72% of unstable lesions.51
    Authors of another study attempted to predict the success of nonsurgical treatment using MRI and clinical
    criteria52 and found the high signal line the most common sign in patients in whom nonsurgical treatment
    failed. In a comparison of MRI and arthroscopic findings, staging accuracy improved from 45% to 85%
    when the authors interpreted a high signal line on T2weighted images as a predictor of instability when accompanied by a breach in articular cartilage seen on
    T1-weighted images.53 Additional research to determine
    if MRI can identify stability and healing potential of
    OCD lesions will be necessary. Recent research suggests
    that the presence of multiple factors associated with instability, including a high T2 signal intensity rim, surrounding cysts, high T2 signal intensity cartilage fracture line, and a fluid-filled osteochondral defect, can
    collectively improve the sensitivity and specificity of
    predicting lesion stability.54
    Nonsurgical treatment is often regarded as the treatment of choice for small, stable lesions in skeletally immature patients. Nonsurgical management focuses on
    significant activity modification by limiting high-impact
    activities. Short-term immobilization and protected
    weight bearing may be helpful. Alternatively, bracing
    and range-of-motion knee exercises may be beneficial.
    Typically, a period of 3 to 9 months of nonsurgical
    treatment is initiated, with success rates from 50% to
    94%. Skeletally immature patients with wide, open
    physes and no signs of instability on MRI are more
    likely to respond to nonsurgical measures. The prognosis for OCD lesions is worse in patients who have
    reached skeletal maturity.
    Authors of a 2008 study evaluated 42 skeletally immature patients and 47 knees with stable lesions and
    used a multivariable logistic regression model to determine potential predictors of healing status from the independent variables. After 6 months of nonsurgical
    treatment, 16 of 47 stable lesions (34%) did not progress to healing. It was found that the size of the lesion
    determined by MRI was the strongest prognostic variable.55
    Surgical treatment should be considered for patients
    with unstable or detached lesions, for patients with persistently symptomatic lesions despite nonsurgical measures, and in those with persistent lesions who are approaching skeletal maturity. The goals of surgical
    treatment are to promote healing of subchondral bone,
    791

    Section 6: Pediatrics

    Figure 10

    A, Bone scan showing stress fracture in the superior femoral neck region. B, Screw fixation for a superior femoral
    neck stress fracture. (Copyright Intermountain Orthopaedics, Boise, ID.)

    to maintain joint congruity, to fix rigidly unstable fragments, and to replace osteochondral defects with cells
    that can replace and grow cartilage.56 Surgical treatment of stable lesions with intact articular cartilage involves drilling the subchondral bone with the intention
    of stimulating vascular ingrowth and subchondral bone
    healing. In one study, 11 knees in 10 children treated
    with arthroscopic drilling were reviewed. In 1 year
    there was evidence of healing in 9 of 11 knees.57 In another study of 23 patients (30 knees) who failed to heal
    with 6 months of nonsurgical treatment and who also
    subsequently underwent arthroscopic transarticular
    drilling, radiographic healing was achieved at an average of 4.4 months after drilling.58
    When the lesion is unstable and hinged, fixation is
    indicated to fix the osseous portion of the fragment to
    allow healing and stabilization of the overlying articular surface. Arthroscopic or open reduction and internal fixation can be performed with a variety of implants. Osteochondral plugs have recently been
    presented as a biologic alternative to the use of implant
    fixation of the lesion.59 In a series of 20 patients treated
    for unstable OCD lesions of the knee using osteochondral plugs, 19 were reported to meet the criteria of normal and 1 patient met the criteria of nearly normal at 2
    years after surgery.59

    Stress Fractures

    6: Pediatrics

    Stress fractures are more common in adolescents and


    older high school-age athletes; however, they can also
    occur in the preadolescent athlete.60 These injuries are
    more common in sports that require a significant volume of running for practice and competition. Stress
    fractures in both male and female athletes may be associated with osteopenia or osteoporosis, especially in endurance athletes. Athletes with recurrent stress fractures and with a history of amenorrhea, menstrual
    irregularities, or eating disorders may need formal evaluation for management of underlying metabolic bone
    disorders. Repetitive loads that exceed the threshold of
    intrinsic bone healing are believed to lead to the development of stress fractures.
    792

    Orthopaedic Knowledge Update 10

    Pain from stress fractures occurs insidiously, may


    worsen with activity, and improve with rest. The clinical examination, radiographs, and other imaging modalities (bone scan and MRI) are used to make the
    diagnosis. Treatment in most cases is activity modification; training errors are believed to be the main cause
    of these injuries in many patients. In addition to reducing their running mileage, athletes may incorporate
    more cross-training into their training program. This
    may include weight training, exercise bike training,
    swimming, or a pool-based running program. These
    types of training modifications will allow the athletes
    to maintain some of their aerobic conditioning, while
    allowing for healing of the stress fracture.
    The tibia is the most common location for lower extremity stress fractures; other locations include the lumbar spine, pelvis, femoral neck or shaft, patella, tibia,
    medial malleolus, talus, tarsals, metatarsals, and sesamoids. In the upper extremity, stress fracture can be
    found in the distal radius, clavicle, and olecranon, especially in those who participate in throwing and upper
    extremity weight-bearing sports such as baseball and
    gymnastics.41 Stress injury or fracture can occur in the
    diaphysis, metaphysis, physis, and epiphysis in the long
    bones of skeletally immature patients.
    Femoral neck stress fractures have been rare in
    younger patients, although this entity has been seen in
    the skeletally immature patient.61 Patients present with
    groin or anterior thigh pain, although specific areas of
    tenderness may not be identified on physical examination. Plain radiographs may not identify the lesion, and
    bone scans or MRIs may be necessary (Figure 10, A).
    Femoral neck stress fractures should be treated with
    great caution because of the possibility of a displaced
    femoral neck fracture that can lead to osteonecrosis.
    The risk of fracture progression and displacement is
    higher for tension-side than compression-side fractures.62 It is, therefore, prudent to have a lower threshold for prophylactic fixation to prevent progression
    and/or displacement of the fracture in tension-side fractures (Figure 10, B). Other high-risk stress fractures include patella, medial malleolus, talus, navicular, fifth
    metatarsal, and great toe sesamoids fractures.63

    2011 American Academy of Orthopaedic Surgeons

    Chapter 61: Injuries and Conditions of the Pediatric and Adolescent Athlete

    Shin splints, or medial tibial stress syndrome, is characterized by pain along the posteromedial border of the
    tibia. This condition is common in young, running athletes. Treatment of this condition is challenging because
    definitive treatment is still not defined.64 In patients
    with more significant symptoms, radiographic and/or
    MRI evaluation may be necessary to rule out a tibial
    stress fracture.65

    Injuries in youth soccer: A subject review. American


    Academy of Pediatrics. Committee on Sports Medicine
    and Fitness. Pediatrics 2000;105(3, pt 1):659-661.

    3.

    Shea KG, Pfeiffer R, Wang JH, Curtin M, Apel PJ: Anterior cruciate ligament injury in pediatric and adolescent soccer players: An analysis of insurance data. J Pediatr Orthop 2004;24(6):623-628.

    4.

    Faigenbaum AD, Micheli LJ: Preseason conditioning for


    the preadolescent athlete. Pediatr Ann 2000;29(3):156161.

    5.

    Hewett TE, Myer GD, Ford KR: Reducing knee and anterior cruciate ligament injuries among female athletes:
    A systematic review of neuromuscular training interventions. J Knee Surg 2005;18(1):82-88.

    6.

    Hinton RY, Sharma KM: Acute and recurrent patellar


    instability in the young athlete. Orthop Clin North Am
    2003;34(3):385-396.

    7.

    Fithian DC, Paxton EW, Stone ML, et al: Epidemiology


    and natural history of acute patellar dislocation. Am J
    Sports Med 2004;32(5):1114-1121.

    8.

    Fucentese SF, von Roll A, Koch PP, Epari DR, Fuchs B,


    Schottle PB: The patella morphology in trochlear dysplasia: A comparative MRI study. Knee 2006;13(2):
    145-150.

    9.

    Desio SM, Burks RT, Bachus KN: Soft tissue restraints


    to lateral patellar translation in the human knee. Am J
    Sports Med 1998;26(1):59-65.

    10.

    Palmu S, Kallio PE, Donell ST, Helenius I, Nietosvaara Y: Acute patellar dislocation in children and adolescents: A randomized clinical trial. J Bone Joint Surg
    Am 2008;90(3):463-470.
    This randomized prospective study evaluated the outcomes of surgical and nonsurgical treatment of traumatic patellar dislocation in patients younger than 16
    years. Family history of patellar dislocation was identified as a significant factor for recurrence of dislocation,
    and surgery did not affect the long-term functional outcome.

    11.

    Takeda Y, Ikata T, Yoshida S, Takai H, Kashiwaguchi S: MRI high-signal intensity in the menisci of
    asymptomatic children. J Bone Joint Surg Br 1998;
    80(3):463-467.

    12.

    Noyes FR, Barber-Westin SD: Arthroscopic repair of


    meniscal tears extending into the avascular zone in patients younger than twenty years of age. Am J Sports
    Med 2002;30(4):589-600.

    13.

    Accadbled F, Cassard X, Sales de Gauzy J, Cahuzac JP:


    Meniscal tears in children and adolescents: Results of
    operative treatment. J Pediatr Orthop B 2007;16(1):
    56-60.
    This retrospective case series of 12 patients demonstrated relatively poor healing rates for surgically repaired

    Physeal Stress Reactions/Avulsions


    Because the physis is composed of cartilage, it may be
    prone to overuse injury or even small acute fracture/
    avulsion in some cases. Sever disease, Osgood-Schlatter
    disease, Sinding-Larsen-Johansson syndrome, and pelvic apophysites are examples of physeal stress injury in
    different regions.
    Sever disease is characterized by pain in the area of
    the calcaneal apophysis. It is common in athletes who
    participate in running and jumping sports, and it occurs frequently before or during peak growth in both
    males and females. The diagnosis can be based on a
    tight Achilles tendon and a positive squeeze test as well
    as pain over the calcaneal apophysis. Treatment includes activity modification, Achilles tendon stretching,
    and the application of ice before and after activities. In
    rare cases, calcaneal cysts may present with findings
    similar to those of Sever disease, and radiographs may
    be helpful in some cases to rule out this diagnosis. In
    young athletes, treatment usually consists of activity
    modification, stretching, use of heel cups, and other local measures. In most cases, the symptoms resolve
    within 1 to 2 years.
    Osgood-Schlatter disease is associated with anterior
    knee pain with involvement of the proximal tibial
    apophyseal region. Sinding-Larsen-Johansson syndrome is a chronic apophysitis or minor avulsion injury
    from the inferior pole of the patella. Although nonsurgical management is indicated in most patients, older
    patients with significant symptoms and proximal tubercle anomalies may benefit from surgery.66
    Pelvic apophyses can occur at the ischial tuberosity
    and the iliac crest. In most cases, the symptoms will resolve with time and activity modifications. In rare
    cases, surgical treatment to produce a fusion of the
    apophyses may be necessary.67
    Treatment of these different disorders includes activity modification and reduction in training that overloads these regions. Local measures, including ice application and strapping/sleeves to decrease tension on the
    apophysis, may also provide some benefit.

    Annotated References
    1.

    Bijur PE, Trumble A, Harel Y, Overpeck MD, Jones D,


    Scheidt PC: Sports and recreation injuries in US children
    and adolescents. Arch Pediatr Adolesc Med 1995;
    149(9):1009-1016.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    2.

    793

    Section 6: Pediatrics

    dren: A 3-dimensional study using magnetic resonance


    imaging. Arthroscopy 2009;245(12):1415-1422.
    The authors determined the volume of injury to the
    physis during ACL reconstruction in children and concluded that a better understanding of the relationship of
    the ACL and physis may help guide drill-hole placement
    and lead to a lower risk of physeal arrest.

    meniscus tears in children at an average follow-up of


    3 years. Although this was a small series, the healing rate
    for meniscus repair in children was lower than previous
    studies have suggested.
    14.

    Meyers MH, McKeever FM: Fracture of the intercondylar eminence of the tibia. J Bone Joint Surg Am 1970;
    52(8):1677-1684.

    15.

    Kocher MS, Micheli LJ, Gerbino P, Hresko MT: Tibial


    eminence fractures in children: Prevalence of meniscal
    entrapment. Am J Sports Med 2003;31(3):404-407.

    16.

    Monto RR, Cameron-Donaldson ML, Close MA, Ho


    CP, Hawkins RJ: Magnetic resonance imaging in the
    evaluation of tibial eminence fractures in adults. J Knee
    Surg 2006;19(3):187-190.

    17.

    Ahn JH, Lee YS, Lee DH, Ha HC: Arthroscopic physeal


    sparing all inside repair of the tibial avulsion fracture in
    the anterior cruciate ligament: Technical note. Arch Orthop Trauma Surg 2008;128(11):1309-1312.
    This paper describes an arthroscopy suture technique
    for fixing tibial spine or eminence fractures. It may be
    useful for smaller or comminuted injuries.

    18.

    19.

    20.

    6: Pediatrics

    21.

    794

    Bonin N, Jeunet L, Obert L, Dejour D: Adult tibial eminence fracture fixation: Arthroscopic procedure using
    K-wire folded fixation. Knee Surg Sports Traumatol Arthrosc 2007;15(7):857-862.
    The retrospective case series reports the outcomes of arthroscopic Bankart repair in a group of pediatric and
    adolescent patients with traumatic anterior shoulder instability.
    Eggers AK, Becker C, Weimann A, et al: Biomechanical
    evaluation of different fixation methods for tibial eminence fractures. Am J Sports Med 2007;35(3):404-410.
    The authors reported that suture fixation of tibial eminence fractures provided more fixation strength than
    screw fixation based on biomechanical data.
    Graf BK, Lange RH, Fujisaki CK, Landry GL, Saluja
    RK: Anterior cruciate ligament tears in skeletally immature patients: Meniscal pathology at presentation and
    after attempted conservative treatment. Arthroscopy
    1992;8(2):229-233.
    McCarroll JR, Shelbourne KD, Porter DA, Rettig AC,
    Murray S: Patellar tendon graft reconstruction for midsubstance anterior cruciate ligament rupture in junior
    high school athletes: An algorithm for management. Am
    J Sports Med 1994;22(4):478-484.

    22.

    Kocher MS, Saxon HS, Hovis WD, Hawkins RJ: Management and complications of anterior cruciate ligament
    injuries in skeletally immature patients: Survey of the
    Herodicus Society and The ACL Study Group. J Pediatr
    Orthop 2002;22(4):452-457.

    23.

    Shea KG, Belzer J, Apel PJ, Nilsson K, Grimm NL,


    Pfeiffer RP: Volumetric injury of the physis during single
    bundle anterior cruciate ligament reconstruction in chil-

    Orthopaedic Knowledge Update 10

    24.

    Kocher MS, Garg S, Micheli LJ: Physeal sparing reconstruction of the anterior cruciate ligament in skeletally
    immature prepubescent children and adolescents.
    J Bone Joint Surg Am 2005;87(11):2371-2379.

    25.

    Kocher MS, Smith JT, Zoric BJ, Lee B, Micheli LJ:


    Transphyseal anterior cruciate ligament reconstruction
    in skeletally immature pubescent adolescents. J Bone
    Joint Surg Am 2007;89(12):2632-2639.
    This retrospective study reports a series of skeletally immature pubescent adolescents who underwent transphyseal reconstruction of the ACL with use of an autogenous quadrupled hamstrings-tendon graft with
    metaphyseal fixation. This group demonstrated excellent functional outcome with a low revision rate and a
    minimal risk of growth disturbance.

    26.

    Anderson AF: Transepiphyseal replacement of the anterior cruciate ligament using quadruple hamstring grafts
    in skeletally immature patients. J Bone Joint Surg Am
    2004;86(pt 2, suppl 1):201-209.

    27.

    Handoll HH, Rowe BH, Quinn KM, de Bie R: Intervensions for preventing ankle ligament injuries. Cochrane
    Database Syst Rev 2001;3:CD0000018.

    28.

    Caine DJ, Nassar L: Gymnastics injuries. Med Sport Sci


    2005;48:18-58.

    29.

    Bishop JY, Flatow EL: Pediatric shoulder trauma. Clin


    Orthop Relat Res 2005;432:41-48.

    30.

    Deitch J, Mehlman CT, Foad SL, Obbehat A, Mallory


    M: Traumatic anterior shoulder dislocation in adolescents. Am J Sports Med 2003;31(5):758-763.

    31.

    Rowe CR: Prognosis in dislocations of the shoulder.


    J Bone Joint Surg Am 1956;38(5):957-977.

    32.

    Chen FS, Diaz VA, Loebenberg M, Rosen JE: Shoulder


    and elbow injuries in the skeletally immature athlete.
    J Am Acad Orthop Surg 2005;13:172-185.

    33.

    Bedi A, Ryu RK: The treatment of primary anterior


    shoulder dislocations. Instr Course Lect 2009;58:293304.
    The authors present a systematic review of the literature
    on the treatment of traumatic anterior instability of the
    shoulder. The evidence comparing the outcomes of nonsurgical and surgical treatment based on open and arthroscopic surgery is provided.

    34.

    Itoi E, Sashi R, Minagawa H, Shimizu T, Wakabayashi


    I, Sato K: Position of immobilization after dislocation of
    the glenohumeral joint: A study with use of magnetic

    2011 American Academy of Orthopaedic Surgeons

    Chapter 61: Injuries and Conditions of the Pediatric and Adolescent Athlete

    This article presents a comprehensive summary of hand


    trauma in children.

    resonance imaging. J Bone Joint Surg Am 2001;83(5):


    661-667.
    35.

    36.

    Finestone A, Milgrom C, Radeva-Petrova DR, et al:


    Bracing in external rotation for traumatic anterior dislocation of the shoulder. J Bone Joint Surg Br 2009;91(7):
    918-921.
    This randomized prospective study compared bracing in
    internal and external rotation for the treatment of primary anterior shoulder dislocation. The differences in
    dislocation rates were statistically significant, suggesting
    that external rotation bracing may not be as effective as
    previously reported.
    Brophy RH, Marx RG: The treatment of traumatic anterior instability of the shoulder: Nonoperative and surgical treatment. Arthroscopy 2009;25(3):298-304.
    This case series reviewed the outcomes of patients with
    unstable OCD lesions treated with mosaicplasty. At
    short term follow-up, the clinical results and MRI evaluation showed evidence of significant healing.

    37.

    Micheli LJ: Pediatric and Adolescent Sports Medicine.


    Boston, MA, Little, Brown, 1984, p 218.

    38.

    Rajasekhar C, Kumar KS, Bhamra MS: Avulsion fractures of the anterior inferior iliac spine: The case for surgical intervention. Int Orthop 2001;24(6):364-365.

    39.

    Klingele KE, Kocher MS: Little league elbow: Valgus


    overload injury in the paediatric athlete. Sports Med
    2002;32(15):1005-1015.
    Petty DH, Andrews JR, Fleisig GS, Cain EL: Ulnar collateral ligament reconstruction in high school baseball
    players: Clinical results and injury risk factors. Am J
    Sports Med 2004;32(5):1158-1164.

    41.

    Rettig AC, Wurth TR, Mieling P: Nonunion of olecranon stress fractures in adolescent baseball pitchers: A
    case series of 5 athletes. Am J Sports Med 2006;34(4):
    653-656.

    42.

    Cain EL Jr, Dugas JR, Wolf RS, Andrews JR: Elbow injuries in throwing athletes: A current concepts review.
    Am J Sports Med 2003;31(4):621-635.

    43.

    DiFiori JP, Caine DJ, Malina RM: Wrist pain, distal radial physeal injury, and ulnar variance in the young
    gymnast. Am J Sports Med 2006;34(5):840-849.

    44.

    Mandelbaum BR, Bartolozzi AR, Davis CA, Teurlings


    L, Bragonier B: Wrist pain syndrome in the gymnast:
    Pathogenetic, diagnostic, and therapeutic considerations. Am J Sports Med 1989;17(3):305-317.

    45.

    Bae DS, Waters PM: Pediatric distal radius fractures and


    triangular fibrocartilage complex injuries. Hand Clin
    2006;22(1):43-53.

    46.

    Waters PM: Operative carpal and hand injuries in children. J Bone Joint Surg Am 2007;89(9):2064-2074.

    2011 American Academy of Orthopaedic Surgeons

    Bhave A, Baker E: Prescribing quality patellofemoral rehabilitation before advocating operative care. Orthop
    Clin North Am 2008;39(3):275-285, v.
    This is an evidence-based review of the literature for the
    treatment of medial tibial stress syndrome, a common
    problem in young athletes. This study confirms that
    there is insignificant evidence to recommend any specific
    treatment of this condition.

    48.

    Dye SF, Stubli HU, Biedert RM, Vaupel GL: The mosaic of pathophysiology causing patellofemoral pain:
    Therapeutic implications. Op Tech Sports 1999;7(2):
    46-54.
    This study compares the fixation strength of screws and
    sutures for the repair of tibial spine/tibial eminence fractures.

    49.

    Lindn B, Telhag H: Osteochondritis dissecans: A histologic and autoradiographic study in man. Acta Orthop
    Scand 1977;48(6):682-686.

    50.

    Fairbanks H: Osteochondritis dissecans. J Bone Joint


    Surg Br 1933;21:67-82.

    51.

    De Smet AA, Ilahi OA, Graf BK: Untreated osteochondritis dissecans of the femoral condyles: Prediction of
    patient outcome using radiographic and MR findings.
    Skeletal Radiol 1997;26(8):463-467.

    52.

    Pill SG, Ganley TJ, Milam RA, Lou JE, Meyer JS, Flynn
    JM: Role of magnetic resonance imaging and clinical
    criteria in predicting successful nonoperative treatment
    of osteochondritis dissecans in children. J Pediatr Orthop 2003;23(1):102-108.

    53.

    OConnor MA, Palaniappan M, Khan N, Bruce CE: Osteochondritis dissecans of the knee in children. A comparison of MRI and arthroscopic findings. J Bone Joint
    Surg Br 2002;84(2):258-262.

    54. Kijowski R, Blankenbaker DJ, Shinki K, Fine JP, Graf


    BK, De Smet AA: Juvenile versus adult osteochondritis
    dissecans of the knee: Appropriate MR imaging criteria
    for instability. Radiology 2008;248(2):571-578.
    In a retrospective study, the authors compared the sensitivity and specificity of MRI criteria in the detection of
    instability in patients with OCD of the knee. Results indicated that MRI criteria for OCD instability have high
    specificity for adult but not juvenile lesions of the knee.
    55.

    Wall EJ, Vourazeris J, Myer GD, et al: The healing potential of stable juvenile osteochondritis dissecans knee
    lesions. J Bone Joint Surg Am 2008;90(12):2655-2664.
    This study identified factors that predicted healing potential in stable OCD lesions. Smaller size lesions and those
    without mechanical symptoms at presentation are more
    likely to heal with nonsurgical treatment protocols.

    56.

    Smillie IS: Treatment of osteochondritis dissecans.


    J Bone Joint Surg Br 1957;39(2):248-260.

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    40.

    47.

    795

    Section 6: Pediatrics

    57.

    Bradley J, Dandy DJ: Results of drilling osteochondritis


    dissecans before skeletal maturity. J Bone Joint Surg Br
    1989;71(4):642-644.

    63.

    Boden BP, Osbahr DC: High-risk stress fractures: Evaluation and treatment. J Am Acad Orthop Surg 2000;
    8(6):344-353.

    58.

    Kocher MS, Micheli LJ, Yaniv M, Zurakowski D, Ames


    A, Adrignolo AA: Functional and radiographic outcome
    of juvenile osteochondritis dissecans of the knee treated
    with transarticular arthroscopic drilling. Am J Sports
    Med 2001;29(5):562-566.

    64.

    Craig DI: Medial tibial stress syndrome: Evidence-based


    prevention. J Athl Train 2008;43(3):316-318.

    59.

    Miniaci A, Tytherleigh-Strong G: Fixation of unstable


    osteochondritis dissecans lesions of the knee using arthroscopic autogenous osteochondral grafting (mosaicplasty). Arthroscopy 2007;23(8):845-851.
    This case series reviewed the outcomes of patients with
    unstable OCD lesions treated with mosaicplasty. At
    short-term follow-up, the clinical results and MRI evaluation showed evidence of significant healing.

    60.

    Maezawa K, Nozawa M, Sugimoto M, Sano M, Shitoto


    K, Kurosawa H: Stress fractures of the femoral neck in
    child with open capital femoral epiphysis. J Pediatr
    Orthop B 2004;13(6):407-411.

    61.

    Maezawa K, Nozawa M, Sugimoto M, Sano M, Shitoto


    K, Kurosawa H: Stress fractures of the femoral neck in
    child with open capital femoral epiphysis. J Pediatr Orthop B 2004;13(6):407-411.

    65.

    Aoki Y, Yasuda K, Tohyama H, Ito H, Minami A: Magnetic resonance imaging in stress fractures and shin
    splints. Clin Orthop Relat Res 2004;421:260-267.

    66.

    Weiss JM, Jordan SS, Andersen JS, Lee BM, Kocher M:


    Surgical treatment of unresolved Osgood-Schlatter disease: Ossicle resection with tibial tubercleplasty. J Pediatr Orthop 2007;27(7):844-847.
    The authors evaluated the functional outcome of ossicle
    excision and tibial tubercleplasty for unresolved
    Osgood-Schlatter disease.

    67.

    Holmstrom MC, Greis PE, Horwitz DS: Chronic ischial


    apophysitis in a gymnast treated with transapophyseal
    drilling to effect apophysiodesis: A case report. Am J
    Sports Med 2003;31(2):294-296.

    Lehman RA Jr, Shah SA: Tension-sided femoral neck


    stress fracture in a skeletally immature patient: A case
    report. J Bone Joint Surg Am 2004;86(6):1292-1295.

    6: Pediatrics

    62.

    This is an evidence-based review of the literature for the


    treatment of medial tibial stress syndrome, a common
    condition in young athletes. This study confirms that
    there is insignificant evidence to recommend any specific
    treatment for this condition.

    796

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 62

    Skeletal Dysplasias,
    Connective Tissue Diseases,
    and Other Genetic Disorders
    Jose A. Morcuende, MD, PhD

    Benjamin A. Alman, MD

    Introduction
    Musculoskeletal syndromes can be broadly categorized
    into groups by the function of the causative gene encoding a protein that is structural, regulates developmentally important signaling pathways, is implicated in
    neoplasia, has a role in processing molecules (such as
    an enzyme), or has a role in nerve or muscle function.
    The syndromes within each broad group have a similar
    mode of inheritance and similar clinical behavior.

    Disorders Caused by Structural Genes


    A variety of proteins play an important role in the
    structure of connective tissues, including the bones, articular cartilage, ligaments, and skin. A mutation in
    such a gene disrupts the structural integrity of the connective tissue in which it is expressed. The phenotype
    evolves with time as the abnormal structural components slowly fail or wear out during the individuals
    growth. The deformity often recurs after surgery because the structural components are abnormal and will
    wear out again. If the structural abnormality involves
    cartilage, a growth abnormality may be caused by
    physeal mechanical failure, or an early degenerative
    disease of the joints may be caused by articular cartilage failure. If the affected protein is important for lig-

    2011 American Academy of Orthopaedic Surgeons

    Marfan Syndrome
    Marfan syndrome is associated with long limbs and involvement of the cardiovascular, ocular, and skeletal systems.1 In a patient with Marfan syndrome, scoliosis is
    sometimes diagnosed first. It is important for the orthopaedist to recognize the underlying condition, as a referral for appropriate prophylactic management of the cardiovascular abnormities can be life saving.
    Marfan syndrome is caused by a mutation in the
    gene encoding for the fibrillin protein, which has a role
    in maintaining the normal mechanical properties of the
    soft tissues, especially in resistance to cyclic stress.2 The
    clinical findings of laxity and subluxation of the joints,
    as well as the weakening of arterial walls with resultant
    aortic dilatation, are easily understood based on the
    function of fibrillin. The tall stature and arachnodactyly associated with the syndrome are more difficult to
    attribute to the fibrillin mutation; the explanation is
    that the extracellular matrix contains growth factors
    that are bound to extracellular matrix proteins. Fibrillin mutations cause some of these extracellular growth
    factors, such as transforming growth factor, to become more readily accessible to cell receptors.3 The increased availability of growth factors probably increases cellular growth and rapid longitudinal bone
    growth, leading to the development of tall stature as
    well as long, thin fingers and toes. The increased availability of growth factors also may be partly responsible
    for many of the changes in the mechanical properties of
    the soft tissues (Figure 1). It is possible that growth factor activity modulation could be used to treat some of
    the sequelae of Marfan syndrome, and studies of such
    an approach are under way.3
    Hyperlaxity is responsible for many clinical aspects
    of Marfan syndrome, including subluxation of joints, a

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Neither Dr. Morcuende nor any immediate family member has received anything of value from or owns stock
    in a commercial company or institution related directly
    or indirectly to the subject of this chapter. He or an immediate family member serves as a board member,
    owner, officer, or committee member of the Pediatric
    Orthopaedic Society of North America, American Academy of Orthopaedic Surgeons, and US Bone and Joint
    Decade. Dr. Alman or an immediate family member
    serves as a board member, owner, officer, or committee
    member of the Pediatric Orthopaedic Society of North
    America and Shriners Research Advisory Board.

    ament or tendon strength, joint subluxation often occurs; Marfan syndrome and osteogenesis imperfecta
    are two of the most common such disorders. Other disorders are caused by mutations in a gene that encodes
    structural proteins, such as spondyloepiphyseal dysplasia.

    797

    Section 6: Pediatrics

    Osteogenesis Imperfecta

    Figure 1

    MRI of the lumbar spine of a patient with Marfan


    syndrome. Dural ectasia and scalloping of the
    posterior vertebral bodies can be seen.

    6: Pediatrics

    predisposition to sprains, and scoliosis. Mild scoliosis


    can be managed in a manner similar to that of idiopathic scoliosis, although bracing appears to be less effective in a patient with Marfan syndrome.4 Surgery is
    considered for a rapidly progressing curve in a skeletally immature patient or a large curve in a skeletally
    mature patient. The complication rate in scoliosis surgery is higher for patients with Marfan syndrome than
    for those with idiopathic scoliosis. Infection, instrumentation failure, pseudarthrosis, or coronal and sagittal curve decompensation occurs in 10% to 20% of patients.5 Overcorrection can cause cardiovascular
    complications; reducing the amount of correction in a
    patient treated with a growing rod was found to reverse cardiac failure in a case report.6 Other unusual
    spine deformities can occur, such as subluxation of vertebrae. Traction should be used with caution, as it can
    worsen the subluxation, especially if the patient has underlying kyphosis.7 Infection often is associated with a
    dural tear. Perioperative death from valvular insufficiency has been reported.
    Marfan syndrome is associated with mild osteopenia. Patients do not seem to be especially susceptible to
    fracture, however, and it is not clear whether intervention is warranted.8,9 Protrusio acetabula is present in a
    third of patients with Marfan syndrome, but it is not
    related to bone mineral density and usually is asymptomatic.10 Prophylactic fusion of the triradiate cartilage
    can be used for protrusio acetabula but is not warranted for most patients.
    798

    Orthopaedic Knowledge Update 10

    Osteogenesis imperfecta (OI), often called brittle bone


    disease, is a spectrum of disorders characterized by abnormal bone fragility. The incidence is 1 in 20,000 children. OI occurs from mutations in the genes that code
    for type I collagen (COL1A1 and COL1A2). Type I
    collagen has a complex structure in which a triple helix
    is composed of three tightly packed procollagen chains;
    abnormality in one of these chains affects the structural
    properties of the molecule. Two different types of collagen abnormalities can cause OI. One type is a quantitative defect in collagen production, usually as the result of a premature stop codon that leads to abnormal
    messenger RNA and, therefore, to less protein production. The second type is the production of abnormal
    types of collagen, usually as the result of the substitution of glycine by another amino acid, leading to abnormal structural properties in the collagen molecule.
    Histologic examination of bone affected by OI reveals
    a decreased number of trabeculae and decreased cortical thickness, with an increased number of osteoblasts
    and osteoclasts. Although fractures in patients with OI
    occur frequently during childhood, they heal at the normal rate. The phenotype of OI is quite variable. Some
    individuals are only mildly affected, with no skeletal
    deformity. Others have short stature, extensive bone
    fragility, and multiple fractures. The most severe form
    of OI is fatal during the perinatal period.
    The Sillence classification is most commonly used
    clinical classification of OI and has been modified to
    include biochemical and genetic information.11,12 Type I
    is a mild disorder characterized by normal or lownormal height and blue sclerae; multiple bone fractures
    occur during childhood but are less common after puberty. Fifty percent of patients have deafness. Type II is
    the lethal perinatal form of OI, in which the child has
    short, crumpled femurs and ribs as well as hypoplastic
    lungs. Central nervous system malformations and hemorrhage are common. Type III is the most severe of the
    survivable types of OI. The patient has a large skull and
    a characteristic underdeveloped triangular appearance
    of the facial bones; pale blue sclerae, which become
    normal at puberty; and multiple long bone and vertebral fractures, which lead to kyphosis and severe scoliosis. Many patients with type III OI use a wheelchair
    for mobility. Muscle weakness and ligament hyperlaxity may be present. Type IV is a moderate form of OI
    characterized by short stature. Many patients with type
    IV OI have bowing bones and vertebra fractures but
    are less severely affected than in type III (Figure 2). The
    sclera typically is white. Most patients with type IV OI
    are ambulatory. Type V OI has a characteristic hypertrophic callus after fracture, with ossification of the interosseous membrane between the tibia and fibula and
    the radius and ulna.13 Type VI is moderate and similar
    to type IV, but there are abnormalities of mineralization
    rather than collagen.14 In type VII OI, the patient has
    rhizomelia and coxa vara.15

    2011 American Academy of Orthopaedic Surgeons

    Chapter 62: Skeletal Dysplasias, Connective Tissue Diseases, and Other Genetic Disorders

    Table 1

    The Cardinal Clinical Findings for


    the Diagnosis of Neurofibromatosis
    Six or more caf-au-lait spots (larger than 5 mm in diameter
    in a child or 15 mm in an adult)
    Two neurofibromas or a single plexiform neurofibroma
    Freckling in the axilla or inguinal region
    An optic glioma
    Two or more Lisch nodules (hamartoma of the iris)
    A distinctive osseous lesion such as vertebral scalloping or
    cortical thinning
    A first-degree relative with neurofibromatosis type 1

    Figure 2

    AP radiograph of the tibia of a patient with


    osteogenesis imperfecta, showing stabilization
    of the tibia with solid nonexpansile rods. The
    thin, gracile diaphysis and enlarged epiphyses
    with popcorn calcifications in the marrow space
    can be seen.

    Disorders Caused by Tumor-Related Genes


    and Overgrowth Syndromes
    A variety of cellular proteins and signaling pathways
    are important in regulating cell reproduction or proliferation. A mutation that results in the dysregulation of
    such a pathway can cause overgrowth of a cell type or
    organ. These pathways are commonly dysregulated in a
    neoplasia.

    Neurofibromatosis

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Neurofibromatosis (NF) is the most common singlegene disorder in humans. NF has several forms. Orthopaedic manifestations are common in type 1 (NF1).
    The typical findings are not present at birth. The diagnosis is made as the child grows, based on at least two
    of the seven cardinal clinical findings (Table 1).
    NF is caused by a mutation in the NF1 gene. Its protein product, neurofibromin, acts as a tumor suppressor, stimulating the conversion of Ras-GTP to RasGDP, activating the RAt Sarcoma (Ras) signaling
    system, which is involved in the control of cell growth.
    Tumors in affected individuals have only the mutated
    gene because of loss of the normal copy. The gene defect provides a clue to potential therapies; pharmaco-

    logic agents that block Ras signaling could be used to


    treat the disorder. Farnesyl transferase inhibitors block
    the downstream effects of Ras signaling activation and,
    thus, have potential use in the treatment of some neoplastic manifestations of NF1. Statin inhibitors such as
    lovastatin, which regulates Ras signaling by interfering
    with its membrane binding, also could be used.16,17
    Clinical studies of these agents are ongoing.
    The orthopaedic manifestations of NF include scoliosis, overgrowth of the limbs, and pseudarthrosis. A
    scoliotic curve is categorized as idiopathic or dystrophic. A dystrophic curve is a short, sharp, single curve
    that is kyphotic and typically involves four to six segments. The onset of a dystrophic curve is early in childhood, and it is relentlessly progressive. A curve that initially appears in a child younger than 7 years has a
    nearly 70% likelihood of becoming dystrophic. The
    most important risk factors for progression are early
    age of onset; a high Cobb angle; and an apical vertebra
    that is severely rotated, scalloped (with concave loss of
    bone), and located in the middle to lower thoracic area
    (Figure 3). Dystrophic curves are refractory to brace
    treatment. Sagittal plane deformities may occur, including an angular kyphosis and a scoliosis that has so
    much rotation that curve progression is more obvious
    on a lateral radiograph than on an AP radiograph. The
    risk of paraplegia is high in patients with an angular
    kyphosis.
    Pseudarthrosis of a long bone typically is associated
    with NF. The pseudarthrosis usually affects the tibia,
    with a characteristic anterolateral bow that is obvious
    in infancy. There is a hamartoma of undifferentiated
    mesenchymal cells at the pseudarthrosis site, which in
    some patients is associated with loss of the normal allele of the NF1 gene.18,19 A study using a mouse model
    suggested that lovastatin could be used as a treatment,
    but clinical studies of this approach are needed.16 Direct installation of bone morphogenetic protein into the
    pseudarthrosis site during reconstruction could help in
    achieving union. Variable results have been reported,
    however, and it is not known whether the use of bone
    799

    Section 6: Pediatrics

    Figure 4

    Figure 3

    PA radiograph of the spine of a patient with neurofibromatosis showing a thoracic scoliosis with
    dysplastic ribs and a short, sharply angulated
    curve. MRI is required to rule out paraspinal
    plexiform neurofibroma or another intraspinal
    lesion.

    6: Pediatrics

    morphogenetic protein in patients with an inherited


    premalignant condition could have long-term harmful
    consequences.20
    The reported incidence of malignancy in patients
    with NF ranges from less than 1% to more than 20%.5
    There is a risk of malignant degeneration of a neurofibroma into a neurofibrosarcoma. Distinguishing a malignant lesion from a benign lesion can be difficult, and
    the use of positron emission tomography holds promise
    for identifying malignancy. Children with neurofibroma have a propensity to develop other malignancies, such as Wilms tumor or rhabdomyosarcoma.

    Beckwith-Wiedemann Syndrome
    Beckwith-Wiedemann syndrome is linked to the insulinlike growth factor gene. Paternal genomic imprinting
    plays a role in the inheritance. The childs initial symptom often is hemihypertrophy. Beckwith-Wiedemann
    syndrome is characterized by organomegaly, omphalocele, and a large tongue that regresses in size as the child
    ages. Pancreatic islet cell hyperplasia causes hypoglycemia, and neonatal hypoglycemic episodes can cause
    symptoms resembling those of cerebral palsy. There is a
    800

    Orthopaedic Knowledge Update 10

    MRI of the hips and thigh of a patient with Proteus syndrome. Note the enlarged left leg, with
    infiltration of fat into the pelvis and fascial
    planes.

    10% risk of a benign or malignant tumor; the most


    common is Wilms tumor. Screening for Wilms tumor
    with abdominal ultrasonography and -fetoprotein levels should be done at regular intervals until the child
    reaches age 6 to 8 years. Some other types of tumors,
    such as alveolar rhabdomyosarcoma, may be present at
    birth.21

    Russell-Silver Syndrome
    Patients with Russell-Silver syndrome have low birth
    weight and a triangular face shape, with an average
    head circumference. Hemihypertrophy is present in
    80% of affected individuals.5 The patients growth
    curve may not follow the normal predictive charts, and
    managing leg-length equality can be difficult. Growth
    hormone has been administered in an attempt to increase stature. Although growth hormone does increase
    growth velocity, whether ultimate height is increased
    has not yet been determined. A case report of Wilms tumor in a patient with Russell-Silver syndrome led to a
    recommendation that patients with Wilms tumor be
    screened, like other patients with hemihypertrophy.22

    Proteus Syndrome
    Proteus syndrome is characterized by hemihypertrophy,
    macrodactyly, and partial giantism of the hands, feet,
    or both (Figure 4). The characteristic appearance of the
    plantar surface of the feet often is described as resembling the surface of the brain. The symptoms worsen
    over time, and new symptoms appear. Unlike other

    2011 American Academy of Orthopaedic Surgeons

    Chapter 62: Skeletal Dysplasias, Connective Tissue Diseases, and Other Genetic Disorders

    overgrowth syndromes, Proteus syndrome is not associated with an increased incidence of malignancy. The
    skeletal deformities include focal and regional gigantism, scoliosis, and kyphosis. The patient has relatively
    large vertebral bodies (megaspondylodysplasia). Angular malformations of the lower extremities, especially
    genu valgum, are common. Recurrence after surgical
    intervention is very common. Although osteotomies
    can correct angular malformations, the decision to undertake surgical correction must take into account the
    possibility of a rapid recurrence of the deformity.
    Guided growth is a promising approach to managing
    limb angular deformity, but data on its results are lacking.23 Nerve compression can be managed using decompression, but spinal cord compression is difficult or impossible to successfully treat surgically because of the
    vertebral overgrowth. Scoliosis apparently is caused by
    overgrowth of one side of the spine.

    Disorders Caused by Developmentally


    Important Signaling Pathways
    Cell signaling systems are activated in a coordinated
    manner during embryonic development to cause cells to
    proliferate, move, and undergo programmed cell death,
    so that the organism will develop into adulthood in a
    normal pattern. The normal patterning is altered by
    mutations in the genes that encode proteins having a
    role in these pathways. Environmental events such as
    exposure to a teratogen also can dysregulate these
    pathways, resulting in a phenotype similar to that of a
    gene mutation. A musculoskeletal malformation can result if such an event occurs in a pathway important for
    skeletal development. Surgery to correct such a malalignment usually is successful.

    Achondroplasia and Related Disorders

    2011 American Academy of Orthopaedic Surgeons

    Lateral radiograph of the spine of a 5-year-old


    boy with achondroplasia showing thoracolumbar kyphosis with symptoms consistent with spinal stenosis.

    of the elbows and subluxation of the radial heads are


    present. The nonorthopaedic manifestations include
    difficulty with weight control, sleep apnea, recurrent
    otitis media, and hydrocephalus. The patient has normal intelligence, and life expectancy is not significantly
    diminished.
    The manifestations of hypochondroplasia are similar
    to those of achondroplasia but are less severe. The gene
    mutation is in a different location than in achondroplasia and, thus, there is more variability in the phenotype.
    The clinical features may not be apparent at birth, and
    mild features may remain undiagnosed until puberty.
    The features of hypochondroplasia include short stature, small hands, lumbar stenosis, and genu varum.28
    Thanatophoric dysplasia is severe and almost always
    is fatal before the patient reaches age 2 years. It is characterized by severe rhizomelic shortening, platyspondyly, a protuberant abdomen, and a small thoracic cavity that is responsible for cardiorespiratory failure.

    6: Pediatrics

    A mutation in the fibroblast growth factor receptor-3


    (FGFR-3) gene can cause skeletal dysplasias of varying
    severity, including achondroplasia, hypochondroplasia,
    and thanatophoric dysplasia. Achondroplasia is the
    most common skeletal dysplasia. This disorder can be
    inherited as an autosomal dominant trait, although it
    results from a sporadic mutation in at least 80% of patients. The risk increases with paternal age. The mutation results in uncontrolled activation of the FGFR-3
    receptor that leads to an impaired growth in the proliferative zone of the physis.24-27 Achondroplasia is clinically characterized by rhizomelic shortening with normal trunk length (the proximal bones are most
    affected), frontal bossing, and trident hands. Spine deformities include foramen magnum and upper cervical
    stenosis, which results in spinal cord compression as
    early as the first 2 years of life. Thoracolumbar junction kyphosis and lumbar spinal stenosis also are common (Figure 5). The lower extremity malalignment typically involves genu varum with associated tibial
    torsion. Ligamentous laxity at the knee and ankles is
    common. In the upper extremities, flexion contractures

    Figure 5

    Camptomelic Dysplasia
    The term camptomelic refers to a bowing of the long
    bones, primarily the tibia and femur. Camptomelic dysplasia appears to be caused by an abnormality in the
    formation of the cartilage anlagen during fetal development. The endochondral ossification is normal, but the
    diaphyseal cylinderization is markedly abnormal. Clin-

    Orthopaedic Knowledge Update 10

    801

    Section 6: Pediatrics

    ically, camptomelic dysplasia is a severe form of shortlimbed dwarfism that sometimes is fatal. The defective
    tracheal cartilage and lower respiratory tract may cause
    respiratory failure during the neonatal period. Bowing
    of the long bones and early, progressive spine deformity
    (kyphosis and scoliosis) are common. The spine deformity further compromises pulmonary function.29 Hydromyelia and diastematomyelia have been reported,
    and neurologic complications and pseudarthrosis are
    common after spine treatment.30 The other clinical features of camptomelic dysplasia include a flattened
    head, a cleft palate, micrognathia, defects of the heart
    and kidneys, and sex reversal (a female has an XY
    karyotype).

    Cleidocranial Dysplasia
    Cleidocranial dysplasia is characterized by abnormality
    of the bones formed by intramembranous ossification
    (primarily the clavicles, cranium, and pelvis). This disorder is inherited as an autosomal dominant trait. The
    gene mutation is in runt-related transcription factor 2
    (RUNX2), an osteoblast-specific transcription factor
    that regulates osteoblast differentiation.31 Clinically, the
    characteristic finding is hypoplasia or absence of the
    clavicles. If the disorder is bilateral, the child can touch
    the shoulders together in front of the chest. Mild short
    stature, a high palate, and abnormal permanent teeth
    development also are present. Widening of the symphysis pubis, coxa vara (which may require treatment), and
    a short femoral neck are common, with lumbar spondylolysis occurring in 24% of patients.32

    Nail-Patella Syndrome

    6: Pediatrics

    The gene mutation in nail-patella syndrome is in the


    LIM homeobox transcription factor 1 (LMX1B),
    which is involved in patterning of the dorsoventral axis
    of the limbs and early morphogenesis of the glomerular
    basement membrane. The disorder is inherited as an
    autosomal dominant trait, but there is marked intrafamilial and interfamilial variation in its clinical features.33 The characteristic features are dystrophy of the
    nails, an absent or hypoplastic patella, and iliac horns.
    Femoral condyle dysplasia and genu valgum are common. Cubitus valgus (hypoplasia of the lateral side of
    the humerus) of varying severity may occur, with radial
    head posterior subluxation or dislocation.34,35 Abnormal pigmentation of the iris occurs in 50% of patients,
    with glaucoma and nephropathy leading to renal failure in the third or fourth decade of life.

    Cornelia de Lange Syndrome


    Heterozygous mutations in the nipped-B homolog
    (NIPBL) gene have been documented in 47% of unrelated individuals with Cornelia de Lange syndrome.
    The familial inheritance is autosomal dominant.
    NIPBL encodes delangin, a protein that is important to
    chromosome function and DNA repair.36 The orthopaedic manifestations vary widely in severity and can include short thumbs, clinodactyly of the fifth finger,
    flexion contractures of the elbow with radial head dis802

    Orthopaedic Knowledge Update 10

    location, and radial hemimelia with ray deficiency. In


    the lower extremities, hip dysplasia, syndactyly of the
    second and third toes, and hallux valgus can occur.37
    Patients have short stature, microcephaly, mental retardation, cleft palate, and distinctive facial features, including bushy eyebrows, a small nose, and full eyelashes. Approximately 30% of patients have a
    congenital heart malformation.

    Disorders Caused by Multiple Genes


    and Chromosome Abnormalities

    Down Syndrome
    Down syndrome (trisomy 21) is the most common and
    most readily recognizable trisomy disorder. Down syndrome is clinically characterized by hypotonia with
    joint hyperlaxity, specifically of the upper cervical spine
    (atlantoaxial and occipitoatlantal instability), relatively
    short stature, a flat face, and mental retardation to a
    varying extent. Orthopaedists and pediatricians often
    are asked to confirm a childs eligibility for participation in the Special Olympics, and, therefore, knowledge
    of the guidelines for athletic participation by patients
    with Down syndrome is important.38-40 In particular,
    tumbling activities should be avoided. The routine use
    of radiographs for surveillance of a child with Down
    syndrome is controversial. Surgical intervention probably should be reserved for children with symptoms because the rate of surgical complications is high. Acetabular dysplasia or hip dislocation is not congenital but
    occurs between age 2 to 10 years; it is found in 5% of
    patients. Slipped capital femoral epiphysis and osteonecrosis also can occur. A patient with Down syndrome
    and slipped capital femoral epiphysis should undergo
    bilateral pinning of both the symptomatic and the contralateral hip (Figure 6). All children with Down syndrome should undergo testing for thyroid dysfunction.
    Short and broad hands, patellofemoral instability, flatfoot and hallux valgus, a congenital heart defect, and
    thyroid dysfunction are common in patients with
    Down syndrome.

    Turner Syndrome
    Turner syndrome is a complete or partial absence of
    one of the X chromosomes. Cell mosaicism, in which
    some cells have the normal two pairs of X chromosomes, is common.41 The effects of the chromosomal
    abnormality probably are caused by imprinting and
    may depend on whether the abnormality is derived
    from the father or the mother. The clinical features of
    Turner syndrome include short stature, a wide and
    webbed neck, low-set ears and hairline, cubitus and
    genu valgum, swollen hands and feet, scoliosis, and a
    chest that is broad, flat, and shield shaped.42 Patients
    typically have gonadal dysfunction, which results in inadequate production of estrogen, leading to absent or
    incomplete development at puberty, infertility, diabetes,
    weight gain, osteoporosis, and a high incidence of fractures. Congenital heart disease and kidney abnormali-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 62: Skeletal Dysplasias, Connective Tissue Diseases, and Other Genetic Disorders

    ties are common, as are cognitive deficits related to


    memory, mathematics, and visuospatial discrimination.
    The life expectancy is normal.

    Noonan Syndrome
    Noonan syndrome is a relatively common congenital
    disorder that affects girls and boys equally. Often it is
    confused with Turner syndrome because the two conditions share several clinical characteristics. Several causative genes have been identified (PTPN11, SOS1, and
    KRAS, NRAS, RAF, BRAF and SHOC2), although asyet-undiscovered genes also may cause this disorder.43
    Noonan syndrome is one of the most common syndromes associated with a congenital heart defect. Other
    clinical features include short stature, cervical spine fusion, low-set ears and hairline, scoliosis, pectus carinatum or excavatum, impaired blood clotting, hypotonia,
    and learning disabilities. Some patients have severe
    joint or muscle pain, often with no identifiable cause.
    Type I Arnold-Chiari malformation is found in some
    patients.44,45

    Prader-Willi Syndrome
    Prader-Willi syndrome is a disorder caused by a deletion of a small part of chromosome 15 of paternal origin. The distinction of chromosome by paternal origin
    results from imprinting, and Prader Willi syndrome
    thus has a sister syndrome, Angelman syndrome, that
    affects maternally imprinted genes in the region.
    Prader-Willi syndrome is characterized by hypotonia,
    hypogonadism, mild mental retardation, short stature
    that responds well to growth hormone therapy, and a
    failure to thrive during the early years that is followed
    by an extreme and insatiable appetite (often leading to
    morbid obesity). The orthopaedic manifestations include scoliosis in as many as 90% of patients, small
    hands and feet, hip dysplasia, and joint hyperlaxity.46-48
    Patients with Prader-Willi syndrome have increased
    morbidity after surgery because of an abnormal physiologic response to hypercapnia and hypoxia, obstructive sleep apnea, thick secretions, obesity, a prolonged
    and exaggerated response to sedatives, and an increased risk of aspiration. Growth hormone therapy
    leads to improvement in weight and behavior.49 The effect of growth hormone therapy on skeletal deformity
    is unclear, but a recent randomized study suggested that
    it does not have a negative effect on the sequelae of
    spine deformity.50

    There are two relatively distinct types of trichorhinophalangeal syndrome (TRPS), with some overlapping
    of clinical features. Both types are caused by mutation
    or loss of the TRPS1 gene. TRPS type II also has a loss
    of the adjacent exostosin (EXT-1) gene, which is responsible for hereditary multiple exostoses and explains the exostoses associated with TRPS type II. Patients with TRPS type I have a bulbous and pearshaped nose, prominent ears, sparse hair, cone
    epiphyses, and short fourth and fifth metacarpals. They

    2011 American Academy of Orthopaedic Surgeons

    AP radiograph of the pelvis in a 13-year-old girl


    with Down syndrome showing pinning of both
    hips after slipped capital femoral epiphysis developed in the left hip. Pinning of the contralateral hip is recommended in children with Down
    syndrome because of the association of thyroid
    disorders and contralateral slipped capital femoral epiphysis.

    have mild mental retardation. Their hips are radiographically and symptomatically similar to hips with
    Legg-Calv-Perthes disease. The key distinguishing feature of TRPS type II is the presence of multiple exostoses, especially in the lower extremities.51,52 Patients
    with TRPS type II also have microcephaly and mental
    retardation. Marked ligamentous laxity and redundant,
    loose skin may be as severe as in Ehlers-Danlos syndrome.

    Disorders Caused by Protein-Processing Genes


    (Enzymes)
    Enzymes modify molecules or other proteins. They often modify substances for degradation, and mutations
    cause cell dysfunction as these substances accumulate.
    Mutations in genes that encode for enzymes can have a
    wide variety of effects on cells, resulting in a broad
    range of abnormalities in cell function and a wide
    range of clinical findings. In many disorders, there is an
    excess accumulation of proteins in cells. The cells become abnormally large, leading to increased pressure in
    the bones, osteonecrosis, and increased extradural material in the spine that can cause paralysis. Medical
    treatments have been developed to replace the defective
    enzyme in many of these disorders. Such treatments often can arrest but not reverse the skeletal manifestations of the disorder. Orthopaedists are treating a
    slowly decreasing number of patients with these disorders because of early diagnosis and appropriate medical
    treatment.

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Trichorhinophalangeal Syndrome

    Figure 6

    803

    Section 6: Pediatrics

    Table 2

    The Mucopolysaccharidoses
    Designation

    Syndrome

    Enzyme Defect

    Stored
    Substance

    Inheritance Pattern

    MPS I

    Hurler
    Scheie

    -l-iduronidase

    HS + DS

    Autosomal recessive

    MPS II

    Hunter

    Iduronidase-2-sulfatase

    HS + DS

    X-linked recessive

    MPS IIIA

    Sanfilippo A

    Heparin-sulfatase (sulfamidase)

    HS

    Autosomal recessive

    MPS IIIB

    Sanfilippo B

    -N-acetylglucosamidase

    HS

    Autosomal recessive

    MPS IIIC

    Sanfilippo C

    Acetyl-CoA: -glucosaminideN-acetyltransferase

    HS

    Autosomal recessive

    MPS IIID

    Sanfilippo D

    Glucosamine-6-sulfatase

    HS

    Autosomal recessive

    MPS IVA

    Morquio A

    N-acetyl galactosamine-6-sulfate sulfatase

    KS, CS

    Autosomal recessive

    MPS IVB

    Morquio B

    -d-galactosidase

    KS

    Autosomal recessive

    MPS IVC

    Morquio C

    Unknown

    KS

    Autosomal recessive

    MPS V

    Formerly called Scheie


    disease

    MPS VI

    Moroteux-Lamy

    Arylsulfatase B, N-acetylgalactosamine-4sulfatase

    DS, CS

    Autosomal recessive

    MPS VII

    Sly

    -d-glucuronidase

    CS, HS, DS

    Autosomal recessive

    Glucosamine-6-sulfatase

    CS, HS

    Autosomal recessive

    MPS VIII

    CS = chondroitin sulfate, DS = dermatan sulfate, HS = heparan sulfate, KS = keratan sulfate, MPS = mucopolysaccharidosis.

    Mucopolysaccharidoses

    6: Pediatrics

    The mucopolysaccharidoses are characterized by excretion of mucopolysaccharide in the urine. There are at
    least 13 types of mucopolysaccharidosis (MPS), all of
    which are autosomal recessive, except for mucopolysaccharidosis type II (Hunter syndrome), which is X
    linked (Table 2). The most common mucopolysaccharidoses are type I (Hurler syndrome) and type IV
    (Morquio syndrome). The mucopolysaccharidoses can
    be diagnosed by urine screening using a toluidine bluespot test.
    Each type of MPS has a deficiency of a specific lysosomal enzyme. The incomplete degradation product accumulates in lysozymes in tissues such as the brain, viscera, and joints. This accumulation is responsible for
    osteonecrosis, which presumably develops because of
    too much material in the intramedullary space, and it
    contributes to symptoms of spinal cord compression
    caused by accumulation of material in the spinal canal.
    Mucopolysaccharidosis Type I
    The Hurler and Scheie forms represent the severe and
    mild ends of the clinical spectrum in MPS type I. Children with the Hurler form have progressive mental retardation, multiple severe skeletal deformities, and organ and soft-tissue deformities. These children die
    before age 10 years. The Scheie form is characterized
    by stiffness of the joints and corneal clouding but not
    by mental retardation. The diagnosis usually is made
    during the teen years, and patients have a normal life
    804

    Orthopaedic Knowledge Update 10

    expectancy. Marrow transplantation is used to treat the


    more severe forms, but its effect on the bones varies.
    Most children develop the typical skeletal phenotypic
    features despite the success of the bone marrow transplant.53 Musculoskeletal deformities that persist after
    marrow transplantation require further treatment.54
    Malalignment of the limbs can occur, and guided
    growth or osteotomies may be necessary to treat genu
    valgum. Approximately one fourth of the patients have
    an abnormality of the upper cervical spine. The accumulation of degradation products in closed anatomic
    spaces, such as the carpal tunnel, causes finger triggering and carpal tunnel syndrome.
    Mucopolysaccharidosis Type IV
    The three types of Morquio syndrome are classified as
    subtypes of MPS IV. All are caused by enzyme defects
    involved in the degradation of keratan sulfate. An affected child has a short trunk and ligamentous laxity.
    There is significant genu valgus, aggravated by the lax
    ligaments. Realignment osteotomies can restore plumb
    alignment, but recurrence is common, and osteotomies
    may not control the instability during ambulation.
    Guided growth is an attractive alternative to osteotomies because it avoids a possible recurrence, but comparative studies are lacking. Early arthritis develops in
    the hips and knee. The hips develop progressive acetabular dysplasia. Radiographs may reveal a small femoral
    ossific nucleus, but MRI or arthrography will show a
    much larger cartilaginous femoral head. Patients may

    2011 American Academy of Orthopaedic Surgeons

    Chapter 62: Skeletal Dysplasias, Connective Tissue Diseases, and Other Genetic Disorders

    require total joint arthroplasty.55 Odontoid hypoplasia


    or aplasia is common, with resulting C1-C2 instability.
    A soft-tissue mass in the spinal canal contributes to
    cord compression. The upper and lower extremities often are flaccid rather than spastic. C1-C2 fusion before
    the onset of symptoms is controversial; some authors
    recommend it, but others prefer to reserve surgical intervention for symptomatic patients.5 No comparative
    studies have evaluated the outcomes of different management approaches. Elsewhere in the spine, the vertebrae show a progressive platyspondia with a thoracic
    kyphosis. A progressive deformity should be surgically
    stabilized. Despite the severity of the disorder, many
    patients with Morquio syndrome live for decades. Cardiorespiratory disease is common, but the upper cervical spine accounts for most of the disabilities.

    Contracture Syndromes
    Contractures are common in a variety of orthopaedic
    conditions, and they are the most prominent phenotypic feature of several disorders. These syndromes
    have a wide variety of etiologies, including mutations
    that cause developmental problems, mutations that
    dysregulate muscle function, and fetal environmental
    causes. Many of these syndromes are associated with
    muscle dysfunction. For example, distal arthrogryposis
    is caused by mutations that disrupt fast-twitch muscle
    fiber activity. There is some overlap in phenotype between these conditions and some of the myopathies.
    Despite their different etiologies, these disorders have
    similar management guidelines.
    Arthrogryposis is a physical finding, not a diagnosis,
    in a large group of disorders characterized by joint contractures present at birth. These disorders can be considered as contracture syndromes and grouped into
    three general categories, each of which can be represented by a prototypic disease.

    Contracture Syndromes Involving


    All Four Extremities

    2011 American Academy of Orthopaedic Surgeons

    Photograph of a newborn boy with arthrogryposis multiplex congenita, showing hyperflexion of


    the hips, extended knees, and the typical extended elbows with wrist deformity.

    level and coping skills than to the magnitude of the


    joint contractures.
    The overall goals of managing arthrogryposis multiplex congenita are lower limb alignment and stability
    for ambulation and upper extremity motion for selfcare. The outcome appears to be improved if surgery
    on joints is done when the child is younger than 4 to 6
    years, when adaptive intra-articular changes begin to
    occur. Approximately two thirds of patients have developmental dysplasia of the hip or frank dislocation, and
    there is considerable controversy about the management of the hips in these children. Closed reduction is
    rarely or never successful. There is significant variability in the functionality of these children because of the
    underlying severity of the disease. The range of motion
    of the hips may be important for functioning. Hip contractures, especially those that cause flexion deformity,
    adversely affect the gait pattern. Surgery to correct a
    dislocated hip therefore can lead to worse functioning
    if it results in significant contracture. A unilateral dislocation generally is treated surgically. Bilateral dislocation management is more controversial. Because of the
    relatively good results of early surgery, at least one
    early attempt at surgical relocation of bilaterally dislocated hips may be worthwhile.
    Although the knees in arthrogryposis multiplex congenita are classically described as hyperextended, most
    are in flexion. Ambulation is difficult if the flexion deformity is greater than 30 because of the associated
    relative weakness of the quadriceps. A posterior soft-

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Arthrogryposis Multiplex Congenita


    Arthrogryposis multiplex congenita is the best known
    of the multiple congenital contracture syndromes. The
    etiology of arthrogryposis multiplex congenita is unknown. Some mothers of children with arthrogryposis
    have serum antibodies that inhibit fetal acetylcholine
    receptor function. The number of anterior horn cells in
    the spinal cord is decreased. The childs shoulders typically are adducted and internally rotated, the elbow is
    more often extended rather than flexed, and the wrist is
    severely flexed, with ulnar deviation. In the lower extremities, the hips are flexed, abducted, and externally
    rotated; the knees are typically in extension, although
    flexion is possible; and clubfeet are typical (Figure 7).
    Joint motion is restricted. At least 25% of affected patients are nonambulatory, and many others are limited
    to household ambulation. Among adults, the level of
    dependency appears to be more related to educational

    Figure 7

    805

    Section 6: Pediatrics

    Figure 8

    MRI of the cervical spine of a 2-year-old girl with


    severe cervical kyphosis secondary to Larsen syndrome. She was treated with anterior and posterior decompression and fusion.

    6: Pediatrics

    tissue procedure initially improves the range of motion


    and function, but the contractures usually recur, along
    with a loss of motion.56-58 Soft-tissue releases may need
    to be repeated later, before skeletal maturity. Supracondylar osteotomies of the femur are recommended toward the end of growth to correct residual deformity.
    Femoral shortening is a useful addition to the osteotomies. A guided growth approach at the distal femoral
    growth plate may correct flexion deformity of the knee,
    although its effectiveness for correcting the quadriceps
    mechanism is unclear.59
    A severe clubfoot is characteristic of arthrogryposis
    multiplex congenita. Traditionally it was believed that
    extensive surgery was necessary to correct the deformity. However, the Ponseti method, with minor modifications, has good results in many patients.60-62
    Most patients do not require upper extremity surgical procedures. It is ideal to achieve elbow flexion to
    90 from the fixed extended position. If both elbows
    are involved, surgery to increase flexion should be done
    only on one side.63
    Approximately one third of patients develop scoliosis. The curve usually has a C-shaped neuromuscular
    pattern. Surgery is indicated for a progressive curve
    that interferes with balance or function. Some patients
    have regained their ability to ambulate after surgical
    correction of a large, rigid curve and surgery should be
    considered for a patient who loses the ability to ambulate as such a curve develops.5
    806

    Orthopaedic Knowledge Update 10

    Larsen Syndrome
    The essential features of Larsen syndrome are multiple
    congenital dislocations of large joints, a characteristic
    flat face, and ligamentous laxity. Kyphosis and abnormal cervical spine segmentation with instability are typical. Kyphosis often is associated with myelopathy.
    Both autosomal dominant and recessive inheritance
    patterns have been reported.5 Mutations in the gene encoding filamin B sometimes causes autosomal dominant inheritance, and a deficiency of carbohydrate sulfotransferase 3 is responsible for some incidences of
    autosomal recessive inheritance.64 A phenotype has
    been reported in which only one side of the body is affected by Larsen syndrome; this pattern suggests a somatic, or mosaic, mutation.65
    Although knee stability is important for ambulation,
    knee stability in extension is even more important because it allows optimal quadriceps function. The knee
    may remain unstable after reduction because of the
    lack of normal function in the stabilizing ligaments,
    such as the anterior cruciate ligament. Extra-articular
    reconstruction of the anterior cruciate ligament may be
    required.66
    The hips are dislocated in a patient with Larsen syndrome, often despite a relatively normal-appearing acetabulum. There is a good range of motion, although
    the hip may prove to be irreducible. The evolution of
    hip management in Larsen syndrome mirrors that of arthrogryposis multiplex congenita, with a trend toward
    earlier treatment. The major concern involving the
    spine is structural abnormality in the cervical vertebrae.
    This manifestation may occur more frequently than has
    been recognized, and cervical spine radiographs should
    be used during the first year of life to identify it. Kyphosis often results from hypoplasia of the vertebral
    bodies. A combination of cervical kyphosis and forward subluxation may result in quadriplegia and death
    (Figure 8). Posterior stabilization within the first 18
    months of life may prevent significant problems associated with complications of treatment after myelopathy
    has developed and allow a kyphotic deformity to be
    corrected with growth. In a patient with severe kyphosis or a patient with myelopathy, anterior and posterior
    decompression and fusion may be required.67,68

    Contracture Syndromes Primarily Involving


    the Hands and Feet: Distal Arthrogryposis
    Distal arthrogryposis is characterized by fixed hand
    contractures and foot deformities, but the large joints
    of the arms and legs are spared. Type I and type II distal arthrogryposis are distinguished by the absence or
    presence, respectively, of facial features.
    In some patients, distal arthrogryposis type I is
    caused by mutations in the TPM2 gene, which encodes
    -tropomyosin, a protein important in fast-twitch muscle fibers. Type II distal arthrogryposis (FreemanSheldon syndrome) is caused by mutations in an isoform of troponin I that is specific to the troponintropomyosin complex of fast-twitch myofibers. Both
    mutations result in abnormal activity of fast-twitch

    2011 American Academy of Orthopaedic Surgeons

    Chapter 62: Skeletal Dysplasias, Connective Tissue Diseases, and Other Genetic Disorders

    muscle fibers, and dysregulation of these muscle fibers


    may be the common pathophysiologic cause of distal
    arthrogryposis.
    Children with distal arthrogryposis have overall
    good function. The hands function well because the
    shoulders, elbows, and wrists are normal. The most
    common hand surgery is to lengthen the flexor pollicis
    longus and rebalance the extensor of the thumb. The
    feet more frequently require surgery. Some clubfeet can
    be corrected with manipulation and serial casts, but
    most are treated with circumferential releases. The outcome of treatment of clubfoot is better in distal arthrogryposis than in other arthrogrypotic syndromes.

    Contracture Syndromes With Skin Webs:


    Pterygia Syndromes

    Doman I, Kvr F, Ills T, Dczi T: Subluxation of a


    lumbar vertebra in a patient with Marfan syndrome:
    Case report. J Neurosurg 2001;94(1, suppl):154-157.

    3.

    Pearson GD, Devereux R, Loeys B, et al; National


    Heart, Lung, and Blood Institute and National Marfan
    Foundation Working Group: Report of the National
    Heart, Lung, and Blood Institute and National Marfan
    Foundation Working Group on research in Marfan syndrome and related disorders. Circulation 2008;118(7):
    785-791.
    The work group discussed Marfan syndrome and other
    conditions.

    4.

    Ahn NU, Sponseller PD, Ahn UM, Nallamshetty L,


    Kuszyk BS, Zinreich SJ: Dural ectasia is associated with
    back pain in Marfan syndrome. Spine (Phila Pa 1976)
    2000;25(12):1562-1568.

    5.

    Alman BA, Goldberg MJ: Syndromes of orthopaedic


    importance, in Morrissy RT, Weisntein SL, eds: Lovell
    and Winters Pediatric Orthopaedics, ed 6. Philadelphia,
    PA, Lippincott Williams and Wilkins, 2006, pp 251313.

    6.

    Skaggs DL, Bushman G, Grunander T, Wong PC, Sankar WN, Tolo VT: Shortening of growing-rod spinal instrumentation reverses cardiac failure in child with Marfan syndrome and scoliosis: A case report. J Bone Joint
    Surg Am 2008;90(12):2745-2750.
    The authors present a case report on the use of growingrod spinal instrumentation in patients with Marfan syndrome and scoliosis.

    7.

    Yang JS, Sponseller PD: Severe cervical kyphosis complicating halo traction in a patient with Marfan syndrome.
    Spine (Phila Pa 1976) 2009;34(1):E66-E69.
    The authors concluded that cervical kyphosis occurs because of laxity of the connective tissue in patients with
    Marfan syndrome, and halo gravity traction should be
    used with caution.

    8.

    Beighton P, De Paepe A, Steinmann B, Tsipouras P,


    Wenstrup RJ; Ehlers-Danlos National Foundation
    (USA) and Ehlers-Danlos Support Group (UK): EhlersDanlos syndromes: Revised nosology, Villefranche,
    1997. Am J Med Genet 1998;77(1):31-37.

    9.

    Burrows NP, Nicholls AC, Yates JR, et al: The gene encoding collagen alpha1(V)(COL5A1) is linked to mixed
    Ehlers-Danlos syndrome type I/II. J Invest Dermatol
    1996;106(6):1273-1276.

    10.

    Wenstrup RJ, Langland GT, Willing MC, DSouza VN,


    Cole WG: A splice-junction mutation in the region of
    COL5A1 that codes for the carboxyl propeptide of pro
    alpha 1(V) chains results in the gravis form of the
    Ehlers-Danlos syndrome (type I). Hum Mol Genet
    1996;5(11):1733-1736.

    11.

    Sillence DO, Senn A, Danks DM: Genetic heterogeneity


    in osteogenesis imperfecta. J Med Genet 1979;16(2):
    101-116.

    Annotated References
    1.

    Pyeritz RE, McKusick VA: The Marfan syndrome: Diagnosis and management. N Engl J Med 1979;300(14):
    772-777.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    The term pterygium refers to a web and is derived from


    a Greek word meaning little wing. The two most
    common pterygia syndromes are multiple pterygia syndrome and popliteal pterygia syndrome. Multiple
    pterygia syndrome, also called Escobar syndrome, is
    characterized by a web across every flexion crease in
    the extremities, most prominently across the popliteal
    space, the elbow, and the axilla. Webbing across the
    neck laterally and anteriorly from sternum to chin
    draws the facial features downward. The fingers are
    webbed. There is almost always a vertical talus in multiple pterygium syndrome. Often there is a significant
    spine deformity, which may interfere with trunk and
    chest growth and lead to death from respiratory failure
    during the first or second year of life. The patients mobility largely depends on the magnitude of the lower
    extremity webs and the residual motion of the joints.
    Many patients must use a wheelchair for locomotion.
    Popliteal pterygium syndrome is caused by mutations in the gene encoding interferon regulatory
    factor-6. Patients have a cleft lip and palate, lip pits, intraoral adhesions, and sometimes a fibrous band that
    crosses the perineum and distorts the genitalia. A
    popliteal web usually is present bilaterally, running
    from ischium to calcaneus and resulting in a severe
    knee flexion deformity. Within the popliteal web is a
    superficial fibrous band, over which lies a tent of muscle running from the os calcis to the ischium; this feature formerly was referred to as a calcaneoischiadicus
    muscle. The popliteal artery and vein are usually deep,
    but the sciatic nerve is superficial in the web, just underneath the fibrous band. Early popliteal web surgery
    is recommended before further vascular shortening or
    the onset of adaptive changes in the articular surfaces.
    Femoral shortening with an extension osteotomy often
    is required.

    2.

    807

    Section 6: Pediatrics

    22.

    Bruckheimer E, Abrahamov A: Russell-Silver syndrome


    and Wilm Tumor. J Pediatr 1993;122:165.

    23.

    Stevens PM, Klatt JB: Guided growth for pathological


    physes: Radiographic improvement during realignment.
    J Pediatr Orthop 2008;28(6):632-639.
    In children with rickets, early intervention, via guided
    growth, to restore and preserve a neutral axis while
    maximizing the growth potential of the physes is recommended. Level of evidence: IV.

    24.

    Hall JG: The natural history of achondroplasia. Basic


    Life Sci 1988;48:3-9.

    Ward LM, Rauch F, Travers R, et al: Osteogenesis imperfecta type VII: An autosomal recessive form of brittle
    bone disease. Bone 2002;31(1):12-18.

    25.

    Horton WA: Fibroblast growth factor receptor 3 and


    the human chondrodysplasias. Curr Opin Pediatr 1997;
    9(4):437-442.

    Kolanczyk M, Khnisch J, Kossler N, et al: Modelling


    neurofibromatosis type 1 tibial dysplasia and its treatment with lovastatin. BMC Med 2008;6:21.

    26.

    Maynard JA, Ippolito EG, Ponseti IV, Mickelson MR:


    Histochemistry and ultrastructure of the growth plate in
    achondroplasia. J Bone Joint Surg Am 1981;63(6):969979.

    27.

    Yamanaka Y, Ueda K, Seino Y, Tanaka H: Molecular


    basis for the treatment of achondroplasia. Horm Res
    2003;60(suppl 3):60-64.

    28.

    Rousseau F, Bonaventure J, Legeai-Mallet L, et al: Clinical and genetic heterogeneity of hypochondroplasia.


    J Med Genet 1996;33(9):749-752.

    29.

    Coscia MF, Bassett GS, Bowen JR, Ogilvie JW, Winter


    RB, Simonton SC: Spinal abnormalities in camptomelic
    dysplasia. J Pediatr Orthop 1989;9(1):6-14.

    30.

    Thomas S, Winter RB, Lonstein JE: The treatment of


    progressive kyphoscoliosis in camptomelic dysplasia.
    Spine (Phila Pa 1976) 1997;22(12):1330-1337.

    31.

    Lee B, Thirunavukkarasu K, Zhou L, et al: Missense


    mutations abolishing DNA binding of the osteoblastspecific transcription factor OSF2/CBFA1 in cleidocranial dysplasia. Nat Genet 1997;16(3):307-310.

    This study suggests that patients with NF1 have a


    unique generalized skeletal dysplasia, which makes them
    more likely to have localized osseous defects.

    32.

    Senta H, Park H, Bergeron E, et al: Cell responses to


    bone morphogenetic proteins and peptides derived from
    them: Biomedical applications and limitations. Cytokine
    Growth Factor Rev 2009;20(3):213-222.

    Richie MF, Johnston CE II: Management of developmental coxa vara in cleidocranial dysostosis. Orthopedics 1989;12(7):1001-1004.

    33.

    Bongers EM, Gubler MC, Knoers NV: Nail-patella syndrome: Overview of clinical and molecular findings. Pediatr Nephrol 2002;17(9):703-712.

    The authors discuss the use of bone morphogenetic proteins and their derived peptides in biomedical delivery
    systems and gene therapy.

    34.

    Guidera KJ, Satterwhite Y, Ogden JA, Pugh L, Ganey T:


    Nail patella syndrome: A review of 44 orthopaedic patients. J Pediatr Orthop 1991;11(6):737-742.

    35.

    Beguiristin JL, de Rada PD, Barriga A: Nail-patella


    syndrome: Long term evolution. J Pediatr Orthop B
    2003;12(1):13-16.

    36.

    Gillis LA, McCallum J, Kaur M, et al: NIPBL mutational analysis in 120 individuals with Cornelia de

    12.

    Cole WG: The molecular pathology of osteogenesis imperfecta. Clin Orthop Relat Res 1997;343(343):235248.

    13.

    Glorieux FH, Rauch F, Plotkin H, et al: Type V osteogenesis imperfecta: A new form of brittle bone disease.
    J Bone Miner Res 2000;15(9):1650-1658.

    14.

    Glorieux FH, Ward LM, Rauch F, Lalic L, Roughley PJ,


    Travers R: Osteogenesis imperfecta type VI: A form of
    brittle bone disease with a mineralization defect. J Bone
    Miner Res 2002;17(1):30-38.

    15.

    16.

    Lovastatin is potentially useful in the treatment of NF1related fracture healing abnormalities.


    17.

    Korf BR: Statins, bone, and neurofibromatosis type 1.


    BMC Med 2008;6:22.
    The author discusses the major features of NF1.

    18.

    Cho TJ, Seo JB, Lee HR, Yoo WJ, Chung CY, Choi IH:
    Biologic characteristics of fibrous hamartoma from congenital pseudarthrosis of the tibia associated with neurofibromatosis type 1. J Bone Joint Surg Am 2008;
    90(12):2735-2744.
    The authors studied the biologic characteristics of fibrous hamartoma cells to understand the pathogenesis
    of this disease. These cells maintain some of the mesenchymal lineage cell phenotypes but do not undergo osteoblastic differentiation in response to bone morphogenetic protein.

    19.

    6: Pediatrics

    20.

    21.

    808

    Stevenson DA, Moyer-Mileur LJ, Murray M, et al: Bone


    mineral density in children and adolescents with neurofibromatosis type 1. J Pediatr 2007;150(1):83-88.

    Kuroiwa M, Sakamoto J, Shimada A, et al: Manifestation of alveolar rhabdomyosarcoma as primary cutaneous lesions in a neonate with Beckwith-Wiedemann syndrome. J Pediatr Surg 2009;44(3):e31-e35.
    The authors determine that neonatal alveolar rhabdomyosarcoma with Beckwith-Wiedemann syndrome
    may result from an alternative molecular pathway.

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 62: Skeletal Dysplasias, Connective Tissue Diseases, and Other Genetic Disorders

    body mass index, head circumference, body composition, and body proportions.

    Lange syndrome and evaluation of genotype-phenotype


    correlations. Am J Hum Genet 2004;75(4):610-623.
    37.

    Joubin J, Pettrone CF, Pettrone FA: Cornelia de Langes


    syndrome: A review article (with emphasis on orthopedic significance). Clin Orthop Relat Res 1982;171(171):
    180-185.

    38.

    Winell J, Burke SW: Sports participation of children


    with Down syndrome. Orthop Clin North Am 2003;
    34(3):439-443.

    39.

    Pizzutillo PD, Herman MJ: Cervical spine issues in


    Down syndrome. J Pediatr Orthop 2005;25(2):253259.

    40.

    Doyle JS, Lauerman WC, Wood KB, Krause DR: Complications and long-term outcome of upper cervical
    spine arthrodesis in patients with Down syndrome.
    Spine (Phila Pa 1976) 1996;21(10):1223-1231.

    41.

    Gicquel C, Cabrol S, Schneid H, Girard F, Le Bouc Y:


    Molecular diagnosis of Turners syndrome. J Med Genet
    1992;29(8):547-551.

    42.

    Kim JY, Rosenfeld SR, Keyak JH: Increased prevalence


    of scoliosis in Turner syndrome. J Pediatr Orthop 2001;
    21(6):765-766.

    43.

    Tartaglia M, Kalidas K, Shaw A, et al: PTPN11 mutations in Noonan syndrome: Molecular spectrum,
    genotype-phenotype correlation, and phenotypic heterogeneity. Am J Hum Genet 2002;70(6):1555-1563.

    44.

    Wedge JH, Khalifa MM, Shokeir MH: Skeletal anomalies in 40 patients with Noonans syndrome. Orthop
    Trans 1987;11:40-41.

    45.

    Lee CK, Chang BS, Hong YM, Yang SW, Lee CS, Seo
    JB: Spinal deformities in Noonan syndrome: A clinical
    review of sixty cases. J Bone Joint Surg Am 2001;
    83(10):1495-1502.
    Holm VA, Cassidy SB, Butler MG, et al: Prader-Willi
    syndrome: Consensus diagnostic criteria. Pediatrics
    1993;91(2):398-402.

    47.

    Soriano RM, Weisz I, Houghton GR: Scoliosis in the


    Prader-Willi syndrome. Spine (Phila Pa 1976) 1988;
    13(2):209-211.

    48.

    Rees D, Jones MW, Owen R, Dorgan JC: Scoliosis surgery in the Prader-Willi syndrome. J Bone Joint Surg Br
    1989;71(4):685-688.

    49.

    Festen DA, de Lind van Wijngaarden R, van Eekelen M,


    et al: Randomized controlled GH trial: Effects on anthropometry, body composition and body proportions
    in a large group of children with Prader-Willi syndrome.
    Clin Endocrinol (Oxf) 2008;69(3):443-451.
    The authors concluded that growth hormone treatment
    in children with Prader-Willi syndrome improves height,

    2011 American Academy of Orthopaedic Surgeons

    de Lind van Wijngaarden RF, de Klerk LW, Festen DA,


    Duivenvoorden HJ, Otten BJ, Hokken-Koelega AC:
    Randomized controlled trial to investigate the effects of
    growth hormone treatment on scoliosis in children with
    Prader-Willi syndrome. J Clin Endocrinol Metab 2009;
    94(4):1274-1280.
    The authors determined that scoliosis should not be
    considered a contraindication for growth hormone
    treatment in children with Prader-Willi syndrome.

    51.

    Bauermeister S, Letts M: The orthopaedic manifestations of the Langer-Giedion syndrome. Orthop Rev
    1992;21(1):31-35.

    52.

    Minguella I, Ubierna M, Escola J, Roca A, Prats J,


    Pintos-Morell G: Trichorhinophalangeal syndrome, type
    I, with avascular necrosis of the femoral head. Acta Paediatr 1993;82(3):329-330.

    53.

    Taylor C, Brady P, OMeara A, Moore D, Dowling F,


    Fogarty E: Mobility in Hurler syndrome. J Pediatr Orthop 2008;28(2):163-168.
    The authors studied mobility in 23 patients at a mean of
    8.5 years after hematopoietic stem cell transplant for the
    treatment of Hurler syndrome. All patients had independent mobility, with restriction of internal hip rotation as
    the most significant clinical finding.

    54.

    Malm G, Gustafsson B, Berglund G, et al: Outcome in


    six children with mucopolysaccharidosis type IH,
    Hurler syndrome, after haematopoietic stem cell transplantation (HSCT). Acta Paediatr 2008;97(8):11081112.
    Early hematopoietic stem cell transplantation in patients
    with mucopolysaccharidosis type I, Hurler syndrome,
    preserves mental ability.

    55.

    Tassinari E, Boriani L, Traina F, Dallari D, Toni A,


    Giunti A: Bilateral total hip arthroplasty in MorquioBrailsfords syndrome: A report of two cases. Chir Organi Mov 2008;92(2):123-126.
    Young age, severe dysplasia, and joint size are the main
    technical problems associated with total hip arthroplasty in patients with Morquio-Brailsford syndrome.

    56.

    Ho CA, Karol LA: The utility of knee releases in arthrogryposis. J Pediatr Orthop 2008;28(3):307-313.
    Although knee releases may improve short-term function in patients with arthrogryposis, function and outcome worsen with age.

    57.

    Devalia KL, Fernandes JA, Moras P, Pagdin J, Jones S,


    Bell MJ: Joint distraction and reconstruction in complex
    knee contractures. J Pediatr Orthop 2007;27(4):402407.
    A retrospective review of joint distraction and reconstruction in complex knee contractures in six patients
    (nine knees) found that all patients were able to move
    with or without an orthosis, and four patients were satisfied with the results of surgery.

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    46.

    50.

    809

    Section 6: Pediatrics

    58.

    van Bosse HJ, Feldman DS, Anavian J, Sala DA: Treatment of knee flexion contractures in patients with arthrogryposis. J Pediatr Orthop 2007;27(8):930-937.
    Posterior knee releases and flexion contracture distraction by Ilizarov fixation were effective in improving mobility in patients with arthrogryposis.

    59.

    Klatt J, Stevens PM: Guided growth for fixed knee flexion deformity. J Pediatr Orthop 2008;28(6):626-631.
    Guided growth is an effective and safe alternative to
    posterior capsulotomy or supracondylar extension osteotomy in the treatment of fixed knee flexion deformity
    in children. Level of evidence: IV.

    60.

    Boehm S, Limpaphayom N, Alaee F, Sinclair MF,


    Dobbs MB: Early results of the Ponseti method for the
    treatment of clubfoot in distal arthrogryposis. J Bone
    Joint Surg Am 2008;90(7):1501-1507.
    The authors early results support the use of the Ponseti
    method to treat distal arthrogrypotic clubfoot. Additional studies are needed to determine the risk of recurrence and the potential need for corrective surgery.

    61.

    van Bosse HJ, Marangoz S, Lehman WB, Sala DA: Correction of arthrogrypotic clubfoot with a modified Ponseti technique. Clin Orthop Relat Res 2009;467(5):
    1283-1293.
    Arthrogrypotic clubfoot can be corrected without extensive surgery in infants and young children.

    62.

    Morcuende JA, Dobbs MB, Frick SL: Results of the


    Ponseti method in patients with clubfoot associated
    with arthrogryposis. Iowa Orthop J 2008;28:22-26.
    The Ponseti method is effective for correcting clubfoot
    associated with arthrogryposis, especially during the
    first few weeks after birth.
    Van Heest A, James MA, Lewica A, Anderson KA: Posterior elbow capsulotomy with triceps lengthening for
    treatment of elbow extension contracture in children
    with arthrogryposis. J Bone Joint Surg Am 2008;90(7):
    1517-1523.

    64.

    Hermanns P, Unger S, Rossi A, et al: Congenital joint


    dislocations caused by carbohydrate sulfotransferase 3
    deficiency in recessive Larsen syndrome and humerospinal dysostosis. Am J Hum Genet 2008;82(6):13681374.
    The authors studied six patients with congenital joint
    dislocations who had carbohydrate sulfotransferase 3
    deficiency.

    65.

    Debeer P, De Borre L, De Smert L, et al: Asymetrical


    Larsen syndrome in a young girl: A second example of
    somatic mosaicism in the syndrome. Genet Couns 2003;
    14:95-100.

    66.

    Johnston CE II, Birch JG, Daniels JL: Cervical kyphosis


    in patients who have Larsen syndrome. J Bone Joint
    Surg Am 1996;78(4):538-545.

    67.

    Madera M, Crawford A, Mangano FT: Management of


    severe cervical kyphosis in a patient with Larsen syndrome: Case report. J Neurosurg Pediatr 2008;1(4):
    320-324.
    The authors discuss the first report of a child with Larsen syndrome in whom an asymptomatic cervical instability was treated before neurologic deterioration with
    synchronous anterior decompression and fixation, posterior fusion and fixation, and halo placement.

    68.

    Sakaura H, Matsuoka T, Iwasaki M, Yonenobu K, Yoshikawa H: Surgical treatment of cervical kyphosis in


    Larsen syndrome: Report of 3 cases and review of the
    literature. Spine (Phila Pa 1976) 2007;32(1):E39-E44.
    Posterior spinal fusion is indicated in patients with mild
    and flexible cervical kyphosis. Anterior decompression
    and circumferential arthrodesis is indicated in patients
    with severe kyphosis.

    6: Pediatrics

    63.

    Elbow capsulotomy with triceps lengthening successfully increased passive elbow flexion and the arc of elbow motion in children with arthrogryposis. None of
    the children in this study underwent subsequent tendon
    transfer surgery.

    810

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 63

    Neuromuscular Disorders
    in Children
    Michael D. Aiona, MD

    Arabella I. Leet, MD

    Introduction

    Dr. Aiona or an immediate family member serves as a


    board member, owner, officer, or committee member of
    the American Academy for Cerebral Palsy and Developmental Medicine and the Pediatric Orthopaedic Society
    of North America. Neither Dr. Leet nor any immediate
    family member has received anything of value from or
    owns stock in a commercial company or institution related directly or indirectly to the subject of this chapter.

    2011 American Academy of Orthopaedic Surgeons

    Cerebral Palsy
    Cerebral palsy (CP) is a group of developmental disorders of movement and posture causing activity restriction or disability, which is attributed to disturbances
    occurring in the fetal or infant brain. The motor impairment varies in severity and may be accompanied by
    a seizure disorder or impairment of sensation, cognition, communication and/or behavior. Although the
    encephalopathy is static, the affected musculoskeletal
    system changes with growth and development. Orthopaedic management addresses the altered biomechanics
    of the musculoskeletal system. Though technical success (such as the ability to straighten limbs) can be
    achieved, correlation to functional outcomes continues
    to be a challenge.2 To meet patient and family goals,
    therapists, pediatricians, physiatrists, orthotists, and social workers provide valuable input in determining a
    treatment plan.
    The incidence of CP has not changed dramatically
    over the past decade, remaining at approximately 2 in
    1,000 births. Improved perinatal care has reduced hypoxic insult at the time of birth as the predominant etiologic factor, along with premature birth, intrauterine
    exposure to infection, and congenital malformations,
    depending on the clinical subtype more commonly associated with the development of CP.3 A genetic-based
    vulnerability may be elucidated with the identification
    of common single nucleotide polymorphism. Decreasing the incidence of CP would have a significant economic impact, as the lifetime cost of one patient is a
    significant social and economic burden, rapidly approaching $1 million,4 with the social and medical care
    costs greatest in childhood because of neonatal care
    and specialized schooling.
    Patients are classified descriptively by the tone abnormality present and the anatomic distribution, for
    example, spastic (velocity-dependent tone) quadriplegia

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Cerebral palsy and neuromuscular disorders have many


    common developments, including an increased awareness that the health risks from obesity in childhood impact children with neuromuscular disorders as well as
    unaffected children. Obesity may be less well tolerated
    in patients with muscle weakness than in children with
    normal muscles. Muscle weakness may also be harder
    to diagnose because the loss of muscle volume may be
    replaced with adipose tissue, giving a more normallooking contour to the limbs and a normal prediction
    of weight on standard growth curves.
    Another common development in the treatment of
    neuromuscular scoliosis includes increased strength of
    segmental fixation to include pedicle and sacral screws,
    which have allowed for increased correction of large
    neuromuscular curves from a posterior approach. In
    neuromuscular disorders, where proximal muscle
    weakness can affect the chest wall musculature and diaphragm, a posterior-only approach can both achieve
    desired correction and decrease some of the risks associated with an anterior approach.
    Some genetic and molecular derangements causing
    neuromuscular conditions are becoming better understood (Table 1); as such there may be new therapies to
    treat patients. Ongoing clinical trials of medical treatments of neuromuscular disorders include deflazacort
    for the treatment of Duchenne muscular dystrophy
    (DMD) or idebenone for the treatment of Friedreich
    ataxia. Deflazacort has been shown to have an effect
    on scoliosis and ambulation in DMD. Whether deflazacort effectively stops curve progression or delays progression until later in life is still unknown.1 The impact
    of these new medical treatments on the development of

    orthopaedic sequelae still requires further clinical research. Gene therapy, which has great potential for curing many neuromuscular disorders, remains an elusive
    treatment because the packaging of many large gene sequencessuch as the gene for dystrophininto a virus is
    a challenge yet to be overcome.1

    811

    Section 6: Pediatrics

    Table 1

    Neuromuscular Conditions
    Disease

    Prevalence

    Gene

    Inheritance

    Molecular
    Defect

    Duchenne
    muscular
    dystrophy

    2-3/10,000

    Xp21.2

    X-linked

    Dystrophin

    Spinal
    muscular
    atrophy

    1/6-10,000

    5q.13

    Autosomal
    recessive

    Survival motor
    Proximal muscle
    neuron protein
    weakness
    Tongue fasiculations

    Scoliosis
    Hip dysplasia

    Charcot-Marie- 36/100,000
    Tooth
    disease

    17p11.2

    Autosomal
    recessive,
    autosomal
    dominant
    X-linked

    Peripheral myelin Loss of sensation


    protein
    including vibration,
    light touch, and
    proprioception
    Absent deep tendon
    reflexes

    Cavovarus feet
    Scoliosis
    Hip dysplasia
    Hand clawing

    Friedreich
    ataxia

    9q13

    Autosomal
    recessive

    Mitochondrial
    protein
    frataxin

    Scoliosis
    Cavovarus feet
    Ataxic gait

    1/50,000

    (four-limb involvement). Although most patients have


    spasticity, many have a mixed pattern with varying degrees of dystonia, a movement disorder manifested by
    involuntary twisting movements and poor motor control. Orthopaedic procedures generally are more successful in treating those patients with pure spasticity
    and less predictable and at times not indicated in other
    patients when dystonic or extrapyramidal tone patterns
    predominate.
    The Gross Motor Function Classification Scale
    (GMFCS) categorizes patients based on function, not
    on geographic distribution or tone. Level I and II patients are independent ambulators, level III patients are
    dependent ambulators, level IV patients walk very
    short distances but use a wheelchair for community
    mobility, and level V patients are nonambulatory with
    global involvement with the lowest function and largest
    disease burden. The usefulness of this classification
    goes beyond description as each level has differing risks
    of developing hip subluxation as well as response to
    surgical intervention, with the greatest risk in GMFCS
    level V.
    6: Pediatrics

    Medical Management of CP
    Intrathecal Baclofen
    Intrathecal baclofen (ITB) is more effective than oral
    baclofen for reduction of tone without diminishing cognitive capacity. Patients using ITB must have a fairly
    stable social situation so the pump can be maintained,
    as sudden withdrawal from ITB can induce seizures. Increasing use of ITB for tone management adds another
    element of complexity to scoliosis management. Its influence on the progression of deformity is unpredictable as studies in the literature report differing findings.
    In comparative studies, patients with and without ITB
    812

    Orthopaedic Knowledge Update 10

    Clinical Features
    Elevated C-reactive
    protein level
    Calf hypertrophy
    Cardiomyopathy

    Cardiomyopathy

    Orthopaedic
    Features
    Scoliosis contractures
    Gait abnormalities

    showed no statistical difference in curve progression,5


    pelvic obliquity, or the incidence of scoliosis.6 In contrast, a review of 19 consecutive patients with spastic
    quadriplegia showed a sixfold increase of curve progression (11 per year) after pump placement. A
    smaller review described four patients with rapid progression of scoliosis after ITB.7 Because ITB is a tone
    management tool, the surgeon and family must weigh
    the benefits of tone reduction separately from its potential influence on spinal deformity in light of this conflicting information. When patients with pumps require
    subsequent spine surgery, pump- and catheter-related
    complications resulted in greater re-operation and hospitalization rates.8,9 There is a reported trend toward
    more wound infections in patients with pumps.
    Botulinum Toxin
    Botulinum toxin, when injected into muscle, blocks the
    release of acetylcholine from vesicles at the neuromuscular junction, allowing muscle relaxation. The drug is
    not FDA approved for the treatment cerebral palsy and
    is used off label. Botulinum toxin can be useful to help
    delay surgical intervention until children are at an age
    where the risk of recurrence of muscle contractures has
    decreased.10 A recent review of the literature by the
    American Academy of Neurology found enough level I
    evidence to prove botulinum toxin efficacious in the
    gastrocnemius-soleus complex, with still undetermined
    success at other muscles sites.11 A randomized controlled study of botulinum toxin injection into the hip
    adductors demonstrated no evidence that the natural
    history of hip instability was altered when children
    were treated with botulinum toxin and hip abduction
    bracing.12

    2011 American Academy of Orthopaedic Surgeons

    Chapter 63: Neuromuscular Disorders in Children

    Figure 1

    A through D, Preoperative and postoperative images after posterior spinal fusion in a premenarchal child with CP.
    Both frontal and sagittal curves are corrected, allowing for better positioning for sitting, while stopping curve
    progression.

    Presurgical Medical Management


    Surgical risks for elective cases can be significant, especially in patients with GMFCS level V involvement.
    Careful preoperative evaluation assuring seizures are
    well controlled, respiratory function is maximized, and
    nutrition and gastrointestinal function are optimal can

    2011 American Academy of Orthopaedic Surgeons

    help decrease medical complications after surgery. Poor


    nutrition or uncontrolled seizures are modifiable risk
    factors in patients with CP and should be addressed before elective orthopaedic intervention.16

    Scoliosis
    The incidence of scoliosis varies with the severity of involvement, with the highest incidence in nonambulatory patients. Although muscle imbalance causes many
    lower extremity deformities, the cause of scoliosis remains elusive. Bracing does not effectively alter the natural history of scoliosis, but may be used to delay surgery for patients who are too young to consider
    definitive surgical treatment. Braces can be prescribed
    in children with trunk hypotonia to assist in positioning and provide comfort.
    Surgical indications vary and are dependent on the
    curve magnitude and family contextual factors. The
    risks of spinal surgery in children with CP are much
    higher than for children with adolescent idiopathic scoliosis and include increased risk of bleeding and infection as well as medical complications. These greater
    risks need to be factored into the clinical decision making process and discussed with the family as part of the
    informed consent process.
    With the advent of more powerful instrumentation,
    it appears that a posterior approach and fusion alone is
    sufficient in most cases.17 In severe curves, osteotomies
    may be performed posteriorly to achieve similar corrections.18 Although the trend is toward more pedicle and
    pelvic screw fixation (Figure 1), the use of a unit rod
    with segmental wire fixation can achieve the same
    curve correction more economically.19 More studies
    comparing screw constructs with other constructs are

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Obesity
    There is a 17% increased prevalence of obesity in the
    ambulatory patient with CP over a 10-year span, which
    is similar to that of the general pediatric population.13
    The ambulatory patients (GMFCS level I and II)
    showed a greater tendency toward being overweight
    than nonambulatory patients (22.7% versus 9.6%).14
    Because children with CP have associated muscle weakness, the extra weight that they carry may reduce ambulatory efficiency.
    Nutrition in patients with CP remains complicated
    and nutritional status needs to be monitored on an individual basis. Children with extensive neurologic involvement (GMFCS level IV and V) tend to have a
    greater incidence of gastrointestinal disorders, with
    feeding problems leading to malnutrition. Level III patients have a lower body mass index than level I and II
    patients as malnutrition may be present in this select
    group of dependent ambulatory patients.15 Although
    there are some questions about the validity of body
    mass index in some neuromuscular disorders, nutritional assessment and counseling can play an important
    role in the overall treatment plan. Individualized care
    of patients with CP should include a strategy to make
    sure all children have adequate nutrition while maintaining an appropriate weight to maximize ambulation
    potential.

    813

    Section 6: Pediatrics

    necessary to demonstrate that pedicle screw fixation is


    able to achieve better results than other constructs
    while being cost-effective. Thus, the specific indications
    for pedicle screw use in CP are still being developed.
    Infection rates after spine fusion are higher in children with CP than in children with adolescent idiopathic scoliosis.20 The complication rate, including infection, is reportedly higher in one series with the use of
    a unit rod compared to a custom rod,20 yet at another
    single institution, the infection rate was as low as 3.9%
    with the use of gentamicin-soaked allograft.21 Although
    caretaker satisfaction, as assessed through surveys, can
    be as high as 96% with spinal fusion, the presence of
    infection adversely affected patients functional status
    with a trend toward greater persistence of pain. Intraoperative blood loss, a major concern, can be significantly reduced by the use of antifibrinolytic agents such
    as aminocaproic acid with resultant decreased transfusion requirements.22

    Hip

    6: Pediatrics

    A dislocated or significantly subluxated hip with femoral head deformity can impact patient function. The etiology of hip subluxation is thought to be muscle force
    imbalance as the hip flexors and adductors dominate
    the hip abductors and extensors. In the nonambulatory patient this condition can affect sitting position, make hygiene difficult, and lead to windswept
    deformity and discomfort. In the ambulatory patient,
    progressive subluxation is less common and may affect
    lever arm function in gait and can cause pain. Dislocated hips are not always painful, but there is no way
    to predict which significantly subluxated hips will go
    on to dislocate without pain. As salvage procedures for
    a dislocated hip are less satisfying than reconstructive
    procedures, prevention of hip deformity is the goal of
    treatment.
    The rate of hip subluxation is correlated with
    GMFCS level, minimal in level I and increasing to 90%
    in level V. Ataxic tone appears to be protective for the
    hips.23 Sequential measures of migration percentage, a
    measure of the percentage of the femoral head that has
    no acetabular coverage, provides the most accurate
    method of identifying and monitoring hip stability.
    Most surgeons would recommend surgery with a migration percentage of 40% to 50% as natural history
    studies have shown that at migration percentages of
    greater than 60% to 70% the hip will dislocate in the
    absence of treatment.24
    The goal of surgical management is to balance the
    muscle forces and to treat any significant bony deformities. Adductor and psoas releases through a medial
    incision with use of an abduction pillow have encouraging initial results in younger children with mild subluxation. Although soft-tissue surgical management
    alone may provide initial stabilization, it is insufficient
    to maintain hip stability until skeletal maturity in many
    cases. Monitoring hip development until skeletal maturity is recommended. Hip monitoring includes clinical
    assessment of hip abduction in extension with
    814

    Orthopaedic Knowledge Update 10

    follow-up radiographs if a hip fails to abduct adequately given the patients clinical picture. Greater deformity usually requires a combination of a proximal
    femoral varus rotational osteotomy and occasionally a
    periacetabular osteotomy.25 Acetabular remodeling is
    not reliable in the older patient population and thus
    correction of acetabular dysplasia should be done in
    the older patient to best protect the reconstruction.26
    Salvage procedures may necessitate removal of the
    femoral head with the complications of heterotopic ossification, migration of the femoral shaft superiorly, or
    incomplete pain relief. The combination of femoral
    head resection and derotational and valgus osteotomy
    helps to position the lower extremity for sitting (Figure
    2).

    Knee
    Excessive stance-phase knee flexion increases patellofemoral pressure, increases demand on the quadriceps
    to maintain upright gait, and causes greater energy demands. As in all lower extremity management, understanding the interplay of joints is crucial in distinguishing primary and secondary deformities. Primary
    deformities need to be addressed, whereas secondary
    compensatory deformities will improve spontaneously
    with treatment of the primary deformity at an adjacent
    joint. Sagittal gait patterns in diplegia have been classified to assist identification of the level of the deformity
    and recommend treatment.27 A similar study describes
    the gait patterns in hemiplegia.28
    The aggressive management of the fixed flexion contracture and quadriceps insufficiency has significantly
    improved technical and functional outcomes. Although
    a 10 improvement of the knee flexion contracture with
    soft-tissue release and casting can be achieved, a fixed
    contracture of 20 or more could be treated with a distal femoral extension osteotomy in the ambulatory adolescent. The Koshina Index can quantify patella alta in
    the immature skeleton.29 Correction of patella alta addresses the quadriceps insufficiency and improves knee
    extension in gait.30 Aggressive rehabilitation and
    ground reaction ankle-foot orthoses are recommended
    to assist knee extension during stance phase. However,
    correction of knee flexion carries the risk of sciatic
    nerve stretch (9.2%), which results in a dysesthetic
    foot. When the ability to bear weight and perform therapy is affected, recovery becomes prolonged. Early recognition by careful postoperative examinations with
    immediate increased knee flexion in response to reports
    of foot pain can reduce tension across the nerve and
    help avoid this complication.31
    In nonambulatory children, identification of knee
    flexion contractures signals hamstring dysfunction that
    can interfere with sitting. Attaching at the pelvis, the
    hamstrings can cause extension of the pelvis out of the
    seating system with strapping of the feet to the foot
    plate of the wheelchair. Thus, hamstring lengthening
    alone may be indicated to improve sitting tolerance and
    wheelchair mobility in children with significant knee
    flexion contractures (popliteal angle greater than 90)

    2011 American Academy of Orthopaedic Surgeons

    Chapter 63: Neuromuscular Disorders in Children

    Figure 2

    A nonambulatory 7-year-old girl with spastic quadreparesis presented with painless deformity of her right leg (A).
    Surgical intervention to reconstruct the right hip was offered, but refused. One year later the patient returned
    with reports of new onset of hip pain. Plain films (B) demonstrated flattening of the femoral head not seen in the
    previous radiographs; loss of the cartilage surface was confirmed with MRI (C). The patient underwent a femoral
    head resection and valgus osteotomy (D). The femoral head demonstrated an extensive cartilage defect (E).

    when other medical modalities such as ITB cannot be


    used.

    Foot and Ankle

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    The goal of foot management is a plantigrade, painless,


    braceable foot. Fixed deformities require more aggressive intervention, whereas flexible deformities are generally treated with bracing.32 Though equinus remains
    the most common ankle deformity, it cannot be overemphasized that a dynamic toe-toe gait does not necessarily mean an equinus deformity requiring surgery.
    Brace-intolerant dynamic deformities are best treated
    with casting and adjuvant botulinum toxin injections to
    the gastrocnemius-soleus complex to reduce tone. Surgical management of equinus should be reserved for
    fixed contractures and to prevent recurrence. Surgery is
    most successful in patients at least 6 to 7 years of age.
    At the time of surgery, the ankle should be reexamined
    because the physical examination can change under anesthesia. The trend is to perform less traditional Z
    lengthening (zone 3), as isolated gastrocnemius lengthening (Strayer) (zone 1) or intramuscular fascial length-

    ening (Vulpius) (zone 2) have lesser chance of postoperative weakness when soleus muscle power is preserved
    (Figure 3). Despite concerns that lengthening procedures could produce significant weakness, the use of ultrasound demonstrates increased volume of the medial
    gastrocnemius 1 year after Vulpius lengthening.33 Similar increases in volume (17%) were documented
    3 months after plantar flexion strengthening resistive
    exercises.34 Ultrasound may prove an excellent tool for
    investigations on muscle architecture after a variety of
    interventions.
    Equinovalgus deformity, common in the diplegic patient, is a combination of midfoot abduction and heel
    valgus. This instability and loss of leverage can affect
    ankle rocker function. In symptomatic patients surgery
    can include calcaneal neck lengthening, which theoretically preserves motion. Calcaneal cuboid subluxation35
    or the use of allograft36 do not compromise the results
    of os calcis lengthening. Subtalar fusion or calcaneal
    sliding osteotomy is reserved for severe, rigid deformities. Midfoot osteotomy may be needed to correct residual supination, which was noted in a subtalar fusion
    815

    Section 6: Pediatrics

    Myelomeningocele
    Myelomeningocele includes the spectrum of spine and
    spinal cord defects resulting from failure of closure of
    the neural tube. A multicenter clinical trial sponsored
    by the National Institutes of Health is currently comparing outcome of fetal surgery to close the defect with
    postnatal surgical closure of exposed neural tissues.

    Spine

    Figure 3

    Surface anatomy of the calf showing the location


    of popular sites of muscle releases for equinus.
    An Achilles tendon lengthening, or a lengthening of the conjoined gastrocnemius and soleus
    fascia (Vulpius) lengthens both gastrocnemius
    and soleus muscles. If the soleus is not contracted, these more distal lengthening procedures will result in significant loss of ankle
    power. Thus, more proximal lengthening procedures are indicated, particularly in diplegic patients, if the ankle can be dorsiflexed past neutral with the knee flexed (Silfverskoid sign).
    (Reproduced with permission from Professor H.
    Kerr Graham, MD, Melbourne, Australia.)

    6: Pediatrics

    group using foot pressure studies.37 Calf muscle lengthening and other soft-tissue rebalancing is necessary
    when performing either procedure.
    Equinovarus foot causes significant lateral foot pressure with the tendency to lead to significant inversion
    strain. Varus positioning can result from imbalance due
    to overpull of the anterior or posterior tibialis. Which
    muscle to treat via combinations of transfer or lengthening is hard to assess clinically; fine-wire electromyography has not been as helpful as had been hoped. A
    recent study has shown physical examination tests such
    as the confusion test to be imperfect, and by electromyography and gait analysis, rebalancing of the varus
    foot would need to address both the anterior and posterior tibialis in two thirds of feet.38 Tendon transfers or
    lengthening are useful in the flexible varus foot whereas
    calcaneal osteotomy or midfoot osteotomies should
    also be considered if the foot deformity is rigid.

    816

    Orthopaedic Knowledge Update 10

    Spinal deformities (including scoliosis, kyphosis, and


    lordosis) are commonly seen in children with myelomeningocele and many result from muscle imbalance and
    weakness as well as structural vertebral anomalies.
    Other factors that affect curve progression include
    shunt malfunction, tethered cord, compensatory pelvic
    obliquity, and/or hip deformity. The prevalence of scoliosis ranges between 50% to 90%, with curve progression determined by the age of the patient, location of
    the dysraphism, ambulation potential, and curve size.39
    Curve progression tends to occur before age 15 years.
    A patient with a curve of 40 or greater can be expected to experience curve progression at a rate of approximately 5 per year.39
    Bracing can be used to provide support and delay
    surgical intervention until the child is older, but bracing
    is not effective in preventing curve progression. Surgical
    intervention carries a high complication rate, including
    surgical blood loss measured in liters, poor wound
    healing, and loss of curve correction over time. In a recent retrospective study of 84 patients undergoing spinal stabilization, the cohort was divided into three
    groups for comparison: (1) posterior spinal fusion and
    instrumentation, (2) posterior and anterior spinal fusion with posterior-only instrumentation, and (3) anterior and posterior spinal fusion and instrumentation.
    The patients in the third group maintained curve correction better than those in group 1; hence, the authors
    recommend anterior and posterior fusion.40 Complications related to hardware were found in one third of
    patients, and loss of correction was directly related to
    hardware failure.40
    The goal of spinal surgery is to improve sitting balance as well as stop curve progression. Pressure mapping has been studied as a tool to assess spinal surgery
    outcome. In 19 wheelchair ambulators undergoing spinal surgery, Cobb angles and pelvic obliquity were significantly corrected radiographically and pressure skin
    ulcers resolved after surgery, but sitting pressure mapping did not show a significant improvement. Because
    the patients appeared to achieve curve correction and
    relief of pressure at the apex of the kyphosis, the authors wondered if pressure mapping was a useful outcomes tool in children with myelomeningocele.41
    Timing of spinal correction remains controversial. In
    a small series of 12 patients undergoing neonatal
    kyphectomy at a single institution and with surgery
    performed by a single surgeon, surgery was found to be
    safe with no reported complications. Although the initial correction of kyphosis was almost 80, the average

    2011 American Academy of Orthopaedic Surgeons

    Chapter 63: Neuromuscular Disorders in Children

    loss of correction after an average of almost 7 years


    was 55. However, the authors noted that the resultant
    kyphotic deformity was different from the natural history of kyphosis in myelomeningocele; the recurrent
    kyphosis was noted to occur over more levels with a
    sagittal contour that was more rounded and technically
    less difficult to manage surgically.42
    In a second retrospective study, nine children at an
    average age of 10.8 years undergoing multilevel spinal
    fusion and cord transaction achieved an average correction of 81.9 of kyphosis, but had a complication rate
    of 89%. Most of the reported complications were
    wound issues; however, an additional 22% of children
    had shunt revision within 6 weeks of surgery, suggesting alterations in cerebrospinal fluid dynamics with
    cord transaction in this age group. The authors propose
    careful preoperative shunt assessment and even suggest
    temporarily externalizing the shunt to better monitor
    shunt function in the acute postoperative period.42-44

    Figure 4

    Hip
    Hip dysplasia is commonly seen in myelomeningocele
    with treatment individualized for the level of function.
    Anterior soft-tissue releases including iliopsoas, rectus
    femoris, tensor fascia lata, and the hip capsule can be
    performed for hip flexion contractures greater than 20
    to facilitate standing in children who do not have active
    motor control about the hip. For children with lowerlevel lesions and who have the potential to ambulate independently, surgical reduction of the hip is indicated
    for unilateral dislocations in children who have good
    quadriceps function (L3 motor level).40 Children with
    bilateral hip dislocations rarely show functional loss
    and may, therefore, benefit from surgical release of hip
    flexion contractures while the hips are left dislocated.
    In patients with sacral level injury, surgical reduction of
    the hips is usually indicated. Ambulatory patients with
    lower-level lesions can have excessive lumbar lordosis
    as compensation for hip flexion contractures as demonstrated by the correlation between hip flexion contracture angle as measured by the Thomas test with the
    sagittal Cobb angle.43

    Foot

    2011 American Academy of Orthopaedic Surgeons

    35 idiopathic clubfeet, the recurrence rate was 68% in


    the myelomeningocele group compared with 26% in
    the idiopathic group. Feet that were insensate had more
    complications with casting when compared to sensate
    feet. In addition, two children in the myelomeningocele
    group sustained nondisplaced fractures. Bracing resulted in more blistering of the feet in the myelomeningocele group.45 Yet despite the fact that the Ponseti approach does not have the same ultimate success rate as
    seen in idiopathic clubfeet, partial correction, which decreases the extent of required surgery, can be achieved
    in children with spina bifida.
    Calcaneovalgus feet develop secondary to plantar
    flexion weakness and can cause loss of toe-off, crouch
    gait, and heel pad ulcers (Figure 4). Early treatment includes bracing, release of foot and toe dorsiflexors, or
    transfer of the anterior tibialis to the gastrocnemiussoleus complex; late treatment may include osteotomy
    and arthrodesis. Gait analysis and dynamic foot pressure measurements were used to study the results of anterior tibialis tendon transfer combined with correction
    of osseous deformity in 18 patients with low lumbar or
    sacral lesions and calcaneal deformity. Patients with excessive coronal or transverse plane pelvic movement or
    with loss of knee extension in stance phase did not
    show improvement in pressure transfer from the hindfoot to the midfoot and forefoot after surgery compared with the more normalized foot pressures seen in
    patients without pelvic and knee dyskinetic movements.46

    6: Pediatrics

    Foot deformities in myelomeningocele include clubfeet,


    calcaneovalgus deformity, metatarsus adductus, and
    congenital vertical talus; the level of the cord lesion is
    not predictive of foot deformity, thus suggesting a multifactorial etiology.45 Traditionally clubfoot deformities
    have been managed by surgical release. In a retrospective review of 167 clubfeet managed with peritalar release, a plantigrade corrected foot was achieved in 83%
    of the cohort, with 17% of children requiring reoperation. The authors concede that the results of surgical
    release were much better than those previously reported in the literature.40 Recently the trend to use the
    Ponseti method for treatment of clubfoot deformity has
    been reported with some success in patients with myelomeningocele. In a prospective 2-year study comparing 28 clubfeet in children with myelomeningocele with

    Lumbar level spina bifida in a 2-year-old boy. On


    his right foot there is L4-level calcaneus deformity due to unopposed pull of the anterior tibialis. On the left foot he has L3 level paralysis
    and a rigid clubfoot.

    Fractures
    The long bones in patients with myelomeningocele are
    often gracile and extremely osteoporotic. The fracture
    rate reportedly is close to 70% in children who have
    high thoracic lesions. Diagnosis of fractures can be
    complex because a fracture can easily mimic an infec-

    Orthopaedic Knowledge Update 10

    817

    Section 6: Pediatrics

    responsible for another 22% of clinically significant ulcers. In comparison, only 7% of skin ulcers in the study
    were caused by a wheelchair cushion or a mattress.40

    Duchenne Muscular Dystrophy

    Figure 5

    Radiograph showing a thoracic-level myelomeningocele in a patient who sustained a femur fracture. Note the prolific amount of callus formation. Arrows point to the gracile femoral
    cortices. Fractures in this patient population can
    be suspicious for infectious process, with a red,
    swollen knee the presenting complaint.

    6: Pediatrics

    tious process with leukocytosis, fever, increased erythrocyte sedimentation rate, and a warm, swollen limb
    (Figure 5). In a recent study, no relationship was found
    between bone mineral density as determined by dualenergy x-ray absorptiometry scan, and the incidence of
    fracture in children with myelomeningocele.47 Thus,
    identification of children at risk for fracture can only
    be approximated based on the level of the cord lesion.
    Fractures heal well in this population, but the rate of
    refracture after immobilization has been reported to be
    as high as 50%. Thus, patients need to be immobilized
    for a minimum amount of time and returned to baseline weight bearing as quickly as possible in an attempt
    to lessen the risk of a refracture.

    Skin Ulcers
    Skin breakdown often occurs on areas of bone prominence. The combination of loss of sensation and other
    deformities such as contractures, hip dislocations, and
    kyphosis commonly lead to ulceration. Iatrogenic
    causes of skin ulceration must also be considered. In a
    recent study of 415 patients admitted to the hospital
    for skin ulcer management, the use of medical devices
    was found to cause 51% of ulcers; cast application was
    818

    Orthopaedic Knowledge Update 10

    DMD has an X-linked pattern of inheritance, although


    one third of all cases are caused by a spontaneous mutation. Because DMD is caused by a single frame shift
    gene defect encoding the dystrophin protein (Xp21),
    great hope exists for a cure with gene therapy. Without
    functioning dystrophin there is poor muscle fiber regeneration, and thus there is a progressive replacement of
    muscle tissue with fat and fibrous tissues. Over time,
    skeletal and cardiac muscle undergo loss of elasticity
    and strength. Clinically, boys present between ages 3 to
    6 years with complaints such as delayed walking or toe
    walking. Often a history is given of difficulty climbing
    stairs, hopping, or jumping. The first symptoms of
    DMD can be subtle, with weakness often being attributed to lack of effort, and the child is deemed lazy instead of weak. Clinical features include pseudohypertrophy of the calf and the presence of a positive Gower
    sign or Trendelenburg sign. Proximal muscle weakness
    is greater than weakness in distal musculature; lumbar
    lordosis is a common compensation for gluteal weakness, whereas circumduction of the limb compensates
    for weakness in the hip flexors. Other orthopaedic concerns include joint contractures and scoliosis.
    Diagnosis of DMD can be suspected when serum
    creatine phosphokinase level is significantly elevated
    above normal early in the disease course. Dystrophin
    gene anomalies can be detected in more than half of
    cases, and muscle biopsy with dystrophin staining can
    often be helpful in making the diagnosis of DMD if
    other tests are inconclusive. Becker muscular dystrophy
    occurs with a less disruptive gene mutation than DMD
    and has a more benign course. Abnormal dystrophin is
    produced and, unlike in DMD, can be detected on muscle biopsy.
    Glucocorticoids have been found to improve muscle
    strength, prolong walking, and reduce scoliosis. Prednisone has been found effective but has side effects including weight gain, loss of bone density, and behavioral changes that frequently necessitate tapering of the
    drug. Deflazacort (available in Canada and Europe) has
    been shown to have the same benefits as prednisone
    with fewer side effects.
    Scoliosis in DMD begins when patients lose ambulatory capacity; thus, screening for curve progression
    should commence when children become wheelchair
    dependent. Scoliosis in DMD is associated with increased kyphosis in the thoracolumbar or lumbar spine
    as well as pelvic obliquity. Patients are best managed
    surgically for curves between 20 and 30 to avoid
    complications. Patients with DMD are at increased risk
    for malignant hyperthermia and intraoperative cardiac
    events. A careful preoperative assessment should include studies of cardiac function (such as with an
    echocardiogram) as well as lung function depending on

    2011 American Academy of Orthopaedic Surgeons

    Chapter 63: Neuromuscular Disorders in Children

    the needs of the patient. Fusion is usually carried to the


    pelvis to treat pelvic obliquity, which if left uncorrected
    may interfere with sitting balance. Pelvic obliquity may
    be difficult to treat later because of worsening cardiac
    and pulmonary function.48

    Spinal Muscular Atrophy

    2011 American Academy of Orthopaedic Surgeons

    Figure 6

    AP scoliosis radiograph of a 4-year-old child with


    type 1 SMA. Note the long C-shaped curve consistent with paralytic scoliosis and the particular
    bell-shaped thorax, which is a result of intercostal paralysis and is characteristic of SMA.

    Hereditary Motor Sensory Neuropathies


    Hereditary motor sensory neuropathies are a group of
    disorders characterized by sensory neuropathies and
    progressive wasting of distal musculature caused by degeneration of the peripheral nerves. Charcot-MarieTooth (CMT) disease is the most common of the hereditary motor sensory neuropathies that is part of a
    heterogeneous group of genetic disorders with more
    than 30 known gene mutations involving many different nerve functional pathways such as myelination, axonal transport, Schwann cell differentiation, and nerve
    cell function.
    There is a wide clinical spectrum to this disease, including all forms of mendelian inheritance patterns,
    variable age of onset, and of disease progression. Although hip dysplasia is seen in less than 10% of all patients with CMT, a recent study documented hip dysplasia occurring after age 8 years in four patients51
    (Figure 7). Hip dysplasia presenting later in childhood
    is a possible presenting clinical feature in CMT. In children who have late dysplasia and a broad-based gait, a
    work-up for CMT should be performed.51 Common orthopaedic findings include cavovarus feet, wasting of
    the intrinsic muscles of the hand, and clawing of the
    toes. Patients can also have loss of sensation, including

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Spinal muscular atrophy (SMA) is an autosomal recessive disorder with proximal muscle weakness caused by
    primary degeneration of the anterior horn cells in the
    spinal cord. The incidence of SMA is 1 in 6,000, but
    SMA is among the most lethal genetic childhood disorders. The gene defect has been identified in chromosome 5q, which codes for the survival motor neuron
    proteins SMN 1 and SMN 2the disorder occurs with
    loss of SMN 1, whereas the severity is predicted by the
    copy number of SMN 2. The higher the copy number
    of SMN 2, the milder the phenotype.
    SMA is classified into three types; type 1 is often
    identified at birththe infant is floppy and has loss of
    deep tendon reflexes and tongue fasciculation. Although the diaphragm is spared, the clearing of airway
    secretions is diminished due to intercostal weakness in
    patients with type 1 SMA, leading to atelectasis and
    pneumonia. Type 2 SMA has a milder course and presents later in life, between age 6 months and 2 years.
    Muscle weakness is greater in the lower extremities
    than the upper extremities, making ambulation difficult. Type 3 SMA is characterized by later presentation
    and a normal life expectancy.
    Progressive scoliosis is the most common orthopaedic concern (Figure 6). Bracing is ineffectual in halting
    curve progression and can exacerbate respiratory difficulties, and thus should be avoided. Children with
    SMA are more likely to experience increased survival
    rates,49 believed to be secondary to better nutritional
    management and advances in pulmonary care; as a result, spinal deformity management should not be withheld under the assumption that the child with type 1
    SMA will not survive. Posterior spinal fusion down to
    the pelvis for curves greater than 40 should be considered before the curve gets large enough to become a
    contributing factor to diminished respiratory function.
    An anterior approach to the spine should be avoided
    whenever possible.
    Other orthopaedic sequelae of SMA include hip dysplasia and joint contractures. Hip dysplasia may require treatment after taking into account walking potential as well as unilateral versus bilateral hip
    involvement. Contractures can be managed with
    stretching or surgical releases.
    As with CP, patients with SMA have been found to
    be at risk for obesity with increased fat mass and reduced lean mass despite low body mass index.50 Increased weight can impede function in children with
    weakness and should be of concern in this patient population. Awareness of the potential for obesity and referral for dietary management may help optimize function.50

    819

    Section 6: Pediatrics

    Figure 8

    Figure 7

    Radiograph of the pelvis of a 12-year-old girl with


    bilateral foot deformities and left hip pain. She
    had a history of CMT disease and bilateral hip
    dysplasia that was worse on the left side.

    vibration, light touch, and proprioception, as well as


    absent deep tendon reflexes.
    Analysis of gait patterns in patients with CMT
    shows that the hip flexors compensate for weakness in
    ankle plantar flexion by taking over the task of initiation of swing phase. When patients develop hip flexor
    fatigue, walking velocity and duration are reduced.
    With fatigue, trunk flexion increases as a secondary
    compensation. The gait analysis data cause one to wonder whether possible selective proximal muscle
    strengthening of hips and trunk might help patients improve walking stamina by helping to maintain gait
    compensations.
    Although high-dose ascorbic acid was shown to
    have a beneficial effect in a mouse model of CMT
    where remyelination was demonstrated after drug use,
    initial clinical trials in children did not reproduce the
    same results seen in the mice but no toxicity was reported as a result of the dosing regimen.52

    6: Pediatrics

    Friedreich Ataxia
    Friedreich ataxia is the most common of the spinocerebellar degenerative disorders.53 The condition is an autosomal recessive disorder caused by a defect on chromosome 9 that causes a loss of the mitochondrial
    protein fraxatin. The lack of fraxatin causes iron to accumulate in mitochondria, causing oxidative stressparticularly in nerve and muscle tissues. The disorder is
    progressive with development of an ataxic gait,
    areflexia, dysarthria, muscle weakness, and loss of vibratory sense and proprioception. Orthopaedic concerns include scoliosis, pes cavovarus, and gait devia820

    Orthopaedic Knowledge Update 10

    Posterior and side radiographic view of the foot


    of a boy with Friedreich ataxia and a cavovarus
    foot. On the posterior view his heel is in
    marked varus positioning. On the lateral view
    he has a high arch consistent with cavus deformity and with obvious clawing of the toes.

    tions (Figure 8). In general, patients lose ambulation in


    the second or third decade of life, and succumb to cardiomyopathy or respiratory sequelae in the fourth or
    fifth decades.53 Treatment of pes cavovarus includes tenotomy, or transfer of either the anterior or posterior
    tibialis tendon in a supple foot, reserving triple arthrodesis for a rigid foot deformity.
    Scoliotic curves can occur in more than 60% of patients and may be difficult to characterize as neuromuscular curves because no real defined curve pattern exists for Friedreich ataxia. Bracing has recently been
    shown to be of only limited use in slowing curve progression. Bracing is poorly tolerated as it restricts compensatory trunk movement that helps with balance for
    walking. Curve progression is related to age of disease
    presentation, and some patients require spinal fusion.
    The results of spinal fusion using segmental fixation
    have been outstanding.54
    Promising medical management with the short chain
    benzoquinone, idebenone, is in current clinical trials to
    work out optimal dosing and patient selection. Idebenone was developed for cognitive disorders such as
    Alzheimer disease and is similar in structure to coenzyme Q 10. Idebenone allows reversible redux reactions to occur. Already idebenone has proved helpful
    both for improving cardiac hypertrophy as seen on
    echocardiogram and for improving neurologic function.55 However, the effect of the drug on the orthopaedic aspects of Friedreich ataxia such as scoliosis curve
    progression and pes cavovarus are not yet known.

    Annotated References
    1.

    Wagner KR: Approaching a new age in Duchenne muscular dystrophy treatment. Neurotherapeutics 2008;
    5(4):583-591.
    The author reviews novel and emerging therapeutic
    strategies for the treatment of DMD.

    2.

    Oeffinger D, Bagley A, Rogers S, et al: Outcome tools


    used for ambulatory children with cerebral palsy: Re-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 63: Neuromuscular Disorders in Children

    An analysis of the current literature from the American


    Academy of Neurology indicates that there is level I evidence to support the efficacy of botulinum-toxin administration for treatment of equinus; other areas of
    botulinum-toxin administration do not yet have enough
    information in the literature to assess the outcome of
    botulinum-toxin treatment.

    sponsiveness and minimum clinically important differences. Dev Med Child Neurol 2008;50(12):918-925.
    The authors evaluate the minimal change needed in outcome measures to be associated with clinical impact.
    3.

    Nelson KB: Causative factors in cerebral palsy. Clin Obstet Gynecol 2008;51(4):749-762.
    A review article on the causes of cerebral palsy is presented.

    4.

    Kruse M, Michelsen SI, Flachs EM, Brnnum-Hansen


    H, Madsen M, Uldall P: Lifetime costs of cerebral palsy.
    Dev Med Child Neurol 2009;51(8):622-628.
    Studies performed in Europe have findings similar to
    those from earlier studies in the United States.

    5.

    Thompson GH, Florentino-Pineda I, Poe-Kochert C,


    Armstrong DG, Son-Hing J: Role of Amicar in surgery
    for neuromuscular scoliosis. Spine (Phila Pa 1976)
    2008;33(24):2623-2629.
    The authors discuss a group of studies on outcomes of
    spine surgery and ways to decrease the morbidity of
    bleeding and infection.

    6.

    7.

    8.

    Shilt JS, Lai LP, Cabrera MN, Frino J, Smith BP: The
    impact of intrathecal baclofen on the natural history of
    scoliosis in cerebral palsy. J Pediatr Orthop 2008;28(6):
    684-687.
    The authors determined that the progression of scoliosis
    in patients with CP who received ITB treatment is not
    significantly different from that in patients not treated
    with ITB.
    Senaran H, Shah SA, Presedo A, Dabney KW, Glutting
    JW, Miller F: The risk of progression of scoliosis in cerebral palsy patients after intrathecal baclofen therapy.
    Spine (Phila Pa 1976) 2007;32(21):2348-2354.
    Ginsburg GM, Lauder AJ: Progression of scoliosis in
    patients with spastic quadriplegia after the insertion of
    an intrathecal baclofen pump. Spine (Phila Pa 1976)
    2007;32(24):2745-2750.
    Sansone JM, Mann D, Noonan K, Mcleish D, Ward M,
    Iskandar BJ: Rapid progression of scoliosis following insertion of intrathecal baclofen pump. J Pediatr Orthop
    2006;26(1):125-128.
    Clinical studies with differing conclusions about the influence of ITB on scoliosis are discussed.

    10.

    Molenaers G, Desloovere K, Fabry G, De Cock P: The


    effects of quantitative gait assessment and botulinum
    toxin A on musculoskeletal surgery in children with cerebral palsy. J Bone Joint Surg Am 2006;88(1):161-170.

    11.

    Simpson DM, Gracies J-M, Graham H-K, et al; Therapeutics and Technology Assessment Subcommittee of
    the American Academy of Neurology: Assessment: Botulinum neurotoxin for the treatment of spasticity (an
    evidence-based review). Report of the Therapeutics and
    Technology Assessment Subcommittee of the American
    Academy of Neurology. Neurology 2008;70(19):16911698.

    2011 American Academy of Orthopaedic Surgeons

    Graham HK, Boyd R, Carlin JB, et al: Does botulinum


    toxin A combined with bracing prevent hip displacement in children with cerebral palsy and hips at risk?
    A randomized, controlled trial. J Bone Joint Surg Am
    2008;90(1):23-33.
    This study design demonstrates no effect of botulinum
    toxin combined with hip abduction bracing for prevention of hip subluxation.

    13.

    Rogozinski BM, Davids JR, Davis RB, et al: Prevalence


    of obesity in ambulatory children with cerebral palsy.
    J Bone Joint Surg Am 2007;89(11):2421-2426.

    14.

    Hurvitz EA, Green LB, Hornyak JE, Khurana SR, Koch


    LG: Body mass index measures in children with cerebral
    palsy related to gross motor function classification: A
    clinic-based study. Am J Phys Med Rehabil 2008;87(5):
    395-403.
    Analysis of body mass index suggests that patients with
    CP are more likely to be overweight.

    15.

    Feeley BT, Gollapudi K, Otsuka NY: Body mass index


    in ambulatory cerebral palsy patients. J Pediatr Orthop
    B 2007;16(3):165-169.
    Counterintuitive findings regarding the presence of obesity in a group of cerebral palsy patients are presented.
    Confounding variables of malnutrition and mobility affect the findings.

    16.

    Murphy NA, Hoff C, Jorgensen T, Norlin C, Young PC:


    Costs and complications of hospitalizations for children
    with cerebral palsy. Pediatr Rehabil 2006;9(1):47-52.

    17.

    Modi HN, Hong JY, Mehta SS, et al: Surgical correction and fusion using posterior-only pedicle screw construct for neuropathic scoliosis in patients with cerebral
    palsy: A three-year follow-up study. Spine (Phila Pa
    1976) 2009;34(11):1167-1175.
    In a retrospective study of 52 patients with neuromuscular scoliosis and CP, posterior-only pedicle screw fixation resulted in satisfactory coronal and sagittal correction without higher complication rates.

    18.

    Suh SW, Modi HN, Yang J, Song HR, Jang KM: Posterior multilevel vertebral osteotomy for correction of severe and rigid neuromuscular scoliosis: A preliminary
    study. Spine (Phila Pa 1976) 2009;34(12):1315-1320.
    The authors studied the effectiveness of posterior multilevel vertebral osteotomy in patients with severe and
    rigid neuromuscular scoliosis and determined that one
    reason the technique should be recommended is because
    it provides release of the anterior column without an anterior approach.

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    9.

    12.

    821

    Section 6: Pediatrics

    19.

    20.

    21.

    22.

    Sponseller PD, Shah SA, Abel MF, et al; Harms Study


    Group: Scoliosis surgery in cerebral palsy: Differences
    between unit rod and custom rods. Spine (Phila Pa
    1976) 2009;34(8):840-844.
    The outcomes and varying techniques in the management of neuromuscular scoliosis are discussed. It is suggested that correction can be achieved with posterior instrumentation and fusion alone though the choice of
    instrumentation varies with some discussion of the cost
    differences between the unit rod and pedicular screws.
    Borkhuu B, Borowski A, Shah SA, Littleton AG, Dabney KW, Miller F: Antibiotic-loaded allograft decreases
    the rate of acute deep wound infection after spinal fusion in cerebral palsy. Spine (Phila Pa 1976) 2008;
    33(21):2300-2304.
    This study reports a decrease in the incidence of deep
    wound infection after spinal fusion in 220 children with
    CP scoliosis from 15% to 4% with the use of prophylactic antibiotics in the corticocancellous allograft bone.
    Caird MS, Palanca AA, Garton H, et al: Outcomes of
    posterior spinal fusion and instrumentation in patients
    with continuous intrathecal baclofen infusion pumps.
    Spine (Phila Pa 1976) 2008;33(4):E94-E99.
    A descriptive study of complications in patients with
    continuous ITB pumps is presented.

    23.

    Soo B, Howard JJ, Boyd RN, et al: Hip displacement in


    cerebral palsy. J Bone Joint Surg Am 2006;88(1):121129.

    24.

    Miller F, Bagg MR: Age and migration percentage as


    risk factors for progression in spastic hip disease. Dev
    Med Child Neurol 1995;37(5):449-455.

    6: Pediatrics

    25.

    26.

    822

    Tsirikos AI, Lipton G, Chang WN, Dabney KW, Miller


    F: Surgical correction of scoliosis in pediatric patients
    with cerebral palsy using the unit rod instrumentation.
    Spine (Phila Pa 1976) 2008;33(10):1133-1140.
    In a retrospective clinical and radiographic consecutive
    case series, it was determined that unit rod instrumentation in the treatment of children with CP is easy to use,
    less expensive than other systems, and can achieve good
    deformity correction with low prevalence of associated
    complications.

    Chung CY, Choi IH, Cho TJ, Yoo WJ, Lee SH, Park
    MS: Morphometric changes in the acetabulum after
    Dega osteotomy in patients with cerebral palsy. J Bone
    Joint Surg Br 2008;90(1):88-91.
    This study reports an increase in mean acetabular volume of 68% with anterosuperior, superolateral, and
    posterosuperior coverage improvement after Dega osteotomy in 17 hips in 12 patients as measured by CT
    scan.
    Schmale GA, Eilert RE, Chang F, Seidel K: High reoperation rates after early treatment of the subluxating hip
    in children with spastic cerebral palsy. J Pediatr Orthop
    2006;26(5):617-623.

    Orthopaedic Knowledge Update 10

    27.

    Rodda JM, Graham HK, Carson L, Galea MP, Wolfe R:


    Sagittal gait patterns in spastic diplegia. J Bone Joint
    Surg Br 2004;86(2):251-258.

    28.

    Riad J, Haglund-Akerlind Y, Miller F: Classification of


    spastic hemiplegic cerebral palsy in children. J Pediatr
    Orthop 2007;27(7):758-764.
    Refinement of the classification of Winters of patterns
    of hemiplegic gait is discussed.

    29.

    Koshino T, Sugimoto K: New measurement of patellar


    height in the knees of children using the epiphyseal line
    midpoint. J Pediatr Orthop 1989;9(2):216-218.

    30.

    Stout JL, Gage JR, Schwartz MH, Novacheck TF: Distal


    femoral extension osteotomy and patellar tendon advancement to treat persistent crouch gait in cerebral
    palsy. J Bone Joint Surg Am 2008;90(11):2470-2484.
    A series of patients reviewed showed that patella advancement improves knee extension over extension osteotomy alone. Level of evidence: IV.

    31.

    Karol LA, Chambers C, Popejoy D, Birch JG: Nerve


    palsy after hamstring lengthening in patients with cerebral palsy. J Pediatr Orthop 2008;28(7):773-776.
    The authors present a descriptive series on a complication that is underrecognized.

    32.

    Westberry DE, Davids JR, Shaver JC, Tanner SL, Blackhurst DW, Davis RB: Impact of ankle-foot orthoses on
    static foot alignment in children with cerebral palsy.
    J Bone Joint Surg Am 2007;89(4):806-813.
    A study using a reproducible standardized radiographic
    measure shows clinically insignificant improvement in
    deformity with the use of an orthosis.

    33.

    Fry NR, Gough M, McNee AE, Shortland AP: Changes


    in the volume and length of the medial gastrocnemius
    after surgical recession in children with spastic diplegic
    cerebral palsy. J Pediatr Orthop 2007;27(7):769-774.
    The application of a new technology to evaluate anatomic outcome in a small series of patients is discussed.

    34.

    McNee AE, Gough M, Morrissey MC, Shortland AP:


    Increases in muscle volume after plantarflexor strength
    training in children with spastic cerebral palsy. Dev Med
    Child Neurol 2009;51(6):429-435.
    This study, using ultrasound, demonstrated that muscle
    volume increased significantly between 7 weeks and
    1 year after Vulpius calf surgery in a group of seven patients.

    35.

    Adams SB Jr, Simpson AW, Pugh LI, Stasikelis PJ: Calcaneocuboid joint subluxation after calcaneal lengthening for planovalgus foot deformity in children with cerebral palsy. J Pediatr Orthop 2009;29(2):170-174.
    Stabilization of the calcaneocuboid joint at the time of
    lateral column lengthening did not significantly reduce
    the incidence or magnitude of subluxation when compared with nonstabilized lengthening and had no significant influence on radiographic outcome or osteoarthritic changes at the calcaneocuboid joint.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 63: Neuromuscular Disorders in Children

    36.

    37.

    38.

    Templin D, Jones K, Weiner DS: The incorporation of


    allogeneic and autogenous bone graft in healing of lateral column lengthening of the calcaneus. J Foot Ankle
    Surg 2008;47(4):283-287.
    Thirty-five lateral column lengthenings in 26 patients
    were reviewed, 30 of which used allograft bone and 5
    autograft. Ninety-seven percent of the allograft cases
    and 80% of the autograft cases were incorporated at final follow-up. The authors recommend the use of allograft as outcome was not adversely affected and donor site morbidity can be avoided.
    Park KB, Park HW, Lee KS, Joo SY, Kim HW: Changes
    in dynamic foot pressure after surgical treatment of valgus deformity of the hindfoot in cerebral palsy. J Bone
    Joint Surg Am 2008;90(8):1712-1721.
    This study demonstrates, through the use of dynamic
    foot pressure measurement, that both extra-articular
    subtalar arthrodesis and calcaneal neck lengthening correct the valgus hindfoot deformity in patients with cerebral palsy. However, residual supination deformity with
    abnormal forefoot pressure was present after fusion
    with postoperative foot pressure distribution more
    closely approximates the normal foot pressure distribution after neck lengthening.
    Michlitsch MG, Rethlefsen SA, Kay RM: The contributions of anterior and posterior tibialis dysfunction to
    varus foot deformity in patients with cerebral palsy.
    J Bone Joint Surg Am 2006;88(8):1764-1768.

    This treatment allowed an average correction of kyphosis of 81.9.


    44.

    Glard Y, Launay F, Viehweger E, Guillaume JM, Jouve


    JL, Bollini G: Hip flexion contracture and lumbar spine
    lordosis in myelomeningocele. J Pediatr Orthop 2005;
    25(4):476-478.

    45.

    Gerlach DJ, Gurnett CA, Limpaphayom N, et al: Early


    results of the Ponseti method for the treatment of clubfoot associated with myelomeningocele. J Bone Joint
    Surg Am 2009;91(6):1350-1359.
    The authors support the use of the Ponseti method to
    treat clubfoot deformity associated with myelomeningocele. Attention to detail is important to avoid complications.

    46.

    Park KB, Park HW, Joo SY, Kim HW: Surgical treatment of calcaneal deformity in a select group of patients
    with myelomeningocele. J Bone Joint Surg Am 2008;
    90(10):2149-2159.
    The authors studied 31 feet in 18 patients and found
    that surgical treatment of calcaneal deformity in patients with myelomeningocele can reduce pressure on
    the calcaneus, increase pressures in the forefoot and
    midfoot, and prevent recurrence of calcaneal deformity.
    Level of evidence: IV.

    47.

    Apkon SD, Fenton L, Coll JR: Bone mineral density in


    children with myelomeningocele. Dev Med Child Neurol 2009;51(1):63-67.
    In a study of 24 children with myelomeningocele, the
    authors found that reduced bone mineral density is a
    major complication.

    Mller EB, Nordwall A, Odn A: Progression of scoliosis in children with myelomeningocele. Spine (Phila Pa
    1976) 1994;19(2):147-150.

    40.

    Akbar M, Bresch B, Seyler TM, et al: Management of


    orthopaedic sequelae of congenital spinal disorders.
    J Bone Joint Surg Am 2009;91(suppl 6):87-100.
    The authors discuss congenital spinal disorders and
    their treatment.

    48.

    Karol LA: Scoliosis in patients with Duchenne muscular


    dystrophy. J Bone Joint Surg Am 2007;89(suppl 1):
    155-162.
    A comprehensive review of the management of scoliosis
    in DMD is presented.

    41.

    Ouellet JA, Geller L, Strydom WS, et al: Pressure mapping as an outcome measure for spinal surgery in patients with myelomeningocele. Spine (Phila Pa 1976)
    2009;34(24):2679-2685.
    The authors studied the effect of improved pressure distribution on patients with myelomeningocele and found
    that pressure mapping may not be useful in predicting
    outcome of spinal surgery.

    49.

    Mannaa MM, Kalra M, Wong B, Cohen AP, Amin RS:


    Survival probabilities of patients with childhood spinal
    muscle atrophy. J Clin Neuromuscul Dis 2009;10(3):
    85-89.
    This study reviews two decades of data on children with
    SMA and finds significantly improved life expectancy in
    patients with type 1 SMA. The positive trend toward
    improved survival is thought to be attributable to better
    nutritional support and pulmonary care.

    42.

    Crawford AH, Strub WM, Lewis R, et al: Neonatal


    kyphectomy in the patient with myelomeningocele.
    Spine (Phila Pa 1976) 2003;28(3):260-266.

    50.

    Sproule DM, Montes JM, Montgomery M, et al: Increased fat mass and high incidence of overweight despite low body mass index in patients with spinal muscular atrophy. Neuromuscul Disord 2009;19(6):391396.
    Obesity is identified in children with SMA as a potential
    source of modifiable morbidity. Body mass index was
    not as predictive of obesity in this patient population as
    in normal children.

    51.

    Bamford NS, White KK, Robinett SA, Otto RK, Gospe


    SM Jr: Neuromuscular hip dysplasia in Charcot-Marie-

    43.

    Ko AL, Song K, Ellenbogen RG, Avellino AM: Retrospective review of multilevel spinal fusion combined
    with spinal cord transection for treatment of kyphoscoliosis in pediatric myelomeningocele patients. Spine
    (Phila Pa 1976) 2007;32(22):2493-2501.
    The authors performed a retrospective review of surgical experience, complications, and insights on nine patients with myelomeningocele and kyphoscoliosis
    treated with spinal cord transaction and spinal fusion.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    39.

    823

    Section 6: Pediatrics

    Tooth disease type 1A. Dev Med Child Neurol 2009;


    51(5):408-411.
    Four patients present with late-onset hip dysplasia. The
    diagnosis of CMT disease is entertained and peripheral
    neuropathies are found clinically followed by a formal
    diagnosis of CMT disease. Thus, hip dysplasia can be a
    presenting sign of CMT disease, which has a wide spectrum of disease severity and presentation.
    52.

    54.

    Milbrandt TA, Kunes JR, Karol LA: Friedreichs ataxia


    and scoliosis: The experience at two institutions. J Pediatr Orthop 2008;28(2):234-238.
    A review of patients with Friedreich ataxia with scoliosis is presented. For those needing surgery,
    somatosensory-evoked potentials were not reliably obtained during surgery.

    55.

    Meier T, Buyse G: Idebenone: An emerging therapy for


    Friedreich ataxia. J Neurol 2009;256(suppl 1):25-30.
    The development of idebenone and the evidence of cardiac and neurologic improvement are reviewed.

    Bernard G, Shevell M: The wobbly child: An approach


    to inherited ataxias. Semin Pediatr Neurol 2008;15(4):
    194-208.

    6: Pediatrics

    53.

    Burns J, Ouvrier RA, Yiu EM, et al: Ascorbic acid for


    Charcot-Marie-Tooth disease type 1A in children: A
    randomised, double-blind, placebo-controlled, safety
    and efficacy trial. Lancet Neurol 2009;8(6):537-544.
    High-dose ascorbic acid was well tolerated in children
    with CMT disease; however, no expected improvements
    in function, strength, or quality of life could be demonstrated.

    Using three case histories, including one child with


    Friedreich ataxia, the authors present a systematic approach to diagnosis and genetic evaluation of children
    with ataxia.

    824

    Orthopaedic Knowledge Update 10

    2011 American Academy of Orthopaedic Surgeons

    Chapter 64

    Pediatric Tumors and


    Hematologic Diseases
    Todd Milbrandt, MD, MS

    Henry J. Iwinski, Jr, MD

    Vishwas R. Talwalkar, MD

    Children with benign tumors may present with a palpable mass, pain with activities, a pathologic fracture, or
    an incidental finding on radiographs. History may reveal pain with activities, which may be indicative of
    weakened bone or sudden onset of pain with minimal
    trauma as a result of a pathologic fracture. The age of
    the patient, history, physical examination, and radiographic features are frequently enough to make a diagnosis. Treatment may range from observation for the
    asymptomatic small lesion with a benign clinical course
    to resection for locally aggressive lesions.

    vealing the nidus. In these cases and especially in the


    spine, fine-cut CT is effective in outlining the lesion and
    planning treatment. Treatment of the lesion depends on
    the location and symptoms. Some lesions will burn
    out and require only observation.1 Medical treatment
    with NSAIDs has also been effective, but typically requires several years of management. Minimally invasive
    ablation using radiofrequency or laser energy has the
    least morbidity and is the most effective treatment
    method, particularly for periarticular lesions.2 Surgical
    treatment is rarely necessary except to obtain tissue for
    diagnosis or for lesions that cannot be safely approached with minimally invasive techniques.

    Osteoid Osteoma

    Osteoblastoma

    Benign Bone Tumors

    Osteoid osteoma is a benign but painful (often at night)


    lesion that occurs in all age groups. It is most frequently
    found in the cortex of the femur and tibia where patients typically present with pain that is progressive and
    well localized. In the limb they may have surrounding
    muscle atrophy and/or gait disturbance, depending on
    location. The tumors also have a predilection for the
    posterior elements of the spine, and a mild scoliosis may
    develop as a result of painful paraspinal muscle spasm.
    Nonsteroidal anti-inflammatory drugs (NSAIDs) are
    particularly effective in relieving symptoms and can assist in making the diagnosis. The lesion is apparent on
    plain radiographs as a fusiform cortical thickening with
    a small radiolucent central nidus less than 1 cm in diameter. The lesion displays markedly increased uptake
    on bone scan. Because of the width of image slices, MRI
    of the involved area may only show widespread inflammatory signal change and soft-tissue edema without re-

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Dr. Milbrandt or an immediate family member serves as a


    board member, owner, officer, or committee member of
    the Pediatric Orthopaedic Society of North America and
    the Scoliosis Research Society and has received research or
    institutional support from DePuy, a Johnson & Johnson
    Company and DJ Orthopaedics. Neither of the following
    authors or any immediate family member has received
    anything of value from or owns stock in a commercial
    company or institution related directly or indirectly to the
    subject of this chapter: Dr. Iwinski, Dr. Talwalkar.

    Osteoblastoma is a benign bone-forming tumor that is


    similar to osteoid osteoma in several ways. It is found
    primarily in the long bones of the lower limbs and the
    posterior spine. Spinal deformity is often apparent in
    patients with spinal lesions. Patients present with pain
    at the lesion and/or signs of disuse. The pain is described as dull and aching but is not relieved by antiinflammatory medications. Bone scan reveals increased
    uptake and may be helpful to localize axial lesions. This
    tumor is less common and is larger in size than osteoid
    osteoma, occurring chiefly in the second decade and
    twice as frequently in males. Osteoblastoma is classically described as a fusiform radiodense cortical lesion
    with a central nidus greater than 1.5 cm in diameter.
    However, in a large series of appendicular lesions, less
    than 50% displayed a characteristic radiographic appearance, and 10% were initially thought to be malignant.3 The lesion may appear locally destructive with
    cortical resorption, soft-tissue invasion, and periosteal
    new bone formation. Thus, the diagnosis may be difficult and is delayed on average by 6 months.4 CT reveals
    specific location, size, and differentiating characteristics
    most clearly. MRI assists in defining surrounding softtissue involvement and proximity to neurovascular
    structures. Osteoblastoma can display locally aggressive
    growth that requires surgical treatment. Intralesional
    resection has yielded a recurrence rate in patients of all
    ages of 15% to 30%. A four-step method of complete
    excision has been described with a 6% recurrence rate.4
    825

    Section 6: Pediatrics

    Figure 2
    Figure 1

    AP radiograph of the humerus of a child with a


    UBC. This image displays the typical appearance
    and location of an active UBC abutting the
    physis. UBCs are centrally located, lytic, and
    demonstrate significant cortical thinning. They
    usually do not expand the bone beyond the
    width of the physis.

    Benign Cystic Lesions of Bone

    Unicameral Bone Cysts

    6: Pediatrics

    Simple or unicameral bone cysts (UBCs) are benign


    bone lesions commonly seen in pediatric patients. They
    are fluid-filled cysts often located in the proximal femur and proximal humerus. Most are asymptomatic
    unless pathologic fracture occurs. Fracture healing usually does not stimulate cyst resolution. Radiographs reveal a centrally located, lytic, well-demarcated metaphyseal lesion with cortical thinning (Figure 1). Biopsy
    is usually indicated for questionable diagnosis based on
    history or atypical imaging. Treatment is usually recommended for large lesions in weight-bearing bones, as
    these are more likely to be painful or lead to fracture
    with resultant deformity and functional disability. In
    the upper extremity, treatment may be recommended
    because of the risk of recurrent pathologic fractures. A
    variety of techniques have been used to induce cyst resolution including injection with steroid, bone marrow
    aspirate, demineralized bone matrix, and calcium sulfate, as well as needle, flexible nail, or cannulated
    screw decompression.5 All have reported some success
    but no single approach has proved to be most advantageous.6,7 Open treatment with curettage and bone grafting is reserved for lesions with questionable diagnosis,
    displaced pathologic fractures that require open reduc826

    Orthopaedic Knowledge Update 10

    AP radiograph of the femur demonstrates an expansive cystic lesion of the distal metaphysis of
    the femur. This finding is consistent with an aneurysmal bone cyst. The diagnosis will be further clarified if fluid-fluid levels are noted on
    MRI. This aneurysmal bone cyst was treated
    with thorough curettage, high-speed burring,
    and bone grafting, with resolution of the cyst
    and spontaneous correction of valgus.

    tion (commonly of the proximal femur), very large lesions, or those that have recurred multiple times. The
    cysts usually resolve as the patient approaches skeletal
    maturity. Many of these lesions abut the physis, which
    can make complete removal difficult and result in
    higher recurrence rates; it should be noted that growth
    arrest occurs, albeit rarely, as a result of the cyst itself
    as well as too-aggressive curettage near the growth
    plate.

    Aneurysmal Bone Cysts


    Aneurysmal bone cysts are benign, cystic lesions composed of blood-filled spaces with thin fibrous septae.
    Radiographs demonstrate an eccentric, lytic, expansile
    metaphyseal lesion with very thin cortical margins. The
    most common location is the metaphyseal region
    around the knee. They are less common and more locally aggressive than UBCs. Aneurysmal bone cyts may
    be considered primary or be secondarily seen in association with other lesions. Primary lesions are associated
    with a rearrangement of chromosome band 17p13. Approximately 75% of patients are younger than 20
    years. Symptoms depend on the location and size of the
    lesion and include increasing pain, warmth, and a palpable bony mass. Spinal lesions usually are in the posterior elements and may present with neurologic signs
    and symptoms (Figure 2). Differential diagnosis in-

    2011 American Academy of Orthopaedic Surgeons

    Chapter 64: Pediatric Tumors and Hematologic Diseases

    cludes UBC and telangiectatic osteosarcoma.


    Because the lesions are locally aggressive, most require open curettage, adjuvant therapy (phenol, cryotherapy, or high-speed burr) and bone grafting. The recurrence rate is approximately 20% but may be higher
    in young children. Percutaneous injection with a variety
    of substances (steroids, demineralized bone matrix, bioglass calcium sulfate, and sclerosing agents) has been
    performed with variable success for lesions that are difficult to approach surgically.8

    Malignant Bone Tumors


    The evaluation of children with suspected musculoskeletal malignancy is similar to that for adults. A thorough assessment of symptoms and the effect of these
    symptoms on function (along with a skillful physical
    examination) guides imaging and/or laboratory evaluation to localize and characterize the process. If additional staging studies and biopsy are necessary, they
    should be performed in consultation with the local
    musculoskeletal tumor center.

    Osteosarcoma

    2011 American Academy of Orthopaedic Surgeons

    Figure 3

    AP radiograph from a 12-year-old girl shows


    characteristic radiographic findings of femoral
    osteosarcoma: a large metaphyseal lesion with
    poorly defined margins, blastic expansion into
    the soft tissues, and periosteal sunbursting.

    phosphatase and lactate dehydrogenase levels. Overall


    5-year survival rates are 60% to 80%.

    Ewing Sarcoma
    Ewing sarcoma is the second most common malignant
    bone tumor in skeletally immature patients age 5 to 30
    years and is most frequently seen in Caucasian males.
    The particular cell type involved has not been completely characterized, but may be of neuronal origin.
    Cytogenetic evaluation has revealed a reciprocal translocation of t(11;22) that ultimately results in the production of transcription factor EWS/FLI1 that may
    have mechanistic importance.11 The tumor may involve
    the axial or appendicular skeleton and is usually painful. The tumor is usually seen as a permeative process
    on plain films with a large soft-tissue mass evident on
    MRI (Figure 4). Prior to surgical treatment, most patients will undergo neoadjuvant chemotherapy to allow
    for tumor shrinkage, increase the chance of clear surgical margins, and facilitate limb salvage. Systemic chemotherapy is essential and has had a dramatic improvement in 5-year survival rates, which are currently 60%
    to 80%.12 Local disease control is obtained surgically in
    most cases, but in rare cases requires radiation therapy.
    It primarily metastasizes to the lungs and other bones,
    but may also involve the bone marrow, thus requiring
    bone marrow aspirate in addition to standard staging
    studies. Poor prognostic signs include metastatic disease at presentation, persistently high serum lactate de-

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Osteosarcoma is a highly malignant bone-producing tumor composed of spindle cells that produce malignant
    osteoid and bone. Its peak incidence is in males in the
    second decade of life. This tumor occurs most often in
    the appendicular skeleton in the metaphyses of the femur and tibia and is usually painful. Pain that occurs at
    night, is worsening, causes limping, changes activity,
    and consistently occurs in the same location is particularly worrisome for a locally destructive process. Initial
    radiographs of the entire bone are taken and usually
    show mixed areas of increased bone density and destruction, poorly defined margins and periosteal reaction described as onion-skinning, sunbursting, and
    Codman triangles (Figure 3). MRI of the entire bone
    should also be performed to evaluate for extent of tumor, skip lesions, soft-tissue involvement, and neurovascular invasion. The role of positron emission tomography in the staging and surveillance of patients with
    sarcomas is still being refined.9 Chest CT and bone
    scan are also vital staging studies to assess for metastatic disease. Although gross metastases are evident in
    10% to 20% of cases, all patients should be assumed to
    have micrometastasis. Biopsy and treatment should be
    performed at a center with experience caring for musculoskeletal malignancy to optimize diagnostic accuracy and appropriate treatment. Surgical resection and
    reconstruction typically occurs after two to three cycles
    of chemotherapy. Neoadjuvant chemotherapeutic protocols have increased 5-year survival rates to almost
    80% at multiple centers in patients with nonmetastatic
    disease and 10% to 20% with metastatic disease.10
    Poor prognostic factors include metastatic disease at
    presentation, poor response to chemotherapy (less than
    90% necrosis of resected tumor), axial location, large
    tumor size, pathologic fracture, and elevated alkaline

    827

    Section 6: Pediatrics

    is performed at the base with resection of the periosteum and perichondrium.13 Care of shortened and deformed limbs in some patients with multiple hereditary
    exostosis may require osteotomy, growth arrest, guided
    growth, or limb lengthening. It is important that patients are aware of the risk of malignant transformation
    (less than 1% for solitary lesions and 3% for multiple
    lesions). This occurs in mature patients, and signs include worsening pain, continued growth after skeletal
    maturity, and a thickened cartilage cap (>1.5 cm).

    Enchondroma

    Figure 4

    A, Coronal T2-weighted MRI of the femur of a


    13-year-old girl with thigh pain, illustrating Ewing sarcoma involving the entire femur. The patient was noted to have metastatic disease at
    presentation, which worsens her prognosis. B,
    Short-tau inversion recovery sequence MRI of
    the same patient showing a large soft-tissue
    mass characteristic of patients with Ewing
    sarcoma.

    Enchondroma is a benign tumor of hyaline cartilage


    that typically involves the diaphysis of the long bones
    and is commonly seen in the hand. These can be solitary lesions or multiple enchondromatosis in two genetic conditions. Ollier disease presents with multiple
    enchondromas in the metaphyses of multiple bones in
    the upper and lower extremities. Affected individuals
    can have limb deformity, shortening, intracranial lesions, and overall short stature. Maffucci syndrome
    consists of similar findings as well as cutaneous hemangioma. Histologically, biopsied tissue is similar to hyaline cartilage except slightly more cellular with atypia
    and pleomorphism. Limb deformities may require similar procedures used in multiple hereditary exostosis.
    The risk of malignant transformation is 1% to 3% in
    Ollier disease, but increased in Maffucci syndrome,
    with an increased incidence of nonskeletal malignancy.

    Chondroblastoma
    hydrogenase despite treatment, large tumor size, and
    pelvic location.

    Cartilage Tumors

    Osteochondroma

    6: Pediatrics

    Osteochondroma (exostosis) is a benign tumor most


    commonly occurring in the metaphyses of the tibia and
    femur around the knee. However, the lesions are seen
    in almost any bone and two patterns of involvement,
    solitary and multiple, are seen. The lesions may limit
    range of motion depending on location or cause pain
    by mechanical irritation of the overlying soft tissues, or
    rarely, compression of adjacent neurovascular structures. Multiple hereditary exostosis is an autosomal
    dominant condition with variable penetrance. In addition to the presence of multiple exostoses, affected patients may have short stature, limb-length discrepancy,
    limb angulation, or bowing. The multiple form is
    linked to mutations in the EXT 1 and EXT 2 tumor
    suppressor genes that code for glycoproteins involved
    in the regulation of endochondral ossification. The true
    incidence of spinal lesions that impinge on neural structures is unknown. Certainly any patient with neurologic signs or symptoms should be evaluated with advanced imaging. Surgical treatment of patients may
    include complete excision of symptomatic lesions; this
    828

    Orthopaedic Knowledge Update 10

    Chondroblastoma is a rare epiphyseal tumor in the


    knee, shoulder, and hip seen in the second decade of
    life. Radiographs show a well-circumscribed epiphyseal
    lesion possibly with stippled calcification. MRI reveals
    significant reactive edema, and bone scan shows increased uptake. Complete resection is difficult, and intralesional resection is often unsuccessful, resulting in a
    20% rate of recurrence. Significant joint deformity and
    pain may result from the tumor as well as the treatment. Rarely, pulmonary metastasis may occur.

    Fibrous Lesions

    Fibrous Dysplasia
    Fibrous dysplasia is a benign fibro-osseous process that
    can occur in one (monostotic) or multiple (polyostotic)
    bones. The polyostotic form usually involves half of the
    skeleton and may be associated with McCune-Albright
    syndrome (fibrous dysplasia, pigmented skin lesions,
    and endocrinopathy). It is usually caused by a postzygotic mutation in the gene GNAS1 (guanine nucleotidebinding protein, alpha stimulating activity polypeptide)
    on chromosome 20q13.14 This results in osteoblastic
    differentiation defects and increased bone resorption.
    Radiographs reveal mild expansion of the bone, thinning of the cortex, endosteal scalloping, and a ground
    glass appearance of the matrix. Progressive deformity
    can be seen with large lesions, particularly proximal

    2011 American Academy of Orthopaedic Surgeons

    Chapter 64: Pediatric Tumors and Hematologic Diseases

    Figure 5

    Radiograph of the tibia of a 5-year-old boy who


    sprained his ankle showing a well-corticated
    metaphyseal lesion consistent with a nonossifying fibroma of bone.

    femoral varus or shepherds crook deformity. Larger lesions at risk for fracture are best treated with curettage,
    bone grafting, and prophylactic fixation. Bisphosphonates have been used in the treatment of polyostotic fibrous dysplasia to relieve bone pain, improve lytic lesions, reduce fracture rates, and increase radiographic
    healing.15 Calcium, vitamin D, and phosphorus supplements may be useful in some patients.

    Nonossifying Fibroma

    Osteofibrous Dysplasia
    Osteofibrous dysplasia (Campanacci disease) is a fibroosseous condition of the anterior tibial diaphysis that is
    usually diagnosed before age 10 years. Multiple lesions
    in the tibia may cause progressive bowing (Figure 6),

    2011 American Academy of Orthopaedic Surgeons

    Lateral radiograph of the tibia of a 3-year-old


    boy with osteofibrous dysplasia.

    pathologic fracture, and/or pain. Radiographs reveal


    the cortex to be focally expanded with a radiolucent
    lobular pattern and a reactive rim of bone around the
    periphery. Because of the high rate of recurrence, en
    bloc resection of a segment of bone is required with reconstruction.17 The aggressive form is difficult to differentiate from malignant adamantinoma, and requires
    surgical treatment. This malignant tumor presents with
    a larger, more painful lesion that is usually found in
    adults, in whom it can metastasize to the lungs. It usually has soft-tissue extension, intramedullary involvement, and a periosteal reaction in the absence of pathologic fracture.18

    Eosinophilic Granuloma
    Isolated eosinophilic granuloma is the most benign
    form of histiocytosis X and commonly occurs in children but can occur at any age. Letterer-Siwe disease is a
    fulminant form that occurs in children younger than 3
    years; it usually is lethal. Hand-Christian-Schller disease is usually seen in children older than 3 years with
    disseminated histiocytosis X and presents with the triad
    of exopthalmos, diabetes insipidus, and skull lesions.
    The most common sites of location for all eosinophilic
    granulomas are the skull, mandible, pelvis, spine, ribs,
    and long bones. Pathologic fractures can occur through
    the lesions. The radiographic appearance differs by location, is nonspecific, and simulates other lesions such
    as osteomyelitis, leukemia, lymphoma, fibrous dysplasia, or Ewing sarcoma. Commonly, diaphyseal lesions
    have a lytic, punched-out appearance with periosteal
    new bone formation or intracortical tunneling. Metaphyseal lesions extend up to but not through the

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    Nonossifying fibroma of bone is a common incidental


    finding. The most common locations are the distal femoral metaphysis followed by the proximal tibial and
    distal tibial metaphyses (Figure 5). Radiographs characterize the lesions as metaphyseal, eccentric, lytic, and
    septated. The cortex can be thinned and there is a rim
    of bone outlining the lesion. The disorder is benign and
    most often asymptomatic. Larger lesions may result in
    pain or a fracture requiring treatment. Treatment is
    usually observation because most go on to spontaneous
    regression starting at the end of adolescence. Curettage
    and prophylactic fixation may be necessary for large
    symptomatic lesions at risk for fracture. Children who
    present with nonossifying fibromas at numerous sites
    may have Jaffe-Campanacci syndrome.16 These patients
    may have systemic and dermal findings similar to neurofibromatosis 1.

    Figure 6

    829

    Section 6: Pediatrics

    growth plate. In the spine, the vertebral body is affected, resulting in the characteristic vertebra plana or
    coin-on-end appearance. Treatment can include observation for the isolated small lesion or vertebral lesions
    without neurologic involvement. Intralesional treatment with steroids, curettage, radiofrequency ablation,19 or low-dose radiation has been reported.

    Soft-Tissue Tumors

    Vascular Malformations
    This highly variable group of lesions is the most common type of benign soft-tissue tumor. They vary in size,
    depth, and type of vascular involvement. Large arterial,
    venous, or lymphatic malformations continue to grow
    with the patient. They may be treated by resection, embolization, or sclerotherapy if they become symptomatic. Surgery is often challenging with the potential
    for large amounts of blood loss and a high rate of recurrence. Local morbidity is also seen from resection of
    lesions that are infiltrative.

    Lipoma
    Although very common overall, these lesions are less
    often seen in children. Lipoblastoma must be considered in the differential diagnosis for infantile fatty tumors. These lesions have an increased recurrence rate
    and cellularity compared to lipoma. Treatment options
    include observation for asymptomatic lesions and marginal excision.

    Rhabdomyosarcoma

    6: Pediatrics

    Embryonal and alveolar subtypes of rhabdomyosarcoma occur in the extremities and are the most common soft-tissue malignancy in children. Patients with
    the embryonal subtype are usually younger than 10
    years, whereas those with the alveolar type are adolescents. Alveolar rhabdomyosarcoma has chromosomal
    translocations: t:(2;13) or t:(1;13). Those with translocation from chromosome 2 usually have a worse prognosis. Patients typically present with a history of a
    growing soft-tissue mass seen on MRI with increased
    signal with gadolinium infusion. Ultrasound may be
    helpful to discern solid from cystic lesions and also to
    evaluate for blood flow. Positron emission tomography
    for staging and surveillance is being used more frequently. Staging by chest CT, bone marrow biopsy, and
    bone scan is also necessary because 20% of patients
    present with gross metastatic disease (lung, bone marrow, lymphatic tissue, and skeletal tissue). Sentinel
    lymph node sampling is often necessary. Effective chemotherapeutic regimens have improved overall survival
    rates from 25% to 70%. Neoadjuvant chemotherapy is
    used in both subtypes, with the addition of radiation
    for the alveolar subtype. The 5-year survival is worse
    overall in alveolar rhabdomyosarcoma (60% survival
    for nonmetastatic and 30% for metastatic disease).
    Within this subtype, large tumor size, incomplete resec830

    Orthopaedic Knowledge Update 10

    tion, and regional lymph node involvement are all poor


    prognostic signs.20

    Synovial Sarcoma
    Synovial sarcoma is the second most common pediatric
    soft-tissue malignancy. It is a lesion that is rarely intraarticular, and the actual tissue of origin is unclear. The
    tumor may grow undetected for many years and present with an indolent course. Pulmonary metastases and
    nodal spread are common. A specific translocation,
    t:(X;18), has been identified that results in several gene
    products, including the SYT-SSX1 fusion protein,
    which also is a poor prognostic sign. Treatment is wide
    excision with adjuvant radiation. The efficacy and role
    of chemotherapy is still being evaluated.21

    Infantile Fibrosarcoma
    Infantile fibrosarcoma is a very rare but unique tumor
    of children. It frequently has a striking presentation at
    birth and is locally aggressive but rarely metastatic. It
    also has a specific translocation: t:(12;15). Neoadjuvant chemotherapy has been helpful. Complete surgical
    excision can be curative, but some nonresectable
    masses may be successfully treated with chemotherapy
    alone.

    Hematologic Diseases

    Hemophilia
    Hemophilia comprises a group of bleeding disorders in
    which the most common forms are due to a deficiency
    in factor VIII (hemophilia A) or factor IX (hemophilia
    B) and are inherited in a sex-linked recessive pattern.
    The role of the orthopaedist is to assist the hematologist in the management of muscular hematomas,
    hemarthroses, and hemophilic joint disease.
    Muscular hematomas are treated with clotting factor
    replacement, prevention of contractures, and rehabilitation. Patients may present with hip pain and a femoral
    nerve palsy indicative of an iliopsoas hematoma. Diagnosis can be confirmed with MRI, CT, or ultrasonography. Pseudotumors can develop from recurrent bleeding
    into the muscle or bone and are managed with a combination of factor replacement, radiation therapy,
    and/or surgical excision.
    Hemarthroses are managed conservatively with immediate factor replacement up to 100% for a week to
    10 days. Aspiration is only necessary for patients with
    vascular compromise or severe pain. Factor replacement is required before any invasive procedure. Affected joints are splinted for 1 to 2 days, after which
    therapy is started to prevent contractures. Recurrent
    hemarthroses can lead to hemophilic joint disease. Iron
    perpetuates a chronic inflammatory state via changes at
    the molecular level and release of cytokines.22 MRI can
    be used to identify the early changes seen with hemophilic joint disease.23 Isotopic, surgical, or chemical
    synovectomy can provide relief from repeated joint
    bleeds.24

    2011 American Academy of Orthopaedic Surgeons

    Chapter 64: Pediatric Tumors and Hematologic Diseases

    Sickle Cell Disease


    Sickle cell disease is a genetic disorder with an abnormal globin chain of hemoglobin resulting in deformation of red blood cells under low oxygen tension.
    About 2 million Americans (or 1 in 12 African Americans) carry the sickle cell gene. Sickle cell anemia is
    seen when two alleles of the abnormal hemoglobin S
    gene are present. Patients with only a single copy of the
    gene (HbAS) have sickle cell trait and are generally
    asymptomatic but may carry a higher risk of exerciserelated sudden death.25 Rarer forms of sickle cell disease include sickle-hemoglobin C disease (HbSC), sickle
    -plus-thalassemia (HbS/+) and sickle -zerothalassemia (HbS/0).
    The first manifestation of the disease may be dactylitis (hand-foot syndrome) occurring around age 6
    months as fetal hemoglobin is diminishing and hemoglobin S reaches pathologic significance. Early presentation (before age 6 months) may predict a more severe
    clinical course.26 Patients with sickle cell anemia are
    susceptible to infections due to hyposplenia, intestinal
    infarcts, poor opsonization of polysaccharide antigens
    due to impaired complement activity, and sluggish microcirculation. Patients with sickle cell anemia frequently present with bone and/or joint pain with signs
    that may be confused with osteoarticular infection.
    Bone infarction (much more common) and infections are similar in presentation consisting of fever, tenderness to palpation, bone pain, swelling, and an elevated erythrocyte sedimentation rate (ESR) and
    C-reactive protein (CRP) level. Osteomyelitis should be
    suspected in patients who appear to have sepsis with fever higher than 38.2C and a white blood cell count
    greater than 15,000 cells/mm3 or who do not respond
    after 24 to 48 hours to proper hydration and pain management.27 Bone scan, bone marrow scan, and MRI
    may help differentiate between these two conditions.
    Staphylococcus aureus is the most common organism
    overall, although Salmonella is also very common and
    may be more prevalent in certain areas. Treatment consists of prompt abscess drainage followed by prolonged
    antibiotic treatment.
    Osteonecrosis of the femoral epiphysis can occur
    and frequently is bilateral (50%). Initial treatment consists of crutch ambulation, partial weight bearing, and
    range of motion. Outcome is dependent on the level of
    involvement and age of the patient.

    Acute lymphoblastic leukemia represents 80% of all


    leukemias in children and is the most common cancer
    seen; half of these patients present initially with musculoskeletal complaints. Symptoms include multiple joint
    complaints, migratory bone pain, limp, back pain, fatigue, flu-like illness, fever, and easy bruising.28 Early
    diagnosis is essential and significantly decreases morbidity and mortality. Although early in the disease
    course laboratory values may be normal, later abnormalities include anemia, thrombocytopenia, increased
    lymphoblasts, and an elevated ESR. Radiographic

    2011 American Academy of Orthopaedic Surgeons

    Pediatric Musculoskeletal Infections


    Musculoskeletal infections in children are potentially
    life-threatening processes if left untreated. The sequelae
    of untreated infection include joint destruction, dislocation, growth arrest, and fracture.30-32 Many children ultimately diagnosed with a musculoskeletal infection
    will present with a history of an upper respiratory illness or trauma. Thus, a high index of suspicion is necessary to properly evaluate and treat these infections in
    a timely manner.

    Resistant Bacteria
    Methicillin-resistant S aureus (MRSA) has changed the
    landscape of pediatric musculoskeletal infections. In recent reports, 37% to 74% of community-acquired S
    aureus infections are MRSA (CA-MRSA).33,34 CAMRSA infections are associated with longer hospital
    stays, a higher rate of subperiosteal abscess formation,
    more surgical procedures, and the need for prolonged
    antibiotics. In addition, isolates with the PantonValentine-Leukocidin gene cause more destructive, lifethreatening infections with septic thromboemboli, venous thrombosis, and necrotic pneumonia.35
    The local prevalence of CA-MRSA must not be overlooked because many of the musculoskeletal infections
    are culture negative; thus, empiric coverage for MRSA
    might be appropriate. Treatment of hospital-acquired
    MRSA and CA-MRSA also differ. Therapy for
    hospital-acquired MRSA may include vancomycin,
    daptomycin, or linezolid; for CA-MRSA, the antibiotics
    trimethoprim-sulfamethoxazole and clindamycin are effective.

    6: Pediatrics

    Leukemia

    changes, seen in 40% of patients, include osteolysis,


    metaphyseal bands, osteopenia, osteosclerosis, a permeative pattern, pathologic fractures, and periosteal reaction.29 The diagnosis is made via peripheral smear
    and/or bone marrow biopsy. Patients are treated with
    chemotherapy.
    In patients with acute lymphoblastic leukemia, the
    incidence of skeletal complications is approximately
    30% over a 5-year period during maintenance therapy.
    Patients may present with chemotherapy-induced neuropathy that can be treated with gabapentin and bracing. Patients treated with high-dose steroids may present to the orthopaedist with secondary osteonecrosis.
    Vertebral compression fractures and other pathologic
    fractures can occur as a result of the disease or due to
    the osteopenia associated with treatment. Bisphosphonate use has shown some promise in the management
    of the diffuse bone loss and the pain associated with
    vertebral compression fractures.

    Osteomyelitis
    The frequency of osteomyelitis is dependent on geographic location. Some reports in colder climates reveal
    a rate of 13 cases per 100,000, whereas in warmer climates the rate is closer to 1 case in 5,000 and has been
    increasing.36,37 Acute hematogenous infection is the
    most common type of osteomyelitis. The most frequent

    Orthopaedic Knowledge Update 10

    831

    Section 6: Pediatrics

    Figure 7

    AP (A) and lateral (B) radiographs of the femur of a 14-year-old boy with fever and leg pain. No radiographic evidence of infection is present. C, Axial T2-weighted MRI of the femur of the same child showing a subperiosteal
    abscess that was surgically drained. Cultures subsequently grew MRSA.

    6: Pediatrics

    locations, in descending order, are the distal femur, pelvis, tibia, calcaneus, and humerus. S aureus is the most
    common infecting organism, followed by group A
    streptococcus and Streptococcus pneumoniae.
    Many families will report a traumatic event before
    the onset of pain. A history of fever and inability to
    bear weight are common. In preambulatory children,
    pseudoparalysis may occur. Laboratory studies should
    include measurement of white blood cell count, CRP
    (peaks within a few days), and ESR (peaks at 3 to 5
    days). Blood cultures may be helpful, but are only positive in one third of patients. Imaging of the suspected
    area is crucial in confirming this diagnosis. Plain radiographs may show periosteal reaction and bone changes
    but lag behind the clinical findings. MRI (Figure 7) is
    the gold standard because it not only confirms the intraosseous infection but also delineates abscess formation, thus guiding surgical intervention in difficult areas
    such as the pelvis.38 Additional studies such as color
    power Doppler sonography may assist in diagnosing
    deep venous thrombosis, found in older children with
    CA-MRSA.35
    Identification of an organism and its antibiotic sensitivity are the mainstays of treatment with parenteral
    antibiotic therapy. In cases where no bacteria are isolated, local prevalence of resistant bacteria may influence antibiotic choice. The decision to switch to oral
    antibiotics should be based on clinical and laboratory
    improvement of the CRP and ESR. Surgical dbridement is indicated if abscess or sequestrum is noted. Persistently elevated CRP and continued fevers or symptoms despite treatment require evaluation for septic
    joint or repeat MRI to rule out reformation of abscess.

    Septic Arthritis
    Septic arthritis in children presents in a manner similar
    to that of acute osteomyelitis. The patient can be febrile
    832

    Orthopaedic Knowledge Update 10

    and be unable to bear weight on the affected extremity.


    Physical examination reveals a tender, erythematous,
    swollen joint that is painful to range of motion. Septic
    arthritis is common in the knee (35%), the hip (35%),
    the shoulder/elbow/wrist (15%), or ankle (10%). If the
    hip is affected, the process must be differentiated from
    other primary hip conditions such as transient synovitis. Ultrasound examination can confirm the presence
    of effusion at the hip.
    Diagnostic testing should evaluate CRP, ESR, and
    white blood cell count. Specifically, if a child is febrile,
    is not bearing weight, and has an ESR greater than 40
    mm/h, a white blood cell count greater than 12,000
    cells/mm3, and a CRP greater than 2 mg/dL, the likelihood of septic arthritis is 98%.39,40
    Other laboratory tests to consider include a rapid
    strep test, antistreptolysin O, Lyme antibodies, gonococcal swabs of mucosal surfaces, and a tuberculosis
    test. Radiographs may delineate the presence of associated osteomyelitis. However, aspiration of the affected
    joint for fluid examination and culture is the gold standard.
    Unfortunately, culture-negative aspirations are common. Placing the aspirate into blood culture bottles
    may increase the diagnostic yield by allowing growth of
    both common bacteria (such as S aureus) and uncommon bacteria (such as Kingella kingae).
    Timely surgical drainage of pus followed by parenteral antibiotics is essential to avoid joint destruction because of the presence of proteolytic enzymes in both the
    synovium and bacterium. Arthroscopic and open lavage techniques are equally effective in cases of early
    joint infection. Drainage tubes are essential following
    either technique. Antibiotic duration is generally 3 to 4
    weeks but may be longer if concomitant osteomyelitis
    is present (found in 21% of patients).41

    2011 American Academy of Orthopaedic Surgeons

    Chapter 64: Pediatric Tumors and Hematologic Diseases

    Pyomyositis
    Recent attention has been paid to CA-MRSA causing
    nontropical pyomyositis in immunocompetent children.42,43 Compartment syndrome, septic pulmonary emboli, and toxic shock have all been reported. Intensive
    medical management including respiratory support may
    also be required. MRI will confirm the diagnosis. If abscess formation is present, surgical or CT-guided drainage coupled with parenteral antibiotics is suggested.

    The authors concluded that the rate of healing of simple


    bone cysts was low following injection of either bone
    marrow (23%) or methylprednisolone (42%). Healing
    rates were superior following injection of methylprednisone.
    Docquier PL, Delloye C: Treatment of aneurysmal bone
    cysts by introduction of demineralized bone and autogenous bone marrow. J Bone Joint Surg Am 2005;87(10):
    2253-2258.

    9.

    Vlker T, Denecke T, Steffen I, et al: Positron emission


    tomography for staging of pediatric sarcoma patients:
    Results of a prospective multicenter trial. J Clin Oncol
    2007;25(34):5435-5441.
    This prospective multicenter study compares the efficacy
    of positron emission tomographic scanning and conventional imaging modalities (MRI, CT, bone scan, and ultrasound) in 46 pediatric patients with histologically
    proven sarcoma.

    10.

    Bacci G, Longhi A, Bertoni F, et al: Bone metastases in


    osteosarcoma patients treated with neoadjuvant or adjuvant chemotherapy: The Rizzoli experience in 52 patients. Acta Orthop 2006;77(6):938-943.

    11.

    Gulley ML, Kaiser-Rogers KA: A rational approach to


    genetic testing for sarcoma. Diagn Mol Pathol 2009;
    18(1):1-10.
    This article is a summary of the current state of the clinical use of molecular testing in the evaluation of skeletal
    sarcoma.

    12.

    Bacci G, Longhi A, Ferrari S, Mercuri M, Versari M,


    Bertoni F: Prognostic factors in non-metastatic Ewings
    sarcoma tumor of bone: An analysis of 579 patients
    treated at a single institution with adjuvant or neoadjuvant chemotherapy between 1972 and 1998. Acta Oncol 2006;45(4):469-475.

    13.

    Stieber JR, Dormans JP: Manifestations of hereditary


    multiple exostoses. J Am Acad Orthop Surg 2005;13(2):
    110-120.

    14.

    Weinstein LS: G(s)alpha mutations in fibrous dysplasia


    and McCune-Albright syndrome. J Bone Miner Res
    2006;21(suppl 2):120-124.

    15.

    Chapurlat R: Current pharmacological treatment for fibrous dysplasia and perspectives for the future.
    Joint Bone Spine 2005;72(3):196-198.

    16.

    Mankin HJ, Trahan CA, Fondren G, Mankin CJ: Nonossifying fibroma, fibrous cortical defect and JaffeCampanacci syndrome: A biologic and clinical review.
    Chir Organi Mov 2009;93(1):1-7.
    The authors present a review of nonossifying fibroma
    and differential diagnosis.

    17.

    Lee RS, Weitzel S, Eastwood DM, et al: Osteofibrous


    dysplasia of the tibia: Is there a need for a radical surgical approach? J Bone Joint Surg Br 2006;88(5):658664.

    Annotated References
    1.

    Kneisl JS, Simon MA: Medical management compared


    with operative treatment for osteoid-osteoma. J Bone
    Joint Surg Am 1992;74(2):179-185.

    2.

    Moser T, Giacomelli MC, Clavert JM, Buy X, Dietemann JL, Gangi A: Image-guided laser ablation of osteoid osteoma in pediatric patients. J Pediatr Orthop
    2008;28(2):265-270.
    This article is a retrospective review of 68 pediatric patients with osteoid osteoma treated by image-guided laser ablation. The overall success rate was 98%, reported
    at mean follow-up of 83 months. Seven patients required two procedures. Level of evidence: IV.

    3.

    Lucas DR, Unni KK, McLeod RA, OConnor MI, Sim


    FH: Osteoblastoma: clinicopathologic study of 306
    cases. Hum Pathol 1994;25(2):117-134.

    4.

    Arkader A, Dormans JP: Osteoblastoma in the skeletally immature. J Pediatr Orthop 2008;28(5):555-560.
    The authors present the first report of osteoblastoma in
    children. Also included is a four-step approach to treatment: curettage, high-speed burring, electrocautery, and
    phenol, a regimen noted to be successful in 16 of 17 patients. Level of evidence: IV.

    5.

    6.

    7.

    Thawrani D, Thai CC, Welch RD, Copley L, Johnston


    CE: Successful treatment of unicameral bone cyst by
    single percutaneous injection of alpha-BSM. J Pediatr
    Orthop 2009;29(5):511-517.
    This article evaluated a single injection of -BSM for
    UBC.
    Sung AD, Anderson ME, Zurakowski D, Hornicek FJ,
    Gebhardt MC: Unicameral bone cyst: A retrospective
    study of three surgical treatments. Clin Orthop Relat
    Res 2008;466(10):2519-2526.
    This article evaluated three different treatments (steroids, curettage and bone grafting, or a combination of
    steroids, demineralized bone matrix and bone marrow
    aspirate) and found that curettage was associated with
    the lowest rate of posttreatment pathologic fractures
    and the highest rate of pain and other complications.
    Wright JG, Yandow S, Donaldson S, Marley L; Simple
    Bone Cyst Trial Group: A randomized clinical trial comparing intralesional bone marrow and steroid injections
    for simple bone cysts. J Bone Joint Surg Am 2008;90(4):
    722-730.

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    6: Pediatrics

    8.

    833

    Section 6: Pediatrics

    18.

    19.

    20.

    21.

    22.

    23.

    6: Pediatrics

    24.

    Khanna M, Delaney D, Tirabosco R, Saifuddin A: Osteofibrous dysplasia, osteofibrous dysplasia-like adamantinoma and adamantinoma: Correlation of radiological imaging features with surgical histology and
    assessment of the use of radiology in contributing to
    needle biopsy diagnosis. Skeletal Radiol 2008;37(12):
    1077-1084.
    The aim of this study was to correlate the imaging features with surgical histology for tibial osteofibrous dysplasia, osteofibrous dysplasia-like adamantinoma, and
    classic adamantinoma.

    dactylitis associated with the occurrence of severe events


    in children with sickle cell anaemia. The Paediatric Cohort of Guadeloupe (1984-99). Paediatr Perinat Epidemiol 2006;20(1):59-66.
    27.

    Berger E, Saunders N, Wang L, Friedman JN: Sickle cell


    disease in children: Differentiating osteomyelitis from
    vaso-occlusive crisis. Arch Pediatr Adolesc Med 2009;
    163(3):251-255.
    Multivariate logistic regression showed that the significant predictors of osteomyelitis in sickle cell disease were
    duration of fever (odds ratio, 1.8; 95% confidence interval, 1.2-2.6) and pain (1.2; 1.0-1.4) before presentation
    and swelling of the affected limb (8.4; 3.5-20.0).

    28.

    Sinigaglia R, Gigante C, Bisinella G, Varotto S, Zanesco


    L, Turra S: Musculoskeletal manifestations in pediatric
    acute leukemia. J Pediatr Orthop 2008;28(1):20-28.
    This article emphasizes the frequent clinical (38.3%)
    and radiologic (40.2%) musculoskeletal manifestations
    of leukemia in children.

    29.

    Palmerini E, Staals EL, Alberghini M, et al: Synovial


    sarcoma: Retrospective analysis of 250 patients treated
    at a single institution. Cancer 2009;115(13):2988-2998.
    This review of 30 years of experience at the Rizzoli Institute includes pediatric patients and describes prognostic factors as well as results of treatment.

    Halton J, Gaboury I, Grant R, et al; Canadian STOPP


    Consortium: Advanced vertebral fracture among newly
    diagnosed children with acute lymphoblastic leukemia:
    Results of the Canadian Steroid-Associated Osteoporosis in the Pediatric Population (STOPP) research program. J Bone Miner Res 2009;24(7):1326-1334.
    The authors state that vertebral compression is an underrecognized complication of newly diagnosed acute
    lymphoblastic leukemia (found in 16%).

    30.

    Valentino LA, Hakobyan N, Rodriguez N, Hoots WK:


    Pathogenesis of haemophilic synovitis: Experimental
    studies on blood-induced joint damage. Haemophilia
    2007;13(suppl 3):10-13.
    This article discusses three cellular regulators (p53, p21
    and TRAIL) induced in synovial tissue that are important for iron metabolism.

    Saisu T, Kawashima A, Kamegaya M, Mikasa M, Moriishi J, Moriya H: Humeral shortening and inferior subluxation as sequelae of septic arthritis of the shoulder in
    neonates and infants. J Bone Joint Surg Am 2007;89(8):
    1784-1793.
    The consequences of delayed treatment of septic shoulder are discussed.

    31.

    Forlin E, Milani C: Sequelae of septic arthritis of the hip


    in children: A new classification and a review of 41
    hips. J Pediatr Orthop 2008;28(5):524-528.
    The sequelae of septic hip are discussed.

    32.

    Wada A, Fujii T, Takamura K, Yanagida H, Urano N,


    Surijamorn P: Operative reconstruction of the severe sequelae of infantile septic arthritis of the hip. J Pediatr
    Orthop 2007;27(8):910-914.
    This article focuses on what can be done once the hip
    has been altered by the sepsis.

    Corby RR, Stacy GS, Peabody TD, Dixon LB: Radiofrequency ablation of solitary eosinophilic granuloma of
    bone. AJR Am J Roentgenol 2008;190(6):1492-1494.
    This article describes the novel application of radiofrequency ablation for the treatment of two cases of solitary eosinophilic granuloma of the bone.
    Ferrari A, Miceli R, Meazza C, et al: Soft tissue sarcomas of childhood and adolescence: The prognostic role
    of tumor size in relation to patient body size. J Clin Oncol 2009;27(3):371-376.
    This case series of 553 pediatric patients with soft-tissue
    sarcoma explores the relationship of tumor size relative
    to patient size in staging and prognosis.

    Bossard D, Carrillon Y, Stieltjes N, et al: Management


    of haemophilic arthropathy. Haemophilia 2008;
    14(suppl 4):11-19.
    The treatment options for patients with hemophilic arthropathy are reviewed.
    Rodriguez-Merchan EC, Quintana M, De la CorteRodriguez H, Coya J: Radioactive synoviorthesis for the
    treatment of haemophilic synovitis. Haemophilia 2007;
    13(suppl 3):32-37.
    The procedure should be performed as soon as possible
    to minimize the degree of articular cartilage damage,
    which based on many studies is irreversible.

    25.

    Kark JA, Posey DM, Schumacher HR, Ruehle CJ:


    Sickle-cell trait as a risk factor for sudden death in physical training. N Engl J Med 1987;317(13):781-787.

    26.

    Foucan L, Ekouevi D, Etienne-Julan M, Salmi LR, Diara JP; Paediatric Cohort of Guadeloupe: Early onset

    33. Mongkolrattanothai K, Aldag JC, Mankin P, Gray BM:


    Epidemiology of community-onset Staphylococcus aureus infections in pediatric patients: An experience at a
    Childrens Hospital in central Illinois. BMC Infect Dis
    2009;9:112.
    The changing epidemiology of CA-MRSA is reviewed.
    34.

    834

    Orthopaedic Knowledge Update 10

    Deresinski S: Methicillin-resistant Staphylococcus aureus: An evolutionary, epidemiologic, and therapeutic


    odyssey. Clin Infect Dis 2005;40(4):562-573.

    2011 American Academy of Orthopaedic Surgeons

    Chapter 64: Pediatric Tumors and Hematologic Diseases

    35.

    Hollmig ST, Copley LA, Browne RH, Grande LM, Wilson PL: Deep venous thrombosis associated with osteomyelitis in children. J Bone Joint Surg Am 2007;89(7):
    1517-1523.
    A sequela of MRSA infections is summarized.

    40.

    Kocher MS, Mandiga R, Zurakowski D, Barnewolt C,


    Kasser JR: Validation of a clinical prediction rule for the
    differentiation between septic arthritis and transient
    synovitis of the hip in children. J Bone Joint Surg Am
    2004;86(8):1629-1635.

    36.

    Gafur OA, Copley LA, Hollmig ST, Browne RH,


    Thornton LA, Crawford SE: The impact of the current
    epidemiology of pediatric musculoskeletal infection on
    evaluation and treatment guidelines. J Pediatr Orthop
    2008;28(7):777-785.
    The authors present an overall review of pediatric infections and MRSA management.

    41.

    Lavy CB, Thyoka M: For how long should antibiotics


    be given in acute paediatric septic arthritis? A prospective audit of 96 cases. Trop Doct 2007;37(4):195-197.

    37.

    38.

    39.

    Riise OR, Kirkhus E, Handeland KS, et al: Childhood


    osteomyelitis-incidence and differentiation from other
    acute onset musculoskeletal features in a populationbased study. BMC Pediatr 2008;8:45-55.
    The focus of this article is the epidemiology of osteomyelitis.
    Klein JD, Leach KA: Pediatric pelvic osteomyelitis. Clin
    Pediatr (Phila) 2007;46(9):787-790.
    The sometimes-hidden diagnosis of pediatric pelvic osteomyelitis is discussed.

    This is a larger study regarding the duration of antibiotics in osteomyelitis.


    42.

    Block AA, Marshall C, Ratcliffe A, Athan E: Staphylococcal pyomyositis in a temperate region: Epidemiology
    and modern management. Med J Aust 2008;189(6):
    323-325.
    This is a review of staphylococcal pyomyositis, a nowfrequent occurrence in nontropical climates.

    43.

    Ovadia D, Ezra E, Ben-Sira L, et al: Primary pyomyositis in children: A retrospective analysis of 11 cases. J Pediatr Orthop B 2007;16(2):153-159.
    This is a small retrospective analysis of pyomyositis.

    Caird MS, Flynn JM, Leung YL, Millman JE, DItalia


    JG, Dormans JP: Factors distinguishing septic arthritis
    from transient synovitis of the hip in children: A prospective study. J Bone Joint Surg Am 2006;88(6):12511257.

    6: Pediatrics

    2011 American Academy of Orthopaedic Surgeons

    Orthopaedic Knowledge Update 10

    835

    Index
    Page numbers with f indicate figures
    Page numbers with t indicate tables

    A
    AAOS. See American Academy of
    Orthopaedic Surgeons
    AATB. See American Association of
    Tissue Banks
    Abbreviated Injury Scale (AIS), 129
    ABI. See Ankle-brachial index
    Ablation, percutaneous radiofrequency,
    102
    Absolute risk, 168
    Accessory navicular, 778
    ACDF. See Anterior cervical diskectomy
    and fusion
    Acetabular fracture, 379
    classification of, 386f
    complications with, 390391
    CT of, 91
    evaluation of, 386387
    incidence of, 385386
    treatment of
    bleeding during, 387
    construct stability/supplementation
    in, 389
    dome impaction/arthroplasty in,
    390
    indications for, 387388
    initial management in, 386387
    new techniques in, 388389
    surgical approaches in, 388
    surgical timing in, 387
    types of, 386f
    Acetabular reconstruction
    cages in, 424
    hemispherical porous-coated
    components in, 424
    porous metallic components in, 424
    primary total hip arthroplasty for, 422
    revision total hip arthroplasty for,
    423424
    Achilles tendon
    lacerations of, 529
    pathologies of, 528
    Achondroplasia, 801
    AC joint. See Acromioclavicular joint
    ACL. See Anterior cruciate ligament
    Acromial fracture, 277
    Acromioclavicular joint (AC joint),
    318319
    Acromion process, 277
    Adolescent athletes. See Young athletes
    Advanced Trauma Life Support (ATLS),
    129
    Adverse events
    apologies for, 6
    communication of, 5, 112
    Age
    developmental dysplasia of the hip
    reduction and, 743
    osteoarthritis and, 24, 214
    spinal deformity and, 592593
    Wnt pathway and, 25

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 837

    AIS. See Abbreviated Injury Scale


    Allograft, 1415
    Alveolar rhabdomyosarcoma, 194t
    Alveolar soft-part sarcoma, 194t
    American Academy of Orthopaedic
    Surgeons (AAOS), 3, 138t, 139
    American Association of Tissue Banks
    (AATB), 15
    American Spinal Injury Association
    (ASIA), 573575, 574f
    Aminoglycosides, 50
    Amputation, lower extremity, 538539
    comorbidity management with,
    539541
    follow-up care after, 545
    indications for, 537
    knee salvage with, 537
    level of, 537538
    pain management with, 539
    phantom limb pain/sensation and,
    540t
    residual limb pain and, 541t
    patient education with, 543
    postoperative dressing of, 539
    preoperative management for, 537
    principles of, 53839
    prostheses for
    management of, 543
    prescription of, 544t
    training with, 545
    psychological management with,
    541542
    rehabilitation after, 543
    community reintegration in, 545
    equipment for, 544545
    mobility in, 544
    prosthetic, 545
    range of motion in, 544
    strengthening in, 544
    residual limb management after
    contracture prevention in, 542543
    edema control in, 542
    heterotopic ossification in, 543
    transfemoral, 538
    transtibial, 537
    Amputation, pediatric traumatic, 759
    Amyotrophic lateral sclerosis, 235236
    Amyotrophy, diabetic, 231
    Analgesics
    adjuvant, 263
    opioid, 263264
    Aneurysmal bone cyst, 194t, 554,
    826827
    Anisomelia, 770
    Ankle
    arthrodesis of, 525
    arthroplasty of, 524525
    cerebral palsy and, 815816
    injuries to, 523
    nerve pain with, 52930
    syndesmosis, 523
    ligamentous issues in, 529
    pain in
    nerve, 529530
    treatment of, 525

    reconstruction of, 523


    sprains of, young athletes with, 787
    Ankle-brachial index (ABI), 457
    Ankle fracture, 493. See also Tibial
    plafond fracture
    classification of, 494, 495f
    complications with, 498
    diabetic, 498499
    distal tibiofibular syndesmosis and,
    497
    evaluation of
    clinical, 493
    CT of, 92
    radiographic, 493494, 494f
    isolated medial malleolar fracture and,
    498
    outcomes of, 498
    posterior malleolus and, 497498
    types of
    pronation-abduction, 496497
    pronation-external rotation, 497
    supination-adduction, 496
    supination-eversion, 494496
    Ankylosing spondylitis, 218
    cervical spine trauma with, 635636
    diagnostic criteria for, 219t
    presentation of, 218219
    treatment of, 219
    Anterior cervical diskectomy and fusion
    (ACDF), 665
    Anterior cruciate ligament (ACL)
    function of, 453
    healing ability of, 43
    injuries to, 453454
    lateral meniscus tears as, 453
    young athletes with, 786, 787f
    nutrition of, 41
    reconstruction of
    failure rate of, 453454
    graft options for, 454
    postoperative protocol for, 454t
    Anterior distal tibial angle (ADTA), 764f
    Antibiotic bead pouch, 51, 51f
    Antibiotic therapy, 4950, 50t
    Anti-Nogo antibodies, 575t, 577
    Apert syndrome, 704, 705f
    Apical ectodermal ridge (AER), 697, 697f
    Apophysites, pelvic, 793
    Arthritis, 213. See also specific anatomic
    site; specific arthritis
    aging and, 2425
    prevalence of, 213
    radiography of, 86
    types of, 213
    Arthrodesis, ankle, 525
    Arthrogryposis, distal, 806807
    Arthrogryposis multiplex congenita,
    805806, 805f
    Arthropathy. See also Rotator cuff
    tear arthropathy; Seronegative
    spondyloarthropathy
    neuropathic, 87, 228229
    postoperative, 286
    pyrophosphate, 86
    radiography of, 8687

    Orthopaedic Knowledge Update 10

    837

    1/11/2011 2:21:51 PM

    Index
    Arthroplasty. See also Disk arthroplasty;
    Total hip arthroplasty; Total knee
    arthroplasty
    acetabular fracture treatment with, 390
    ankle, 524525
    biologic total shoulder, 288289
    cervical, 614615
    dome, 390
    facet, 668669
    femoral head osteonecrosis treatment
    with, 421422
    glenohumeral degenerative joint
    disease treatment with, 287289
    hemiarthroplasty, 287288
    patellofemoral, 473
    prosthetic joint, 254t
    proximal humerus fracture treatment
    with, 275276
    reverse, 276
    shoulder resurfacing, 287
    total joint, 73
    total shoulder, 289
    unicompartmental knee, 473
    Arthroscopy
    hip, 401, 416
    knee arthritis dbridement with,
    470471
    rotator cuff tear treatment with, 306
    shoulder instability repair with, 302
    Arthrosis. See Facet arthrosis;
    Pseudarthrosis
    Articular cartilage. See Cartilage
    Aseptic loosening, 7475
    ASIA. See American Spinal Injury
    Association
    Aspirin, 137, 139
    Athletes. See Throwing athletes; Young
    athletes
    Atlantoaxial instability, 722
    Atlantodens interval, 720t
    Atlas fracture
    management of, 630
    pediatric, 721
    ATLS. See Advanced Trauma Life
    Support
    Autogenous bone grafts, 14
    Autonomic neuropathy, 231
    Axial neck pain
    causes of, 611612, 611f, 612f
    evaluation of, 611612
    treatment of, 612613
    Azobactam, 50t
    Aztreonam, 50

    B
    Back pain, 719. See also Discogenic low
    back pain
    Bacteria
    biofilm of, 241242, 242f, 243f
    formation of, 242
    infection promoting properties of,
    243t
    host defense mechanisms and,
    242244

    838

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 838

    in operating room, 239


    osteomyelitis-causing, 244245
    septic arthritis-causing, 246
    Barlow sign, 739, 740f
    Baumann angle, 677f
    Bearing surfaces, 73
    alternative, 7679
    problems, 76
    for THA/TKA, 74t
    types of, 74t
    Beckwith-Wiedemann syndrome, 800
    Bench-top testing, 66
    finite element analysis in, 69f
    loading modes in, 6667
    loading patterns in, 67, 67f
    outcome parameters in, 6869
    specimens for, 66
    Biceps, pathology, 307t
    Biceps tendon, injuries to, 335
    Bilateral fracture, 131, 434, 634
    Biofilm, 241242, 242f, 243f
    formation of, 242
    infection promotion properties of,
    243t
    Biologic model of disease, 151152
    Biologic total shoulder arthroplasty,
    288289
    Biomarkers, in articular cartilage
    assessment, 28
    Biomechanics. See also Bench-top testing
    of bone, 59
    of coronoid fracture, 328329
    of intervertebral disk, 28f
    of joints, 6266
    numeric simulation of, 6970
    of shoulder, 299300
    testing in, 66, 7071
    tribology in, 75
    Biopsy
    of bone lesions, 197198
    fine-needle aspiration, 102
    percutaneous needle, 101102
    of soft-tissue masses, 205207
    Biopsychosocial model of disease, 152
    Bisphosphonates
    long-term side effects of, 14
    osteoporosis treatment with, 188189
    Blood
    donation of, 141
    loss of, in polytrauma, 129
    surgical management of, 140141
    algorithm for, 142f
    intraoperative, 142
    postoperative, 142143
    preoperative, 141
    Blount disease, 765766
    BMI. See Body mass index
    BMP. See Bone morphogenetic protein
    Body mass index (BMI), 215
    Bone. See also specific bones
    biomechanics of, 59
    as calcium reservoir, 186
    density of, 6162
    formation of, 181182
    hormonal regulation of, 186188

    ligaments inserted in, 41


    material properties of, 5961, 60t
    metabolism of, 13, 181, 190
    regenerative capacity of, 181
    remodeling of, 11
    resorption of, 190
    stress-strain curve of, 61f
    structural properties of, 6162
    tendon healing with, 42
    tendons inserted in, 41
    turnover of, 183184
    Bone bridge procedure, 538, 538f
    Bone cyst, 194t, 554, 826827
    Bone graft
    autogenous, 14
    calcaneal fracture treatment with, 511
    Bone healing
    biology of, 11
    enhancement of, 14
    allografts for, 1415
    autogenous bone grafts for, 14
    bone marrow aspirate for, 15
    extracorporeal shock wave therapy
    for, 1617
    low-intensity pulsed ultrasound for,
    1617
    synthetic bone substitutes for, 15
    factors affecting, 1314
    phases of
    hard callus, 13
    inflammatory, 11, 15
    soft callus, 1112
    remodeling in, 11, 13
    stem cells source during, 13
    Bone lesion
    benign aggressive, 198199
    benign latent, 198
    biopsy of, 197198
    clinical evaluation of, 195
    differential diagnosis of, 197t
    fractures and, 198, 199f
    imaging of, 195197
    CT in, 195
    MRI in, 196
    radiography in, 195, 196f
    presentation of, 195
    staging of, 197t
    Bone marrow aspiration, 15
    Bone morphogenetic protein (BMP), 13,
    15, 182
    Bone neoplasm, 199t, 200t
    categories of, 199t, 200t
    pathology of, 199t, 200t
    primary high-grade malignant,
    202203
    primary low-grade malignant, 202
    radiography of, 8788
    syndromes associated with, 194t
    Bone repair. See Bone healing
    Bone scan, 98
    of occult fractures, 98
    of osteomyelitis, 99
    of stress fractures, 9899
    of tumors, 100101
    Bone tumor, pediatric, 825, 827

    Orthopaedic Knowledge Update 10

    1/11/2011 2:21:52 PM

    Index
    Bony fusion, 93
    Botulinum toxin, 812
    Brachial plexus injury, 709710, 710t
    Brain, 225
    Bunionette deformity, 778779
    Burn, 4
    Burst fracture, 633

    C
    Calcaneal fracture, 508
    characteristics of, 508509
    CT of, 92
    imaging of, 509
    injury mechanism of, 508509
    pediatric, 759
    treatment of
    bone grafts in, 511
    decision making for, 509510
    results of, 511
    surgical, 510511
    Calcaneal tuberosity fracture, 511, 512f
    Calcaneovalgus, positional, 774
    Calcitonin
    bone regulation with, 187
    osteoporosis treatment with, 189
    Calcium
    bone as reservoir of, 186
    recommended daily intake of, 187t
    Camptodactyly, 705
    Camptomelic dysplasia, 801802
    Cancer
    clinical research related to, 195
    genetic predisposition to, 194t
    molecular biology of, 193, 195
    population science of, 193
    staging of, 197t
    Capitate, osteonecrosis of, 367
    Capitellum fracture, 329, 330f
    Care, patient-centered, 5
    Carpal bone
    fractures of, 353354, 690691
    instability of, 354
    Carpal tunnel syndrome, 367
    diabetes associated with, 231
    diagnosis of, 368t
    treatment of, 367369, 370t
    Carpectomy, 363
    Carpometacarpal joint, 353, 364365
    Cartilage
    articular
    assessment of, 2728
    cell division in, 25
    function of, 2324
    injury to, 2527, 460
    structure of, 2324
    avascularity of, 23
    composition of, 23
    extracellular matrix of, 23
    composition of, 24
    mechanical stress effect on, 24
    structure of, 23
    Cartilage tumor, pediatric, 828
    Case-control study, 170f, 171
    Cavus foot

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 839

    pediatric, 776777, 777f


    subtle, 527
    Cefazolin, 50t
    Cell
    division of, 25
    lymphocytic, 11
    Schwann, 225
    senescence of, 25
    stem
    mesenchymal, 43
    source of, 13
    white blood, 99
    Central nervous system, 225
    brain in, 225
    components of, 225226
    spinal cord in, 226
    Cephalomedullary nail, 70f
    Cephalosporin, 50
    Ceramic-on-ceramic prostheses, 74t,
    7778
    Ceramic-on-metal prostheses, 74t, 79
    Cerebral palsy (CP), 811812
    management of
    ankle, 815816
    botulinum toxin, 812
    foot, 815816
    hip, 814
    intrathecal baclofen in, 812
    knee, 814815
    medical, 812813
    obesity with, 812813
    scoliosis with, 813814
    Cervical disk arthroplasty (CDA),
    665668, 666f
    Cervical lordosis, 720t
    Cervical spine
    degenerative diseases of, 611
    pediatric fractures of, 721723
    radiography of, 85
    Cervical spine trauma
    ankylosing spine conditions with,
    635636
    assessment of, 623624
    classification of
    cervicothoracic junction injury,
    625626
    lower cervical spine injury, 625626
    upper cervical spine injury in,
    624625
    in elderly patients, 636
    epidemiology of, 623
    future trends in, 636
    management of
    acute steroid administration in, 627
    algorithm for, 628f
    atlas fractures and, 630
    bilateral facet fracture-dislocations
    and, 634
    burst-axial load injuries and, 633
    cervicothoracic junction injuries
    and, 635
    craniocervical injuries and, 630
    emergency, 626627
    extension injuries and, 634635
    flexion-teardrop injuries and, 634

    fracture-dislocations and, 635


    hangmans fracture and, 631
    lower cervical spine injuries and,
    631633
    nonsurgical, 628629
    odontoid fracture and, 630631
    reduction in, 627
    surgical principles in, 629
    transverse atlantal ligament injury
    and, 630
    unilateral facet fracture-dislocations
    and, 633634
    MRI of, 9698
    triage of, 624
    Cervical spondylolisthesis, 611f
    Cervical spondylotic myelopathy
    differential diagnosis of, 616
    patient history of, 616
    physical examination for, 616
    physical findings in, 617t
    radiographic evaluation of, 616617
    treatment of
    anterior decompression and fusion
    in, 618
    combined approaches in, 620
    laminectomy in, 618619
    laminoplasty in, 619620
    nonsurgical, 617618
    surgical, 618
    Cervical spondylotic radiculopathy
    evaluation of
    clinical, 613614
    radiographic, 614
    treatment of
    cervical arthroplasty in, 614615
    diskectomy in, 614615
    fusion in, 614615
    nonsurgical, 614
    posterior decompression in, 615
    surgical, 614615
    Cervicothoracic junction injury
    classification of, 625626
    management of, 635
    Cethrin, 575t, 577
    Charcot deformity, 530, 531f
    Charcot-Marie-Tooth disease, 234235,
    531, 819820
    clinical/orthopaedic features of, 812t
    genetic characteristics of, 812t
    management of, 820
    prevalence of, 812t
    Cheiralgia paresthetica, 371
    Chondroblastoma, 828
    Chondrocytes
    death of, 2526
    lifespan of, 25
    maturation of, 13
    Chondrosarcoma, 194t
    Chordoma, 556
    Chronic inflammatory demyelinating
    polyradiculopathy (CIDP), 232233
    CIDP. See Chronic inflammatory
    demyelinating polyradiculopathy
    Cierny-Mader staging system, 245t
    Ciprofloxacin, 50

    Orthopaedic Knowledge Update 10

    839

    1/11/2011 2:21:52 PM

    Index
    Claudication, 600t
    Clavicle fracture, 271, 675676
    classification of, 271
    distal third, 272273
    fixation complications with, 273
    medial third, 273
    midshaft, 271272
    ORIF for, 273
    presentation of, 271
    radiographic evaluation of, 271
    Claw toe, 527
    Clear cell sarcoma, 194t
    Cleft hand, 701, 702f
    Cleidocranial dysplasia, 183, 184f, 802
    Clinical practice guidelines
    for diaphyseal femoral fractures,
    pediatric, 162t
    for distal radial fracture treatment,
    357t, 358t
    evidence-based medicine, 161162,
    163t
    for glenohumeral arthritis treatment,
    292, 292t
    for knee osteoarthritis, 470t
    for work-related illness/injury, 153
    Clinodactyly, 705, 706f
    Closed fracture, 49, 131
    Closed reduction
    developmental dysplasia of the hip
    treatment with, 742
    radial neck fracture treatment with,
    682683
    supracondylar humerus fracture
    treatment with, 678
    Clubfoot, 772774
    Coagulation, 137
    cascading interactions with, 131
    pharmacologic prophylaxis for,
    137139
    in polytrauma, 132t
    Cohort study, 170171, 170f
    Collagen fibril, 23
    Combination fracture, 131
    Communication
    of adverse events, 5, 112
    educational, 112
    empathy in, 111112
    engagement in, 111
    enhancing, 5
    enlistment in, 112
    malpractice lawsuits caused by,
    110111, 111f
    orthopaedic surgeons training in,
    110111
    patient care affected by, 4
    skills, 111
    Compartment syndrome
    of foot, 508
    of hand, 359360
    neonatal, 711, 711f
    Compression neuropathy, 227228, 367
    electrodiagnostic studies of, 228229
    sites of, 367t
    Computed tomography (CT)
    of acetabular fractures, 91

    840

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 840

    advances in, 6, 89
    of ankle fractures, 92
    of bone lesions, 195
    of bony fusion failure, 93
    of calcaneal fractures, 92
    of elbow fractures, 92
    of extremity fractures, 9192
    of femoracetabular impingement,
    414415
    of hip arthritis, 414
    of osteolysis, 93
    of pelvic fractures, 91
    of postoperative complications, 9293
    of prostheses, 9293
    of spine fractures, 9091
    of thoracolumbar trauma, 642
    of tibial plateau fractures, 92
    of tumors, 101
    of wrist fractures, 9192
    Concierge medicine, 124125
    Condyle fracture, lateral, 680681
    Congenital anomalies. See also specific
    congenital defect
    radiography of, 89
    spinal, 715716
    Congenital femur deficiency, 769
    Congenital fibrosarcoma, 194t
    Congenital knee dislocation, 771
    Congenital patella dislocation, 771
    Congenital rib fusion, 716
    Congenital spondylolisthesis
    epidemiology of, 652
    pathogenesis of, 653
    treatment of, 657
    Congenital tibial pseudarthrosis, 768
    Congenital vertical talus, 772, 772f
    Constriction band syndrome, 708709
    Continuous passive motion (CPM), 344
    Contracture syndrome, 805807
    Coracoid fracture, 277
    Cornelia de Lange syndrome, 802
    Coronoid fracture
    biomechanics of, 328329
    classification of, 328, 328f
    treatment of, 328329
    Coronoid process of the ulna, 345f
    Corticosteroids
    bone healing inhibition by, 14
    uses of, 187
    COX-2. See Cyclooxygenase-2
    Coxa vara, developmental, 744
    CPT. See Current procedural terminology
    Craniocervical injury, management of,
    630
    Crescent fracture, 383
    Crescent sign, 420, 421f
    Crossover design trial, 169
    Crossover toe, 528
    Cruciate ligament. See Anterior cruciate
    ligament
    Crush injury, 131
    Crystal-associated arthritis, 220
    CT. See Computed tomography
    Cubital tunnel syndrome, 369
    Cuboid fracture, 515

    Culture, 112113
    competence in, 115
    diversity of, 114
    health disparities and, 114115
    language divisions in, 114
    of medicine, 113114
    programming of, 113t
    Curly toe, 778
    Current procedural terminology (CPT),
    148
    Cyclooxygenase-2 (COX-2), 11

    D
    Dactyly. See Camptodactyly;
    Clinodactyly; Macrodactyly;
    Polydactyly; Symbrachydactyly;
    Syndactyly
    DDH. See Developmental dysplasia of
    the hip
    Dbridement
    knee arthritis treatment with, 470471
    open fracture wound treatment with,
    51
    osteomyelitis treatment with, 246
    tibial shaft fracture treatment with,
    484485
    Deep venous thrombosis, 139, 427
    Deformity. See also specific deformity
    acquired, 526528
    classification of, 697698, 698t
    constriction band, 708709
    developmental, 710711
    duplication, 706708
    failure of differentiation, 704706
    failure of formation, 698704
    forces of, 531
    overgrowth, 708
    upper extremity, 697
    Degenerative spondylolisthesis
    clinical presentation of, 654
    epidemiology of, 651652
    pathogenesis of, 652
    treatment of
    nonsurgical, 656
    surgical decompression in, 656657
    Degenerative ulnocarpal impaction, 374
    Demineralized bone matrix (DBM), 14
    Dens, ossification center of, 720t
    Dentrocentral synchondrosis, 720t
    Dermatofibrosarcoma protuberans, 194t
    Desmoplastic small round cell tumor,
    194t
    Developmental coxa vara, 744
    Developmental dysplasia of the hip
    (DDH), 739
    diagnosis of
    imaging in, 740741
    physical examination in, 739740
    etiology of, 739
    ischemic necrosis and, 743
    late dysplasia with, 743744
    pathogenesis of, 739
    treatment of, 741
    closed reduction in, 742

    Orthopaedic Knowledge Update 10

    1/11/2011 2:21:52 PM

    Index
    open reduction in, 742
    pelvic osteotomy in, 742473, 743f
    redislocation after, 743
    reduction age limits in, 743
    splinting in, 741742
    dGEMRIC protocol, 28
    Diabetes
    bone healing affected by, 13
    carpal tunnel syndrome associated
    with, 231
    neuropathies associated with,
    230231, 231t, 530
    total knee arthroplasty outcome
    affected by, 471
    Diabetic amyotrophy, 231
    Diabetic ankle fracture, 498499
    Diaphyseal forearm fracture, 331,
    687688, 688f
    Digastric osteotomy, 403f
    Digital replantation, 360
    Dimelia, ulnar, 707708, 708f
    Disability, 152153
    Discogenic low back pain, 604
    clinical features of, 606
    diagnostic imaging for, 604606
    treatment of, 606607
    Disease models
    biologic, 151152
    biopsychosocial, 152
    Disk. See Intervertebral disk
    Disk arthroplasty, 665667
    cervical, 665666, 666f
    lumbar, 667, 667f
    total, 73, 75, 7980
    Diskectomy
    anterior diskectomy and fusion, 665
    cervical spondylotic radiculopathy
    treatment with, 614615
    lumbar disk herniation treatment with,
    603604
    Dislocation. See specific dislocation site
    Distal arthrogryposis, 806807
    Distal interphalangeal joint (DIP joint),
    351, 365
    Distal radioulnar joint (DRUJ), 356, 358
    arthritis at, 363364
    fractures of, 688
    Down syndrome, 802
    Duchenne muscular dystrophy (DMD)
    clinical/orthopaedic features of, 812t
    diagnosis of, 818
    genetic characteristics of, 812t
    management of, 818
    prevalence of, 812t
    Duty, legal, 6
    Dyskinesis, scapular, 318
    Dysplasia. See also Developmental
    dysplasia of the hip; Hip
    camptomelic, 801802
    cleidocranial, 183, 184f, 802
    fibrodysplasia ossificans progressiva,
    182, 183f
    fibrous, 194t, 828829
    late, with, 743744
    osteofibrous, 829

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 841

    Dysplastic spondylolisthesis
    epidemiology of, 652
    pathogenesis of, 653
    treatment of, 657
    Dysraphism, spinal, 718f

    E
    Edema, 542
    Education
    communication as, 112
    with lower extremity amputation, 543
    Elbow
    dislocation of, 331
    complex, 332, 334335
    simple, 331332
    treatment of, 332, 333f, 334335
    disorders of, 319322
    features of, 676f
    fractures of, 92
    free-body diagram of, 63, 63f
    inflammatory arthritis of, 343344
    injuries of, 676677
    instability of, 319321, 331f, 344345
    chronic, 348
    pivot-shift test of, 345, 345f
    posterolateral rotatory, 345346
    recurrent, 345
    valgus, 347348
    varus posteromedial rotatory,
    346347
    laxity of, 65f
    osteoarthritis of, 343
    rotation axes of, 65f
    stabilizers of, 344345
    in static equilibrium, 63f
    stiffness of, 343344
    synostosis across, 705
    terrible triad injury, 332, 334f
    throwers, 789790
    Elderly patients
    cervical spine trauma in, 636
    concerns of, 113t
    pain management for, 263
    Electrical stimulation, 16. See also
    Extracorporeal shock wave therapy
    Electrocautery, as ignition source, 4
    Electrodiagnostic studies, 228229
    Electromyography (EMG), 228229,
    230t
    Electronic medical record (EMR),
    126127
    Enchondroma, 194t, 828
    End-of-life care, 264265
    Enteropathic arthritis, 219
    Eosinophilic granuloma, 554, 829830
    Epidural abscess, 570
    Epiphysiodesis, 769
    Epitenon, 41
    Estrogen, 187, 189
    Evidence-based medicine, 157
    clinical practice guidelines with,
    161162, 163t
    critical appraisal of, 173175, 174t
    evidence levels in, 157, 158t, 161t

    assignation of, 157158, 160


    interrater reliability and, 160
    nontherapeutic studies in, 159160
    orthopaedic literature in, 160161
    randomized controlled trials in, 159
    therapeutic studies in, 159
    use of, 161
    Ewing sarcoma, 556
    demographics of, 193
    pediatric, 827828, 828f
    translocations of, 194t
    Exostoses, 194t
    Expertise-based study design, 170
    Extensor tendon injury, 358, 692
    Extracellular matrix (ECM), 23, 29
    Extracorporeal shock wave therapy
    (ESWT), 1617
    Extraskeletal myxoid chondrosarcoma,
    194t
    Extremity. See also Amputation, lower
    extremity; Lower extremity, pediatric;
    specific extremity
    fractures of
    CT of, 9192
    radiography of, 8586
    injury to, 49, 131

    F
    Facet arthroplasty, 668669
    Facet arthrosis, 611, 612f
    Facet fracture-dislocation, 633634
    Factorial design trial, 169170
    Fanconi anemia, 698699
    Fasciocutaneous flap, 54
    Fat embolism, 436
    Fees, explanation of, 6
    Femoral cutaneous neuropathy, 231
    Femoral fracture. See also Femoral head
    fracture; Femoral neck fracture;
    Femoral shaft fracture
    bilateral, 434
    diaphyseal, 162t
    distal, 436
    classification of, 436
    complications with, 438439
    Hoffa, 437, 437f
    injury mechanism of, 436
    nonunion of, 438439
    periprosthetic, 437
    supracondylar, 436437
    unicondylar, 437438
    intertrochanteric, 404405
    ipsilateral, 133t, 434
    metaphyseal, pediatric, 753
    pathologic, 406
    periprosthetic, 427, 427t, 437
    pertrochanteric, 405f
    physeal, pediatric, 754
    complications with, 755
    growth plate arrest with, 754, 754f
    treatment of, 754756
    proximal, 86
    subtrochanteric
    classification of, 405

    Orthopaedic Knowledge Update 10

    841

    1/11/2011 2:21:52 PM

    Index
    complications from, 729
    pediatric, 729
    treatment of, 406
    Femoral head fracture, 401402
    classification of, 402f
    visualization of, 403f
    Femoral head osteonecrosis
    classification of, 420, 420t
    epidemiology of, 419420
    risk factors associated with, 419420,
    420t
    treatment of, 420422
    Femoral neck fracture
    classification of, 403, 404f405f
    femoral shaft fracture with, 434
    pediatric, 727, 729, 730f
    treatment of, 403404
    Femoral shaft fracture, 431
    classification of, 431, 431t
    comminution of, 431, 431t
    complications with, 434
    fat embolism as, 436
    malunion as, 435
    neurapraxia as, 435
    nonunion as, 435
    pudendal nerve compression as, 435
    femoral neck fracture with, 434
    from gunshot wounds, 434
    injury mechanisms of, 431432
    open, 434
    pediatric, 731, 733f
    complications with, 734
    external fixation for, 734
    intramedullary nails for, 732
    Pavlik harness for, 732
    surgery for, 732
    treatment of, 731, 731t
    treatment of, 432
    antegrade nailing in, 433
    nonsurgical, 432
    plating in, 434
    retrograde nailing in, 433
    vascular injury with, 434
    Femoroacetabular impingement (FAI), 414
    evaluation of, 414415, 415f, 415t
    treatment of, 415416
    Femur. See also Femoral fracture; specific
    femoral part
    amputation of, 538
    anteversion of, excessive, 768
    deficiency of, congenital, 769
    reconstruction of
    cemented stems in, 422, 426
    cementless stems in, 422423
    cylindrical fully porous-coated
    stems in, 425
    impaction grafting in, 425
    modular tapered, 425
    primary THA for, 422423
    revision THA for, 425426
    replacement of, proximal, 425426
    shortening of, closed, 769
    Fibroblast growth factor (FGF), 13, 16
    Fibrodysplasia ossificans progressiva
    (FOP), 182, 183f

    842

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 842

    Fibroma
    neurofibroma, 555
    nonossifying, 829
    Fibromyxoid sarcoma, 194t
    Fibrosarcoma
    congenital, 194t
    infantile, 830
    Fibrous dysplasia, 194t, 828829
    Fibrous lesion, 828830
    Fibula fracture, pediatric, distal, 758
    Fibular collateral ligament (FCL),
    455456, 456t
    Fibular hemimelia, 770, 770f
    Fillet flaps, 5354
    Fine-needle aspiration biopsy, 102
    Finite element analysis, 69f, 70f
    Fixed sagittal imbalance, 589
    causes of, 589t
    pelvic incidence with, 589590
    treatment of, 590
    pedicle subtraction osteotomy in,
    590591
    Smith-Peterson osteotomy in, 590
    vertebral column resection in, 592
    Flatfoot, 775
    Flexible flatfoot, 775
    Flexion-teardrop injury, 634
    Flexor tendon injury, 358359, 692
    Floating shoulder, 278
    Fluorine-18 deoxyglucose (FDG), 98
    Food and Drug Administration (FDA), 5
    Foot, 507
    arthritis of, 525
    cavus
    pediatric, 776777, 777f
    subtle, 527
    cerebral palsy and, 815816
    clubfoot, 772774
    compartment syndrome of, 508
    deficiency of, central, 701
    evaluation of, 507508
    flatfoot, 775
    fractures of
    pediatric, 759
    radiography of, 517
    myelomeningocele and, 817
    osteochondroses of, 777778
    pain in, 507508
    nerve, 529530
    treatment of, 525
    reconstruction of, 523
    skewfoot, 774
    Foraminotomy, 615
    Forearm
    diaphyseal fracture of, 331, 687688,
    688f
    injury to, 325
    trauma of, 687
    Fracture. See also specific fracture
    bilateral, 131, 434, 634
    bone lesions and, 198, 199f
    burst, 633
    closed, 49, 131
    combination, 131
    imaging of, 8586, 9092

    infiltration of, 11
    myelomeningocele with, 817
    occult, 96, 98
    open, 131, 434, 484486 (See also
    Open fracture wound)
    stress, 9899, 792793
    Free tissue flaps, 53
    Freiberg infraction, 777
    Friedreich ataxia, 820
    clinical/orthopaedic features of, 812t
    genetic characteristics of, 812t
    prevalence of, 812t

    G
    Gadolinium, 9596
    Galeazzi sign, 739
    Gastric bypass surgery, 13
    Gender, 214
    Gene therapy, intervertebral disk
    regeneration with, 670
    Genetic(s)
    cancer predisposition, 194t
    intervertebral disk degeneration, 31
    neurofibromatosis, 799
    neuromuscular disorders, 812t
    osteoarthritis, 214215
    osteopetrosis, 185t
    Genetic mutations, in osteopetrosis, 185t
    Genu valgum, 767768
    Giant cell tumor, 555
    Glenohumeral arthritis
    physical therapy for, 286
    treatment of, 292, 292t
    Glenohumeral degenerative joint diseases,
    285286
    treatment of
    biologic total shoulder arthroplasty
    in, 288289
    future directions of, 292293
    hemiarthroplasty in, 287288
    nonprosthetic joint-sparing
    techniques in, 286287
    nonsurgical, 286
    shoulder resurfacing arthroplasty
    in, 287
    total shoulder arthroplasty in, 289
    Glenohumeral ligaments, 300f
    Glenoid fossa fracture, 278
    Glenoid neck fracture, 277278
    Glucocorticoids, 187
    Gross Motor Function Classification
    Scale (GMFCS), 812
    Guidelines. See Clinical practice
    guidelines
    Gunshot wounds, 434

    H
    Hallux valgus, 526527, 775776, 776f
    Halo vest, 629
    Hand
    cleft, 701, 702f
    compartment syndrome of, 359360
    deficiency of, central, 701

    Orthopaedic Knowledge Update 10

    1/11/2011 2:21:53 PM

    Index
    dislocations of, 351, 691692
    fractures of, 351
    pediatric, 691692, 691t
    surgery necessitated by, 691t
    injuries of
    high-pressure injection, 359
    nerve, 359
    pediatric, 691
    soft-tissue, 358
    vascular, 358
    young athletes with, 790
    mirror, 707708, 708f
    trauma of, 687
    Hangmans fracture, 631, 722
    Health Care Quality Improvement Act, 7
    Hemangioma, 555
    Hematologic disease, 830833
    Hemiarthroplasty, 275276, 287288
    Hemiatrophy, 770
    Hemihypertrophy, 770771
    Hemimelia, 770, 770f
    Hemophilia, 830
    Hemorrhage, 131
    Hemorrhagic shock, 129
    HEPA filter. See High-efficiency
    particulate air filter
    Heparin, 137
    Heterotopic ossification (HO)
    as acetabular fracture complication, 391
    in residual limbs postamputation, 543
    High-efficiency particulate air filter
    (HEPA filter), 239
    Highly cross-linked polyethylene, 74t
    High-pressure injection injuries, 359
    Hindfoot, arthritis of, 525
    Hinge joint, 64f
    Hip. See also Developmental dysplasia of
    the hip; Total hip arthroplasty
    arthritis of
    clinical evaluation of, 413414
    CT of, 414
    epidemiology of, 413
    MRI of, 414
    patient history of, 413
    physical examination of, 413414
    radiographic evaluation of, 414
    arthroscopy, 401, 416
    cerebral palsy and, 814
    dislocations of, 399401
    classification of, 400t
    pediatric, 727728
    dysplasia of
    history of, 417
    myelomeningocele with, 817
    osteotomy in treatment of, 418
    physical examination of, 417
    radiograph examination of, 417
    418, 418t
    THA in treatment of, 418419
    fractures of, 402, 406
    injury to, 399
    resurfacing of, 423
    stability of, 399
    wear characteristics of, 74
    HIV. See Human immunodeficiency virus

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 843

    Hoffa fracture, 437, 437f


    Hormones, bone regulation with, 186
    188. See also specific hormone
    Hospital
    infection pathomechanics in, 238239,
    238f
    hospital floor in, 240241
    operating room in, 239240
    as practice setting, 123
    Human immunodeficiency virus (HIV),
    14
    Humeral fracture
    distal
    classification of, 327
    complications with, 328
    treatment of, 327328
    humeral shaft, 278
    nonunion with, 280
    presentation of, 278
    radial nerve palsy with, 280
    radiographic evaluation of, 278
    279, 279f
    treatment of, 279280
    proximal, 273, 676
    classification of, 274
    greater tuberosity fracture with, 275
    nonunion/malunion with, 276
    presentation of, 273
    radiographic evaluation of, 274
    treatment of, 274276
    vascularity and, 273274
    supracondylar, 436437, 677680
    arterial repair with, 679680
    complications with, 678
    flexion-type, 679
    perfusion adequacy and, 679680
    treatment of, 677678
    type I, 677
    type II, 677678
    type IV, 679
    vascular injury with, 679
    Humerus, 273274, 276
    Hyperinsulinemia, 231t
    Hyperostosis, disseminated idiopathic
    skeletal, 635
    Hypoglycemia, 231t
    Hypoplasia, thumb, 699, 701f
    Hypothermia
    cascading interactions with, 131
    spinal cord injury management with,
    575t, 578
    Hypothyroidism, 232

    I
    Iliac wing fracture, 383
    Image-guided intensity modulated
    radiation therapy (IGIMRT), 559,
    561f
    Imaging, 85. See also Computed
    tomography; Magnetic resonance
    imaging; Radiography
    of bone lesions, 195197
    of developmental dysplasia of the hip,
    740741

    of discogenic low back pain, 604606


    fracture, 8586, 9092
    calcaneal, 509
    radial head, 325
    of Legg-Calve-Perthes disease,
    745746
    nuclear, 9899
    of rotator cuff tears, 304305
    of slipped capital femoral epiphysis,
    747748
    of soft-tissue masses, 205
    of spinal infection, 571
    of spinal metastases, 558t
    of thoracic disk herniation, 662
    of thoracolumbar trauma, 642
    of vertebral osteomyelitis, 566,
    566f568f, 569
    Immune system
    impairment of, factors causing, 243t
    local defense by, 243244
    systemic defense by, 242243
    Implanted devices
    operating room best-care practices
    with, 241t
    recalls of, 5
    Indian hedgehog (Ihh), 13
    Infantile fibrosarcoma, 830
    Infection. See also Musculoskeletal
    infection; Periprosthetic joint
    infection; Spinal infection
    as acetabular fracture complication,
    390
    biofilms promotion of, 243t
    neuropathies associated with, 233
    nuclear imaging of, 99
    radiography of, 88
    total hip arthroplasty, 426427
    total knee arthroplasty
    chronic, 474
    risk factors of, 471
    treatment of, 473474
    of wounds, 49
    Infectious arthritis, 220221
    Inferior vena cava (IVC), 139
    Inflammation
    in bone repair, 11, 15
    cascading interactions with, 131
    Inflammatory arthritis, 217
    elbow, 343344
    epidemiology of, 413
    Inflammatory myofibroblastic tumor,
    194t
    Inflammatory neuropathy, 232233
    Informed consent, 6
    Injury Severity Score (ISS), 129
    Instruments
    patient-specific, 472473
    retained, 4
    Intensive care unit, 133134, 134t
    Interleukins, 11
    Interosseous nerve syndrome
    anterior, 369, 371f
    posterior, 371
    Interphalangeal joint. See Distal
    interphalangeal joint; Proximal

    Orthopaedic Knowledge Update 10

    843

    1/11/2011 2:21:53 PM

    Index
    interphalangeal joint
    Interspinous spacers, 669
    Intervertebral disk
    artificial, 80f
    biomechanics of, 28f
    degeneration of
    disk regeneration therapies for,
    669670
    genetic factors in, 31
    matrix metalloproteinase in, 30
    mechanical loading and, 3132
    normal aging vs., 29
    nutritional deficiency and, 30
    soluble factors and, 3031
    development of, 29
    function of, 2829
    maturation of, 29
    regeneration of, 669670
    structure of, 2829
    Intrathecal baclofen, 812
    Ischemic necrosis, developmental
    dysplasia of the hip with, 743
    ISS. See Injury Severity Score
    Isthmic spondylolisthesis
    clinical presentation of, 654
    epidemiology of, 651
    high-grade, 655656
    low-grade, 655
    pathogenesis of, 652
    treatment of
    instrumented fusion in, 655656
    noninstrumented fusion in, 655
    nonsurgical, 654

    J
    Joint(s). See also specific joint
    biomechanics of, 6266
    classification of, 64, 64f
    degrees of freedom of, 65
    kinematics of, 6466
    laxity of, 6566
    loading of, 6264
    types of, 64f
    Joint Commission, 3, 4t
    Joint line congruity angle (JLCA), 764f

    K
    Kienbck disease, 365366, 366f
    Kirner deformity, 705
    Klippel-Feil syndrome, 716
    Knee. See also Total knee arthroplasty
    amputation and, 537
    anatomy of, ligamentous/tendinous,
    455f
    arthritis
    arthroscopic dbridement for,
    470471
    joint-preserving procedures for,
    470471
    proximal tibial osteotomy for, 471
    treatment of, 469, 470t
    arthroplasty, unicompartmental, 473
    cerebral palsy and, 814815

    844

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 844

    dislocation of
    congenital, 771
    traumatic, 457458
    injuries of
    extensor mechanism, 448
    multiligament, 457458, 458f, 458t
    posterolateral corner of, 456457
    osteoarthritis of, 470t
    osteochondritis dissecans of, 791792
    pain in
    clinical evaluation of, 469470
    patient history of, 469
    physical examination of, 469
    radiographic evaluation of,
    469470
    treatment of, nonsurgical, 470
    young athletes with, 790791
    posterolateral corner of, 455
    examination of, 456t
    injury of, 456457
    reconstruction of, 457
    wear characteristics of, 75
    Kohler disease, 777
    Kyphoplasty, 188
    Kyphosis
    axial neck pain caused by, 611612
    Scheuermann, 718719

    L
    Laminectomy, 618619
    Laminoforaminotomy, 615
    Laminoplasty, 619620
    Laminotomy, 603
    Langerhans cell histiocytosis. See
    Eosinophilic granuloma
    Larsen syndrome, 806
    Laser, as ignition source, 4
    Latarjet procedure, 302f
    Lateral condyle fracture, 680681
    Lateral distal femoral angle (LDFA), 764f
    Lateral distal tibial angle (LDTA), 764f
    Lateral proximal femoral angle (LPFA),
    764f
    Lateral ulnar collateral ligament (LUCL),
    345346, 346f
    Lawn mower injury, 759
    Lawsuit, 68
    Legg-Calv-Perthes disease (LCP disease),
    744
    classification of, 745, 745f
    clinical evaluation of, 745746
    epidemiology of, 744
    etiology of, 744
    imaging of, 745746
    natural history of, 746
    pathogenesis of, 744745
    prognosis of, 746
    radiography of, 746f
    treatment of, 746
    Leprosy, 233234
    Lesion. See also Bone lesion
    fibrous, 828830
    osteochondral, 525526
    rotator cuff tear and, 304

    SLAP, 317f
    Leukemia, 831
    Liability, 78
    Li Fraumeni syndrome, 194t
    Ligaments. See also specific ligaments
    bone insertion of, 41
    composition of, 41
    function of, 4142
    healing of, stages of, 43f
    injury of, 4344
    load-elongation curve of, 41, 42f
    nutrition of, 41
    stress-strain behavior of, 42
    structure of, 4142
    Limb lengthening, 769
    Limb pain/sensation
    phantom, 540t
    residual, 541t
    Limb replantation, 53
    Lipoma, 830
    Lisfranc injury, 515516, 516f
    Little leaguers shoulder, 789
    Lordosis, cervical, 720t
    Low back pain. See Discogenic low back
    pain
    Lower extremity. See Amputation, lower
    extremity; specific lower extremity
    Lower extremity, pediatric
    axial alignment/development of, 763
    deformity correction for, 764
    limb-length discrepancy of, 769771
    malalignment of
    conditions causing, 764768
    rotational, 768769
    planning for, 763764
    radiographic analysis of, 763764
    rotational development of, 763
    trauma to, 753
    Low-intensity pulsed ultrasound (LIPUS),
    1617
    Low-molecular-weight heparin (LMWH),
    137, 139
    Lumbar discogenic pain. See Discogenic
    low back pain
    Lumbar disk arthroplasty, 667, 667f
    Lumbar disk herniation
    classification of, 602f
    clinical presentation of, 603
    outcomes of, 604
    pathoanatomy of, 602
    pathophysiology of, 602
    treatment of, 603604
    types of, 602f
    Lumbar nerve, 654655
    Lumbar spinal stenosis
    clinical presentation of, 600
    lateral recess, 599600, 599f
    neurogenic claudication and, 600t
    pathophysiology of, 599600
    treatment of, 600602
    vascular claudication and, 600t
    Lumbar spine
    degenerative disorders of, 599
    Modic classification of changes in,
    605, 605t, 606f

    Orthopaedic Knowledge Update 10

    1/11/2011 2:21:53 PM

    Index
    injuries to, 722
    Lumbar spondylolysis
    incidence of, 651
    pathogenesis of, 652
    treatment of, 654655
    Lunate
    dislocation of, 355356
    osteonecrosis of, 365366
    Lunotriquetral dissociation, 355
    Lyme disease, 234
    Lymphocytic cell, 11

    M
    Macrodactyly, 708, 709f
    Macrophages, 11
    Madelung deformity, 710711, 711f
    Magnesium, 575t, 578
    Magnetic resonance imaging (MRI), 9394
    advances in, 96
    articular cartilage assessment with,
    2728
    of bone lesions, 196
    of cervical spine injuries, 9698
    contrast agents for, 9596
    of femoroacetabular impingement, 415
    of hip arthritis, 414
    of occult fractures, 96
    of proximal femoral fractures, 86
    of radial head/neck fractures, 86
    of scaphoid fractures, 86
    of spinal cord injury, 575576
    sequences, 9495
    of soft-tissue masses, 205
    of thoracolumbar trauma, 642643
    Malignant malalignment, 769
    Malleolus fracture
    isolated medial, 498
    posterior, 497498, 498f
    Malpractice litigation, 68, 110111,
    111f
    Malunion
    femoral shaft fractures with, 435
    proximal humerus, 276
    tibial shaft fracture, 486
    Marfan syndrome, 797798, 798f
    Matrix metalloproteinase (MMP), 30
    McCune-Albright syndrome, 194t
    Mechanical axis deviation (MAD), 764f
    Mechanical loading, of intervertebral
    disks, 3132
    Mechanical stress, cartilage matrix
    affected by, 24
    Medial collateral ligament (MCL)
    bone insertion of, 41
    injuries of, 454455
    nonsurgical treatment of, 454455
    reconstruction indications for, 455
    Medial epicondyle fracture, 681,
    787788, 787f, 788f
    Medial epicondylitis, 321
    Medial patellofemoral ligament (MPFL),
    460
    Medial proximal tibial angle (MPTA),
    764f

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 845

    Median nerve
    compression of, 367369
    palsy, 372373
    Medical practice
    concierge medicine in, 124125
    contracting as, 123124
    electronic medical records and,
    126127
    management of, 121, 125126
    ownerships trends of, 121122
    physician-owned, 122123
    setting of, 121, 121f, 123
    Medicine. See Evidence-based medicine
    Meniscectomy, 459
    Meniscus tear
    classification of, 459
    lateral, 453
    natural history of, 459
    repair of, 459, 459f
    of tibiofemoral joints, 458459
    in young athletes, 785
    Meniscus transplantation, 459460
    Mesenchymal stem cell (MSC), 43
    Metabolic bone diseases. See also specific
    disease
    categories of, 188189
    pediatric, 764765
    Metabolic diseases, 8889
    Metacarpal fracture, 352353
    Metacarpophalangeal joint (MCP joint),
    352, 365
    Metal-on-metal prostheses, 74t, 7677
    Metastases. See Spinal tumor
    Metatarsal fracture, 518
    fifth, 516517, 517f
    pediatric, 759
    treatment of, 518
    Metatarsophalangeal dislocations,
    517518
    Metatarsus adductus, 774
    Methadone therapy, 264
    Methicillin-resistant Staphylococcus
    aureus (MRSA), 254, 255t, 831
    Methylprednisolone, 577
    Microsurgical coverage, 53
    Midfoot
    arthritis of, 525
    pediatric fracture of, 759
    Minocycline, 575t, 577578
    Mirror hand, 707708, 708f
    Miserable malalignment, 769
    Mitochondria, 26
    M line proteins, 37
    Mononeuropathy, 231
    Monteggia fracture-dislocation, 681682
    MRI. See Magnetic resonance imaging
    MRSA. See Methicillin-resistant
    Staphylococcus aureus
    Mucopolysaccharidoses, 804805, 804t
    Multifocal motor neuropathy (MMN),
    232233
    Multiple hereditary exostoses, 194t
    Multiple myeloma, 557
    Multiple organ dysfunction syndrome
    (MODS), 134

    Muscle. See Skeletal muscle; specific


    muscle
    Musculoskeletal imaging. See Imaging
    Musculoskeletal infection, 238
    conditions associated with, 244254
    hospital pathomechanics of, 238239,
    238f
    hospital floor in, 240241
    operating room in, 239240
    pediatric, 831
    Musculoskeletal syndromes, 797
    chromosomal abnormality caused,
    802803
    contracture, 805
    multiple gene-caused, 803
    protein-processing gene-caused, 803
    signaling pathway-caused, 801
    structural gene-caused, 797
    tumor-related gene-caused, 799
    Musculoskeletal system, 59
    Myelination, 225
    Myeloma, 557
    Myelomeningocele, 816
    foot deformities with, 817
    fractures with, 817
    hip dysplasia with, 817
    skin ulcers with, 818
    spinal deformities with, 816817
    Myelopathy. See Cervical spondylotic
    myelopathy
    Myofibers, 38t, 39
    Myofibril, 37
    Myositis ossificans, 40
    Myxoid liposarcoma, 194t

    N
    Nail
    antegrade/retrograde, 433
    cephalomedullary, 70f
    intramedullary, 732
    plate vs., 484485
    Nail-patella syndrome, 802
    National Practitioners Data Bank
    (NPDB), 78
    Neck pain. See Axial neck pain
    Needle EMG, 228229, 230t
    Negative pressure wound therapy
    (NPWT)
    contraindications for, 52
    open fracture wound management
    with, 5153
    pressure range of, 52f
    split-thickness skin grafting and, 53
    vacuum in, 52f
    Negligence, 6
    Neisseria gonorrhoeae, 221
    Neonatal compartment syndrome, 711,
    711f
    Neoplasm. See Bone neoplasm
    Nerve. See also specific nerve
    compression of, sites of, 367t
    conduction velocity studies, 228229,
    229t
    injury of

    Orthopaedic Knowledge Update 10

    845

    1/11/2011 2:21:54 PM

    Index
    acetabular fracture with, 390391
    electrophysiologic response to, 230
    hand/wrist, 359
    pain, 529530
    palsy of, 280, 372373
    Nerve compression syndromes. See
    Compression neuropathy
    Nervous system, 225. See also Central
    nervous system; Peripheral nervous
    system
    Neurofibroma, 555
    Neurofibromatosis (NF), 799800
    clinical findings with, 799t
    genetics of, 799
    neoplasms associated with, 194t
    Neurogenic claudication, 600t
    Neuroma, surgical, 529530
    Neuromuscular disorders, 234, 811,
    812t. See also specific disorder
    Neuropathic arthropathy
    electrodiagnostic studies of, 228229
    radiography of, 87
    Neuropathy
    autonomic, 231
    compression, 227228, 367
    electrodiagnostic studies of,
    228229
    sites of, 367t
    diabetes-associated, 230231, 231t,
    530
    femoral cutaneous neuropathy, 231
    hereditary motor sensory, 819820
    hyperinsulinemia-associated, 231t
    hypoglycemia-associated, 231t
    hypothyroidism-associated, 232
    infection-associated, 233
    inflammatory, 232233
    mononeuropathy, 231
    multifocal motor, 232233
    peroneal, 231
    symmetric sensory polyneuropathy,
    231
    ulnar, 231
    Neuropeptides, 44
    Neurapraxia, 435
    Neurovascular injuries, 319
    New Injury Severity Score, 129
    Nicotine, 13
    NOMS system, 558, 560f
    Nonossifying fibroma, 829
    Nonunion
    of distal femoral fractures, 438439
    femoral shaft fractures with, 435
    humeral shaft, 280
    proximal humerus, 276
    scaphoid, 354
    scaphoid nonunion advanced collapse,
    363, 364t
    tibial shaft fracture, 486488
    Noonan syndrome, 803
    Nuclear imaging, 9899
    Numeric simulation, 6970
    Nutrition
    of ACL, 41
    deficiencies in

    846

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 846

    bone healing impaired by, 13


    intervertebral disk degeneration
    and, 30
    of rotator cuff, 290f

    O
    Obesity
    cerebral palsy with, 812813
    total knee arthroplasty outcome
    affected by, 471
    Observational studies, 170171, 170f
    Occipitoatlantal dislocation, 721
    Occult fracture, 96, 98
    Odds ratio, 168
    Odontoid fracture, 630631, 721722
    Olecranon fracture, 329
    classification of, 329
    complications with, 331
    treatment of, 329331
    Oligodendrocyte progenitors, 575t, 579
    Ollier disease, 194t
    Open fracture, 131, 434, 484486
    Open fracture wound
    contamination of, 49
    management of, 51
    antibiotic bead pouch for, 51, 51f
    antibiotic therapy for, 4950, 50t
    closure in, 53, 485486
    dbridement in, 51
    fasciocutaneous flap for, 54
    fillet flaps for, 5354
    initial, 49
    irrigation in, 50
    microsurgical coverage in, 53
    negative pressure wound therapy
    for, 5153
    perforator flap for, 54
    soft-tissue coverage for, 5354
    Open reduction
    developmental dysplasia of the hip
    treatment with, 742
    femoral physeal fracture treatment
    with, 755
    Open reduction and internal fixation
    (ORIF)
    for clavicle fracture, 273
    of tibial plafond fracture, 500
    Operating room
    bacterial load in, 239
    best-care practices in, 241t
    fire in, 4
    infection pathomechanics in,
    239240
    laminar air flow in, 239f
    time-out in, 3
    Operating room space suits, 239
    Opioid analgesics, 263264
    Orthobiologics, 486
    Orthopaedic medicine. See Evidencebased medicine
    Orthopaedic research. See Research
    Orthopaedic surgeon
    AAOS and, 3, 138t, 139

    communication training of, 110111


    contracting by, 123124
    practice setting of, 121, 121f, 123
    skills of, importance of, 110t
    Ortolani sign, 739, 740f
    Osgood-Schlatter disease, young athletes
    with, 793
    Os odontoideum, 716, 717f
    Osteoarthritis (OA), 213
    classification of, 416t
    clinical features of, 215216
    diagnosis of, 216
    of distal interphalangeal joint, 365
    Eaton classification system for, 364,
    365t
    elbow, 343
    epidemiology of, 413
    incidence of, age-dependence of, 24
    knee, 470t
    of metacarpophalangeal joint, 365
    pathophysiology of, 213214
    of proximal interphalangeal joint, 365
    radiography of, 86
    risk factors for, 214
    age as, 214
    anatomic, 215
    body mass index as, 215
    bone density as, 215
    gender as, 214
    genetic, 214215
    trauma as, 215
    of scaphotrapezial joint, 365
    of thumb carpometacarpal joint,
    364365
    treatment of
    nonsurgical, 216
    surgical, 216217
    surgical reconstruction in, 285
    viscosupplementation in, 286
    Osteoblast, 11
    differentiation of, 181182, 181f
    diseases related to defects in, 182183
    Osteoblastogenesis, 181
    Osteoblastoma, 556, 825
    Osteochondral autologous transfer
    system, 526
    Osteochondral explants, 26f
    Osteochondral lesion (OCL), 525526
    Osteochondritis dissecans (OCD),
    791792
    Osteochondroma, 556, 828
    Osteochondrosis, of foot, 777778
    Osteoclast
    differentiation of, 181f, 183184
    diseases related to defects in, 184186
    Osteoclastogenesis, 183184
    Osteofibrous dysplasia, 829
    Osteogenesis imperfecta (OI), 798, 799f
    Osteoid osteoma, 555556
    pediatric, 825
    radiofrequency ablation for, 102
    Osteolysis, 93
    Osteomalacia, 189190, 190t
    Osteomyelitis. See also Vertebral
    osteomyelitis

    Orthopaedic Knowledge Update 10

    1/11/2011 2:21:54 PM

    Index
    adult, 244246
    bacteria causing, 244245
    bone scans of, 99
    diagnosis of, 245, 248
    labeled WBC scans of, 99
    pediatric, 247248, 831832
    position emission tomography of, 99
    presentation of, 247
    staging system for, 245t
    treatment of, 246, 247
    Osteonecrosis. See also Femoral head
    osteonecrosis
    of capitate, 367
    HIVs effect on, 14
    of lunate, 365366
    of scaphoid, 366367
    treatment of, surgical reconstruction
    in, 285
    Osteopenia, 14
    Osteopetrosis, 184186, 185t
    Osteoporosis, 188
    criteria for, 188t
    hip fracture and, 406
    radiographs of, 185f
    treatment of
    novel, 188
    pharmacologic, 188189
    Osteoprotegerin (OPG), 184
    Osteosarcoma, 193, 557
    pediatric, 827, 827f
    syndromes associated with, 194t
    Osteotomy
    digastric, 403f
    hip dysplasia treatment with, 418
    pediatric lower extremity deformity
    with, 764
    pedicle subtraction, 590591, 593
    pelvic, 742743, 743f
    proximal tibial, 471
    Smith-Peterson, 590
    osterix, 11
    Os trigonum fracture, 525
    Oxidative stress, 26

    P
    Paget disease, 186
    Pain. See also specific pain location
    assessment of, 259t
    classification of, 260t
    cost of, 259
    diagnosis of, 260, 262, 262t
    pathophysiology, 260
    physiology of, 259260
    prevalence of, 259
    Pain management, 259
    acute, 260
    basics of, 259t
    chronic, 260
    diagnostic testing with, 262t
    evaluation for, 260262
    patient history in, 261t
    physical examination in, 261t
    for elderly patients, 263
    in end-of-life care, 264265

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 847

    ethical considerations of, 265


    guidelines for, 263
    nonpharmacologic, 262
    outcomes of, 263
    in palliative care, 264265, 265t
    for pediatric patients, 263
    pharmacologic, 262263
    adjuvant analgesics in, 263
    methadone in, 264
    opioid analgesics in, 263264
    Palliative care, 264265, 265t
    Palsy, nerve, 280, 372373. See also
    Cerebral palsy
    Parallel design trial, 169
    Parathyroid hormone (PTH), 16,
    183184, 187
    Parathyroid hormone-related protein
    (PTHrP), 13, 187
    Patella. See also Nail-patella syndrome
    dislocations of
    congenital, 771
    young athletes with, 784785
    fracture of, 448449
    pediatric, 755756
    treatment of, 448449
    resurfacing of, 472
    Patellar tendon, 449450
    Patellectomy, 449
    Patellofemoral arthroplasty, 473
    Patellofemoral instability, 460461
    Patient(s). See also Education; Elderly
    patients; Young athletes
    complaints of, 5
    cultural diversity of, 114
    handoff of, 4
    injury understanding by, stages of, 152
    instruments specific to, 472473
    safety of, 3
    surgeons skills important to, 110t
    Patient-centered care, 5, 109110
    Pavlik harness, 732
    Pediatric patients. See also Femoral
    fracture; Lower extremity, pediatric;
    Spinal trauma, pediatric
    atlas fractures in, 721
    bone tumors in, 825, 827
    calcaneal fractures in, 759
    cartilage tumors in, 828
    cavus foot in, 776777, 777f
    Ewing sarcoma in, 827828, 828f
    fibula fractures in, 758
    foot fractures in, 759
    hand fractures in, 691692, 691t
    hip dislocations in, 727728
    metabolic bone diseases in, 764765
    metatarsal fractures in, 759
    musculoskeletal infections in, 831
    osteoid osteoma in, 825
    osteomyelitis in, 247248, 831832
    osteosarcoma in, 827, 827f
    patella fractures in, 755756
    pelvis fractures in, 727
    rhabdomyosarcoma in, 830
    rotatory subluxation in, 722
    septic arthritis in, 248249, 832

    soft-tissue masses in, 830


    soft-tissue tumor in, 830
    spondylolysis in, 719
    synovial sarcoma in, 830
    talus fractures in, 759
    tibial physeal fractures in, 756758
    tibial shaft fractures in, 756757
    toe injuries in, 759
    traumatic amputations in, 759
    Pediatric trigger thumb, 710
    Pelvic apophysites, 793
    Pelvic osteotomy, 742743, 743f
    Pelvic ring injury, 379
    anterior, 381382
    classification of, 381t
    examination of, 382f
    fixation of, 381382, 382f
    nonsurgical treatment of, 380381
    posterior, 382385
    ramus fractures and, 381382
    reduction of, 381382
    symphyseal disruptions and, 381
    Pelvis
    apophyseal avulsion of, 788789, 788f
    fracture of, 379
    classification of, 380, 381t
    clinical findings with, 380t
    CT of, 91
    evaluation of, 379380
    internal degloving soft-tissue
    injuries and, 385
    management of, 379380, 385
    outcome studies for, 385
    pediatric, 727
    radiography of, 380
    incidence of
    fixed sagittal imbalance and,
    589590
    normal values for, 590t
    tilt of, 590t
    unstable injuries of, 131133
    Penicillin, 50, 50t
    Pentasaccharide, 139
    Percutaneous needle biopsy, 101102
    Perforator flap, 54
    Perilunate, 355356
    Peripheral nerve
    schematic of, 226f
    structure of, 225
    Peripheral nerve sheath tumor, 194t
    Peripheral nervous system (PNS), 225
    Periprosthetic fracture, 427, 427t, 437
    Periprosthetic joint infection, 250
    compromising factors with, 252t
    evaluation of, 252
    inoculation mechanisms of, 250
    MRSA and, 254, 255t
    presentation of, 251
    staging of, 250, 251t
    treatment of, 252254, 253t
    wound grading and, 251
    Permeability transition pore (PTP), 26
    Peroneal neuropathy, 231
    Peroneal tendinopathy, 528, 529f
    Personal isolator suits, 239

    Orthopaedic Knowledge Update 10

    847

    1/11/2011 2:21:54 PM

    Index
    Pes planus, 527
    Phalangeal fracture, 351
    Phantom limb pain/sensation, 540t
    Phocomelia, 704f
    Physeal stress reactions/avulsions, 793
    Physical therapy, glenohumeral arthritis
    treatment with, 286
    Pigmented villonodular synovitis, 194t
    Piperacillin, 50t
    Pivot joint, 64f
    Pivot-shift test, 345, 345f
    Plate, 434
    fixation of, 481482, 483f
    locking, 275
    nail vs., 484485
    Platelet-derived growth factor (PDGF), 11
    Platelet-rich plasma, 15
    Pleiomorphic rhabdomyosarcoma, 194t
    Pleomorphic soft-tissue sarcoma, 193
    PNS. See Peripheral nervous system
    Poland syndrome, 702, 703f
    Polydactyly
    postaxial, 706707
    preaxial, 706
    thumb, 706, 707f
    toe, 778
    ulnar, 706707
    Polyethylene
    highly cross-linked, 7879
    structure of, 7576
    ultra-high-molecular-weight, 76,
    7879
    Polyethylene prostheses, 74t
    Polymethylmethacrylate bone cement
    (PMMA), 60t, 61f
    Polytrauma, 129
    assessment of, initial, 129
    blood loss in, 129
    cardiovascular status in, 129130
    clinical conditions of, 433t
    intensive care unit and, 133134
    patient condition in
    borderline, 130, 130t
    criteria in, 132t
    grading, 130
    in extremis, 131
    stable, 130
    rehabilitation after, 135
    soft-tissue reconstruction after,
    134135
    unstable, 130
    Popliteofibular ligament (PFL), 455
    Positional calcaneovalgus, 774
    Positron emission tomography (PET), 98
    of osteomyelitis, 99
    of soft-tissue masses, 205
    of tumors, 100101
    Postaxial polydactyly, 706707
    Posterior distal femoral angle (PDFA),
    764f
    Posterior proximal tibial angle (PPTA),
    764f
    Posttraumatic arthritis
    as acetabular fracture complication,
    391

    848

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 848

    epidemiology of, 413


    treatment of, 285
    Prader-Willi syndrome, 803
    Preaxial polydactyly, 706
    Preiser disease, 366367
    Progressive static splint, 344f
    Pronator syndrome, 369
    Prostheses
    amputee
    management of, 543
    prescription of, 544t
    training for, 545
    joint
    ceramic-on-ceramic, 74t, 7778
    ceramic-on-metal, 74t, 79
    CT of, 9293
    metal-on-metal, 74t, 7677
    polyethylene, 74t
    zirconium on polyethylene, 74t
    Prosthetic joint arthroplasty, 254t
    Proteoglycan, 23, 27
    Proteus syndrome, 800801, 800f
    Proximal interphalangeal joint (PIP joint),
    351352, 365
    Pseudarthrosis
    as spinal deformity surgery
    complication, 593
    of tibia, congenital, 768
    Pseudomona aeruginosa, 244445
    Psoriatic arthritis, 219
    Pterygia syndrome, 807
    Pudendal nerve, 435
    Pulmonary embolism
    prevention guidelines, 138t
    as total hip arthroplasty complication,
    427
    Puncture wounds, 249250
    P values, 172, 173f
    Pyomyositis, 833
    Pyrophosphate arthropathy, 86

    Q
    Quadriceps contusion, in young athletes,
    786
    Quadriceps tendon, 449450
    Quinolone, 50

    R
    Radial fracture
    distal, 356, 688690
    angulation in, 689t
    treatment guidelines for, 357t,
    358t
    metaphyseal
    complete, 689
    greenstick, 689
    torus, 688689
    physeal, 689
    Radial head fracture, 325
    classification of, 325, 326f
    examination of, 325
    imaging of, 325
    MRI of, 86

    radiography of, 86
    treatment of, 325327, 326f
    Radial longitudinal deficiency, 698
    classification of, 698
    Fanconi anemia with, 698699
    thrombocytopenia-absent radius
    syndrome with, 698, 699f
    thumb hypoplasia with, 699
    treatment of, 699700, 700f
    VACTERL association and, 699
    Radial neck fracture
    closed reduction of, 682683
    displaced, 682683
    MRI of, 86
    radiography of, 86
    Radial nerve
    compression of, 371
    palsy, 280, 372
    Radiculopathy. See Cervical spondylotic
    radiculopathy; Chronic inflammatory
    demyelinating polyradiculopathy
    Radiofrequency ablation (RFA), 102
    Radiography
    advances in, 85
    of ankle fractures, 493494, 494f
    of arthritis, 86
    of arthropathy, 8687
    of axial neck pain, 612
    of bone lesions, 195, 196f
    cervical spine, 85
    of cervical spondylotic myelopathy,
    616617
    of cervical spondylotic radiculopathy,
    614
    of clavicle fracture, 271
    of congenital anomalies, 89
    extremity fracture, 8586
    of femoroacetabular impingement,
    414, 415f, 415t
    of foot fractures, 517
    of hip arthritis, 414
    of hip dysplasia, 417418, 418t
    of humeral shaft fracture, 278279,
    279f
    of infection, 88
    of knee, 469470
    of Legg-Calv-Perthes disease, 746f
    of metabolic diseases, 8889
    neoplasm, 8788
    of osteoarthritis, 86
    of osteoporosis, 185f
    of pediatric lower extremity alignment,
    763764
    of pediatric spine injuries, 720721
    of pelvic fractures, 380
    of proximal femoral fractures, 86
    of proximal humerus fractures, 274
    of radial head/neck fractures, 86
    of rheumatoid arthritis, 86
    of scaphoid fractures, 86
    of scapular fractures, 277
    of slipped capital femoral epiphysis,
    747f748f
    of seronegative spondyloarthropathy,
    87

    Orthopaedic Knowledge Update 10

    1/11/2011 2:21:54 PM

    Index
    of spinal deformity, 586, 586f
    of thoracolumbar trauma, 642
    Radius. See Radial fracture; Radial
    head fracture; Radial longitudinal
    deficiency; Radial neck fracture
    Ramus fracture, 381382
    Randomized controlled trial (RCT)
    designs of, 168170
    ethics of, 170
    in evidence-based medicine, 159
    in orthopaedic journals, 160f
    Reactive arthritis, 219
    Recalls, of medical devices, 5
    Receptor activator of nuclear factor- B
    ligand (RANKL), 184
    Reconstructions. See Soft-tissue
    reconstruction
    Rehabilitation
    amputation, 543
    community reintegration in, 545
    equipment for, 544545
    mobility in, 544
    prosthetic, 545
    range of motion in, 544
    strengthening in, 544
    after meniscus repair, 459
    after polytrauma, 135
    after rotator cuff tear repair, 308309
    of young athletes, 784
    Relative risk, 167168
    Remak bundles, 225
    Repetitive strain injury (RSI), 215
    Research, 167. See also Observational
    studies; Randomized controlled trial
    bias limitation in, 171
    calculations in, sample, 167t
    cancer-related, 195
    statistics in, 172173, 173f
    subgroup analysis in, 172
    terminology of, 167168
    Residual limb pain/sensation, 541t
    Retinoblastoma, 194t
    Reverse shoulder arthroplasty, 290292
    Rhabdomyosarcoma
    alveolar, 194t
    pediatric, 830
    pleiomorphic, 194t
    Rheumatoid arthritis, 217218
    classification of, 218t
    epidemiology of, 413
    radiography of, 86
    treatment of, 285
    Rib fusion, congenital, 716
    Rickets, 189190, 190t, 764, 766f
    Riluzole, 575t, 578
    Risk
    calculation of, 167168
    management of, 58
    Rotator cuff
    disorders of, 303304
    fatty infiltration of, classification of,
    305t
    healing of, factors affecting, 304t
    impingement of, 303, 304t
    nutrition to, rotator cuff tear

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 849

    arthropathys effect on, 290f


    Rotator cuff tear, 303304
    classification of, 306t, 307f
    diagnostic imaging of, 304305
    history of, 304
    lag signs of, 305t
    lesions associated with, 304
    physical examination of, 304
    treatment of, 305306
    arthroscopic repair in, 306
    augmentation in, 307
    open repair in, 306
    partial-thickness tears and, 306
    rehabilitation after, 308309
    single-row vs. double-row repair
    in, 307
    surgical, 306
    tendon transfers in, 307308
    transosseous repair in, 307
    Rotator cuff tear arthropathy (RCTA),
    289290
    classification of, 290, 291t
    rotator cuff nutrition affected by, 290f
    treatment of, 290292
    Rotatory subluxation, pediatric, 722
    Rothmund-Thompson syndrome, 194t
    runx-2, 11
    Russell-Silver syndrome, 800

    S
    Sacral fracture
    transforaminal, 384f
    U-shaped, 385
    vertical, 384385, 384f
    Sacral slope, normal values for, 590t
    Sacroiliac joint (SI joint), 383384, 384f
    Sacroiliac screw, 384, 384f
    Saddle joint, 64f
    Safety
    checklists, 4
    patient, 3
    Sagittal imbalance. See Fixed sagittal
    imbalance
    Salmonella species, 246
    Sample size, 173
    Sarcomas. See also specific sarcoma
    categories of, 193
    genetic cancer predispositions
    associated with, 194t
    translocations, 194t
    Sarcomeres, 37
    Scaphoid
    fractures of, 86, 690
    nonunion of, 354
    osteonecrosis of, 366367
    Scaphoid nonunion advanced collapse
    (SNAC), 363, 364t
    Scapholunate advanced collapse (SLAC),
    363, 363f, 364t
    Scapholunate ligament
    dissociation, 354355, 355t
    reconstruction of, 363
    Scaphotrapezial joint, 365
    Scapular dyskinesis, 318

    Scapular fracture, 277


    classification of, 277
    injuries associated with, 277
    presentation of, 277
    radiographic evaluation of, 277
    treatment of, 277278
    types of, 277278
    Scheuermann kyphosis, 718719
    Schwann cell, 225
    Scoliosis, 587
    adolescent, 716, 718f
    adult, 592
    cerebral palsy with, 813814
    idiopathic, 716718
    neuromuscular, 592
    treatment of
    approach in, 588
    brace, 717
    curve correction in, 588
    decompression in, 588589
    fusion level selection in, 588
    nonsurgical, 587
    surgical, 588, 717
    Septic arthritis
    adult, 246247
    bacteria causing, 246
    diagnosis of, 247
    joint decompression for, 247, 249
    pediatric, 248249, 832
    presentation of, 246247, 249
    treatment of, 247
    Sequestrectomy, 603604
    Seronegative spondyloarthropathy,
    218220
    pathogenesis of, 218
    radiography of, 87
    undifferentiated, 220
    Serpentine foot, 774
    Sesamoiditis, 528
    Sever disease, young athletes with, 793
    Shock
    hemorrhagic, 129
    in polytrauma, 132t
    Shoulder. See also Glenohumeral
    degenerative joint diseases
    anatomy of, 299
    arthroplasty of
    biologic total, 288289
    resurfacing, 287
    total, 289
    biomechanics of, 299300
    dislocations of, young athletes with,
    787788
    disorders of, 315
    floating, 278
    force couples of, 301f
    internal impingement of, 317318
    laxity of, 316
    little leaguers, 789
    Shoulder instability, 299, 316
    anterior, 301
    arthroscopic vs. open repair of, 302
    Latarjet procedure for, 302f
    natural history of, 301302
    recurrent, 302

    Orthopaedic Knowledge Update 10

    849

    1/11/2011 2:21:55 PM

    Index
    treatment of, 301
    classification of, 300301
    constraints to, 300t
    multidirectional, 303
    nonsurgical treatment of, 303
    surgical treatment of, 303
    posterior, 302
    acute posterior dislocation in,
    302303
    chronic posterior dislocation in, 303
    surgical treatment of, 303
    Shoulder resurfacing arthroplasty, 287
    Sickle cell disease, 831
    Sinding-Larsen-Johansson syndrome,
    young athletes with, 793
    Single photon emission CT (SPECT), 98
    Skeletal muscle. See also specific muscles
    contraction of, 37
    fibers of, 3739, 38t
    function of, 3739
    healing of, 3940, 39f
    injury to, 3940
    number of, 37
    structure of, 3739, 38f
    Skewfoot, 774
    Skin
    closure suture, 53
    graft, 53
    ulcers, 818
    web, 807
    Slipped capital femoral epiphysis (SCFE),
    746
    classification of, 747
    clinical evaluation of, 747
    complications with, 749
    etiology of, 747
    imaging of, 74748
    incidence of, 747
    radiography of, 747f748f
    treatment of, 748749
    SMAD proteins, 182
    Smith-Peterson osteotomy, 590
    Smoking, fracture union delayed by, 13
    Soft-tissue injury
    classification of, 133t
    of hand/wrist, 358
    pelvic internal degloving, 385
    in polytrauma, 132t
    Soft-tissue masses
    biopsy of, 205207
    categories of, 208t209t
    imaging of, 205
    management of, 207, 210
    MRI of, 205
    pathology of, 208t209t
    pediatric, 830
    positron emission tomography of, 205
    presentation with, 204205
    Soft-tissue reconstruction, 134135
    Soft-tissue tumor, pediatric, 830
    Spheroidal joint, 64f
    Spinal column. See also Cervical spine;
    Lumbar spine
    aging of, 592593
    anatomy of

    850

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 850

    development of, 720


    ossification centers in, 720f
    congenital abnormalities of, 715716
    development of, 29, 715
    fractures of, CT of, 9091
    injury of, unstable, 133
    stability of, 643
    surgery on
    advances in, 665, 670671
    dynamic stabilization systems in,
    667668
    facet replacement, 668669
    interspinous spacer technology in,
    669
    thromboembolism after, 139140
    wear characteristics of, 75
    Spinal cord, 226227
    as central nervous system component,
    226
    development of, 715
    schematic of, 227f
    Spinal cord injury (SCI), 573
    evaluation of
    emergency assessment in, 573
    MRI in, 575576
    neurologic assessment in, 573575,
    574f
    incidence of, 573
    pathophysiologic mechanisms of,
    576577
    recovery from, 576577
    treatment of, 576
    novel approaches in, 575t, 577579
    Spinal deformity
    adult, 585
    age and, 592593
    evaluation of
    clinical, 585586
    radiographic, 586, 586f
    intraoperative neurophysiologic
    monitoring and, 592
    with myelomeningocele, 816817
    pseudarthrosis with, 593
    treatment of
    complications with, 593
    goals for, 585
    indications for, 585
    types of, 586587
    Spinal dysraphism, 718f
    Spinal infection, 565
    clinical presentation of, 571
    diagnostic imaging of, 571
    epidemiology of, 570571
    laboratory studies of, 571
    postoperative, 570571
    treatment of, 571
    Spinal muscular atrophy (SMA)
    classification of, 819
    clinical/orthopaedic features of, 812t
    genetic characteristics of, 812t
    prevalence of, 812t
    Spinal stenosis. See Lumbar spinal
    stenosis
    Spinal trauma, pediatric, 719720
    false signs of, 720t

    management of, 721


    radiographic findings with, 720721
    Spinal tumor, 553
    diagnosis of, 554
    epidemiology of, 553
    evaluation of, 553554
    metastatic, 557560
    evaluation algorithm for, 558f
    imaging of, 558t
    NOMS system for, 558, 560f
    radiosensitivity of, 560t
    scoring system for, 559t
    primary benign, 554556
    primary malignant, 556557
    staging of, 554, 555f
    treatment of
    surgical planning in, 554
    surgical technique in, 560561
    types of, 553t
    Spine. See Cervical spine; Lumbar spine;
    Spinal column; Spinal cord; Thoracic
    spine
    Splint
    developmental dysplasia of the hip
    treatment with, 741742
    progressive static, 344f
    Split-thickness skin grafting (STSG), 53
    Spondylitis. See Ankylosing spondylitis
    Spondyloarthropathy. See Seronegative
    spondyloarthropathy
    Spondylolisthesis, 651, 719. See also
    specific spondylolisthesis
    classification of, 651t
    clinical presentation of, 654
    epidemiology of, 651652
    pathogenesis of, 652654
    treatment of, 654657
    Spondylolysis
    lumbar
    incidence of, 651
    pathogenesis of, 652
    treatment of, 654655
    pediatric, 719
    Spondylosis, 635
    Sponges, retained, 4
    Sprengel deformity, 706
    Staphylococcus aureus. See also
    Methicillin-resistant Staphylococcus
    aureus
    infectious arthritis caused by, 221
    osteomyelitis caused by, 244
    septic arthritis caused by, 246
    Statistics, 172173, 173f
    Steel
    material properties of, 60t
    stress-strain curve of, 61f
    Stem
    cemented, 422, 426
    cementless, 422423
    cylindrical fully porous coated, 425
    flat wedge tapered, 423f
    modular tapered, 425
    Stem cell
    mesenchymal, 43
    source of, 13

    Orthopaedic Knowledge Update 10

    1/11/2011 2:21:55 PM

    Index
    Stenosis. See Lumbar spinal stenosis
    Sternoclavicular joint, 675
    Steroids
    bone regulation with, 187188
    cervical spine trauma treatment with,
    627
    corticosteroids
    bone healing inhibition by, 14
    uses of, 187
    glenohumeral injection of, 286
    Streptococcus species, 246
    Stress fracture, 9899, 792793
    Study power, 173
    Subaxial fracture, 722
    Subluxation, rotatory, 722
    Superior labrum anterior posterior
    (SLAP)
    lesions of, 317f
    tears of, 316317
    Supracondylar fracture. See Humeral
    fracture
    Surgery. See also specific procedure
    blood management in, 140141
    algorithm for, 142f
    intraoperative, 142
    postoperative, 142143
    preoperative, 141
    burns during, 4
    complications after, CT of, 9293
    fire during, 4
    instruments retained after, 4
    site marking prior to, 3, 4t
    time-out during, 3
    wound contamination reduction
    measures after, 242t
    wrong-site, 34
    Surgical neuroma, 529530
    Surgical wounds
    clean (type I), 4950, 50t
    clean-contaminated (type II), 4950, 50t
    contaminated (type III), 4950, 50t
    dirty-infected (type IV), 49
    Surveillance, Epidemiology, and End
    Results (SEER), 193
    Suture, 53
    Symbrachydactyly
    diagnosis of, 701
    monodactylous form of, 701702,
    703f
    nubbin formation with, 701702, 703f
    short-finger type of, 702704, 703f
    syndactyly release with, 703
    Symmetric sensory polyneuropathy,
    distal, 231
    Synchondrosis, dentrocentral, 720t
    Syndactyly, 704
    classification of, 704
    reconstruction for, 704, 705f
    Synostosis
    across elbow, 705
    radioulnar, 706, 707f
    Synovial sarcoma
    pediatric, 830
    translocation of, 194t
    Synthetic bone substitutes, 15

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 851

    T
    Talofibular joint, 513
    Talofibular ligament, 529
    Talus, 511512
    fracture of
    body, 513
    lateral process, pediatric, 759
    neck, 512513, 513f, 758759
    lateral process of, 513
    subtalar dislocations and, 513514
    vertical, congenital, 772, 772f
    Tarsal coalition, 775
    Tarsal navicular fracture, 514515, 514f
    Tarsometatarsal injury, 515516, 516f
    Tear. See Meniscus tear; Rotator cuff tear;
    Superior labrum anterior posterior
    Temperature, in polytrauma, 132t
    Tendinopathy, 44
    peroneal, 528, 529f
    treatment of, 44
    Tendon(s). See also specific tendon
    bone insertion of, 41
    composition of, 41
    function of, 4142
    healing of, 42, 43f
    injury of, 42
    treatment for, 4344
    load-elongation curve of, 41, 42f
    origin of, 37
    stress-strain behavior of, 42
    structure of, 4142
    transfers, 307308, 371
    indications for, 372373
    surgical principles of, 372t
    Tenodesis, 307t
    Tenotomy, 307t
    Teriparatide, 189
    Terrible triad injury, 332, 334f
    Testosterone, 187
    THA. See Total hip arthroplasty
    Thoracic disk herniation
    classification of, 661
    clinical presentation of, 661662
    etiology of, 661
    imaging of, 662
    incidence of, 661
    natural history of, 662
    physical examination of, 662
    surgical approach in, 662664
    Thoracic spine, 722
    Thoracolumbar junction, 641
    Thoracolumbar trauma, 641
    assessment of
    CT in, 642
    imaging in, 642
    initial, 641642
    MRI in, 642643
    physical examination in, 642
    radiography in, 642
    classification of, 643644, 644t
    treatment of
    minimally invasive surgery in, 648
    surgical approaches in, 646647,
    646t

    surgical stabilization in, 644645


    Thrombocytopenia-absent radius
    syndrome, 698, 699f
    Thromboembolism, 137
    mechanical prophylaxis for, 139
    pharmacologic prophylaxis for,
    137139
    after spine surgery, 139140
    Thrombosis, deep venous, 139, 427
    Throwers elbow, 789790
    Throwing athletes
    clinical evaluation of, 315316
    injuries of
    acromioclavicular joint, 318319
    internal impingement, 317318
    risk of, 315
    scapular dyskinesis as, 318
    SLAP tears as, 316317
    neurovascular injuries in, 319
    Throwing motion, 316f
    Thumb
    carpometacarpal joint osteoarthritis,
    364365
    deficiency of, 700t
    hypoplasia of, 699, 701f
    pediatric trigger, 710
    polydactyly of, 706, 707f
    Tibia
    amputation of, 537
    angles of, 764f
    bowing of, posteromedial, 770, 771f
    congenital pseudarthrosis of, 768
    healing of, 12f
    local reference frame of, 65f
    Tibial eminence fracture, 785, 786f
    Tibial hemimelia, 770
    Tibial osteotomy, 471
    Tibial physeal fracture, pediatric
    distal, 757758
    proximal, 756
    Tibial plafond fracture, 499
    classification of, 499500
    complications with, 500, 502
    emergency evaluation of, 499
    outcomes of, 500, 502
    treatment of
    external fixation in, 500
    open reduction and internal
    fixation in, 500
    staged management of, 500, 501f
    Tibial plateau fracture, 443
    classification of, 443, 444f
    CT of, 92
    evaluation of, 443444
    injury mechanisms of, 443
    outcomes after, 447
    treatment of
    definitive surgical, 445447
    indications for, 444445
    provisional, 445
    urgent, 445
    Tibial shaft fracture, 479
    classification of, 480, 480t, 482f
    clinical examination of, 479480
    healing of, 486

    Orthopaedic Knowledge Update 10

    851

    1/11/2011 2:21:55 PM

    Index
    malunion of, 486
    nonunion of, 486488
    open, 484
    classification of, 484
    surgical dbridement with, 484485
    wound closure after, 485486
    pediatric, 756757
    treatment of, 133t
    external fixation in, 481, 483f
    intramedullary nailing in, 482483,
    484f
    nonsurgical, 48081
    plate fixation in, 481482, 483f
    plating vs. nailing in, 484485
    surgical, 481484
    Tibial torsion, 768769
    Tibial tubercle fracture, 756
    Tibia vara
    early onset, 765766, 767f
    late onset, 766767
    Tibiofemoral joints, 458459
    Tibiofibular syndesmosis, 497
    Tibiotalar joints
    resection of, 523
    traumatic arthritis of, 523
    Tillaux fracture, 758
    Time-out, in operating room, 3
    Tinel sign, 369
    Titanium
    material properties of, 60t
    stress-strain curve of, 61f
    Tobramycin, 50t
    Toe
    claw toe, 527
    crossover, 528
    curly, 778
    deformities of, 778779
    pediatric injury, 759
    polydactyly of, 778
    Toe walking, 779
    Total disk arthroplasty (TDA), 73, 75,
    7980
    Total hip arthroplasty (THA), 73
    aseptic loosening of, 74
    bearing surfaces for, 74t
    complications of
    deep venous thrombosis as, 427
    infection as, 426427
    instability as, 426
    periprosthetic fractures as, 427
    pulmonary embolism as, 427
    failure of, 74
    hip dysplasia treatment with, 418419
    primary
    acetabular reconstruction with, 422
    femoral reconstruction with, 422
    423
    hip resurfacing with, 423
    revision
    acetabular reconstruction with,
    423424
    femoral reconstruction with,
    425426
    Total joint arthroplasty, 73
    Total knee arthroplasty (TKA), 73, 471

    852

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 852

    aseptic loosening of, 75


    bearing surfaces for, 74t
    design of, 472
    cruciate-retaining, 472
    high-flexion, 473
    mobile-bearing, 472
    posterior cruciate substituting, 472
    diabetes effect on, 471
    failure of, 75
    infection with
    chronic, 474
    risk factors of, 471
    treatment of, 473474
    instruments for, patient-specific,
    472473
    obesitys effect on, 471
    outcome of, 471
    painful, 474
    patellar resurfacing and, 472
    revision
    bone loss in, 474475
    component fixation in, 474475
    component removal in, 474
    constraint in, 475
    evaluation for, 474
    surgical management in, 474
    surgical technique of, 471472
    computer-assisted surgery in,
    472473
    spacer block use in, 472f
    Total shoulder arthroplasty, 289
    Transphyseal fracture, 681
    Transverse atlantal ligament injury,
    management of, 630
    Trauma. See Polytrauma; Posttraumatic
    arthritis; specific body part
    Traumatic arthritis, 523
    Traumatic spondylolisthesis
    epidemiology of, 652
    pathogenesis of, 653654
    treatment of, 657
    Triangular fibrocartilage complex
    (TFCC), 373374, 374t
    Tribology, 75
    Trichorhinophalangeal syndrome (TRPS),
    803
    Trigger finger, 710
    Trochlea fracture
    classification of, 329, 330f
    surgical treatment of, 329
    Tumor. See also Spinal tumor
    bone, pediatric, 825, 827
    cartilage, pediatric, 828
    desmoplastic small round cell, 194t
    evaluation of
    bone scans in, 100101
    CT in, 101
    positron emission tomography in,
    100101
    genes related to, musculoskeletal
    syndromes caused by, 799
    giant cell, 555
    inflammatory myofibroblastic, 194t
    peripheral nerve sheath, 194t
    soft-tissue, pediatric, 830

    Tumor necrosis factor (TNF-), 11


    Turner syndrome, 802803

    U
    Ulcer, skin, 818
    Ulna
    coronoid process of, 345f
    deficiency of, 700701, 702t
    metaphyseal fracture of
    complete, 689
    greenstick, 689
    torus, 688689
    physeal fracture of, 689
    styloid fracture of, 689690
    Ulnar collateral ligament
    lateral, 345346, 346f
    repair of, 321f
    Ulnar dimelia, 707708, 708f
    Ulnar nerve
    compression of, 369, 371
    palsy, 373
    Ulnar neuropathy, 231
    Ulnar pain, 373374
    Ulnar polydactyly, 706707
    Ulnar tunnel syndrome, 369, 371
    Ulnocarpal impaction, degenerative, 374
    Ulnocarpal joint, 374
    Ultra-high-molecular-weight polyethylene
    (UHMWPE), 76, 7879
    Ultrasound, 16. See also Low-intensity
    pulsed ultrasound
    Unicameral bone cyst (UBC), 826
    Unicompartmental knee arthroplasty
    (UKA), 473
    Unicondylar fracture, distal femoral,
    437438

    V
    VACTERL association, 699
    Valgus extension overload, 321322,
    321f
    Vascular claudication, 600t
    Vascular endothelial growth factor
    (VEGF), 13, 1516
    Vascular injury
    femoral shaft fracture with, 434
    of hand, 358
    humeral supracondylar fracture, 679
    throwing athletes with, 319
    of wrist, 358
    Vascular malformations, 830
    Vasculocutaneous catastrophe, of
    newborn, 711
    Venous thrombosis, deep, 139, 427
    Vertebrae. See also Intervertebral disk
    body of, wedging of, 720t
    resection of, 592593
    Vertebral artery injury, 636
    Vertebral compression fracture (VCF),
    647648
    Vertebral osteomyelitis (VO)
    hematogenous, 565
    nonpyogenic

    Orthopaedic Knowledge Update 10

    1/11/2011 2:21:55 PM

    Index
    clinical presentation of, 567, 569
    epidemiology of, 567
    imaging of, 569
    laboratory diagnosis of, 567, 569
    pathogenesis of, 567
    treatment of, 569570
    pyogenic
    clinical presentation of, 566
    epidemiology of, 565
    imaging of, 566, 566f568f
    laboratory assessment of, 566
    pathophysiology of, 565
    Vertebroplasty, 188
    Vertical talus, congenital, 772, 772f
    Viscosupplementation, 286
    Vitamin D, 188
    Volume treatment, 129

    W
    Warfarin, 137138
    Wartenberg sign, 371f
    Wartenberg syndrome, 371
    WBC. See White blood cell
    Wear
    characteristics of
    hips, 74
    knees, 75
    spines, 75
    mechanisms of, 7374
    modes of, 74
    White blood cell (WBC), 99
    Wnt pathway
    age-related changes in, 25
    signaling via, 16
    Workers compensation, 147
    causation in, 149150
    clinical guideline legislation with, 153
    costs of, 147149
    history of, 147
    procedure outcomes and, 148t

    2011 American Academy of Orthopaedic Surgeons

    OKU10_Index.indd 853

    Work-related illness/injury, 147


    assessment after, 151
    biologic vs. biopsychosocial disease
    models with, 151152
    clinical treatment guidelines for, 153
    costs of, 147149
    disability from, 152153
    impairment from, 152153
    return to work after, 150151
    risk and, 151
    work capacity and, 151
    work tolerance and, 151
    Wound(s). See also Open fracture wound;
    Surgical wounds
    contamination reduction, 242t
    gunshot, 434
    infection of, 49
    management of, 49
    periprosthetic joint infection and, 251
    puncture, 249250
    Wrist
    dislocations of, 353
    fractures of, 353
    CT of, 9192
    injuries of
    nerve, 359
    soft-tissue, 358
    vascular, 358
    young athletes with, 790
    pain in, ulnar, 373374
    scaphoid nonunion advanced collapse
    of, 363, 364t
    scapholunate advanced collapse of,
    363, 363f, 364t
    Wrong-site surgery, 34

    ankle sprains in, 787


    apophyseal avulsion of pelvis,
    788789, 788f
    hand injuries in, 790
    injury of
    acute, 784789
    epidemiology of, 783
    overuse, 78993
    risk of, 783
    knee osteochondritis dissecans in,
    791792
    knee pain in, 790791
    medial epicondyle fracture in,
    787788, 787f788f
    meniscus tears in, 785
    Osgood-Schlatter disease in, 793
    patella dislocations in, 784785
    quadriceps contusion in, 786
    rehabilitation of, 784
    Sever disease in, 793
    shoulder dislocations in, 787788
    Sinding-Larsen-Johansson syndrome
    in, 793
    strength training for, 783
    stress fractures in, 792793
    throwers elbow in, 789790
    tibial eminence fracture in, 785, 786f
    wrist injuries in, 790

    Z
    Z-foot, 774
    Zirconium on polyethylene bearing
    surfaces, 74t
    Z lines, 37
    Zone of polarizing activity (ZPA), 697,
    697f

    Young athletes, 783


    ACL injuries in, 786, 787f
    anatomic considerations with, 784

    Orthopaedic Knowledge Update 10

    853

    1/11/2011 2:21:55 PM

    You might also like