INFECTION

ACUTE, SUBACUTE AND CHRONIC OSTEOMYELITIS

APLEYS SYSTEM OF ORTHOPAEDICS AND FRACTURES 8TH EDITION TEAM IV : IK, JS, TS, SF

GENERAL ASPECT OF INFECTION

Micro-organisms enter the bones and joints :

directly : a break in the skin (a pinprick, a stab wound, a laceration, an open fracture or an operation) indirectly via the blood stream from a distant site: the nose or mouth, the respiratory tract, the bowel or the genitourinary tract.

GENERAL ASPECTS OF INFECTION

Acute pyogenic infections are characterized by:

The formation of pus or abscess (Local effect) a concentrate of defunct leucocytes, dead and dying bacteria and tissue debris. Spread further afield via lymphatics or via the bloodstream (systemic effect) causing lymphangitis and lymphadenopathy, bacteraemia and septicaemia, with systemic reaction : vatigue, mild pyrexia, severe illness, fever, toxaemia and shock.

GENERAL ASPECT OF INFECTION

Chronic infection

follow on acute infection or start from beginning The formation of granulation tissue (a combination of fibroblastic and vascular proliferation) fibrosis.

Host Response:
Age of patient (very young or too old is more resistance), state of malnutrition, immuno-supresan other disease like diabetes

Local Factors :
damaged muscle and foreign bodies bone structure itself consist of collection of rigid compartment make it more susceptible for vascular damage and cell death..

GENERAL ASPECT OF INFECTION

The principles of treatment are:

(1) to provide analgesia and general supportive measures; (2) to rest the affected part; (3) effective antibiotic or chemotherapy; and (4) surgical eradication of infected and necrotic tissue.

For acute infections, the timing of surgery is all-important: in the early stages, antibiotics should be given a chance and the clinical condition carefully monitored to detect signs of improvement or deterioration; if there is pus, it must be let out and the sooner the better.

ACUTE HAEMATOGENOUS OSTEOMYELITIS

Acute osteomyelitis is almost invariably a disease of children. This predilection for the metaphysis has been attributed to the peculiar arrangement of the blood vessels in that area: the non-anastomosing terminal branches of the nutrient artery twist back in hairpin loops before entering the large network of sinusoidal veins; the relative vascular stasis favours bacterial colonization.

In young infants, in whom there is still a free anastomosis between metaphyseal and epiphyseal blood vessels, infection can just as easily lodge in the epiphysis In adults, haematogenous infection is more common in the vertebrae than in the long bones.

PATHOLOGY OF
ACUTE OSTEMYELITIS

Inflammation
acute inflammatory reaction, vascular congestion, exudation of fluid, infiltration of PMN, increase of intraosseus pressure

Suppuration
Subperiosteal abscess, end plate and intervertebral disc infection

Necrosis avascular necrosis of growth plate in infant. Bacterial toxins and leucocytic enzymes also may play their part in the advancing tissue destruction.

reactive new bone formation resolution and healing.

NEW BONE FORMATION

New bone forms from the deep layers of the stripped periosteum. This is typical of pyogenic infection and is usually obvious by the end of the second week. With rime the new bone thickens to form an involucrum enclosing the infected tissue and sequestra. If the infection persists, pus and tiny sequestrated splcules of bone may continue to discharge through perforations (cloacae) in the involucrum and track by sinuses to the skin surfaces; the condition is now established as a chronic osteomyelitis.

(A) INFECTION

IN THE METAPHYSIS MAY SPREAD COWARDS THE SURFACE, TO FORM A

SUBPERIOSTEAL ABSCESS (B). NEW BONE AS A SEQUESTRUM SINUSES.

SOME OF THE BONE MAY DIE, AND IS ENCASED IN PERIO STEAL (C).THE ENCASING INVOLUCRUM IS SOMETIMES PERFORATED BY

RESOLUTION

Once common, chronic osteomyelitis following on acute is nowadays seldom seen. If infection is controlled and intraosseous pressure released at an early stage, this dire progress can be aborted. The bone around the zone of infection is at first osteoporotic (probably due to hypcraemia).

CLINICAL FEATURES

The patient, usually a child, presents with severe pain, malaise and a fever; in neglected cases, toxaemia may be marked. X-RAYS NORMAL DURING FIRST 10 DAYS Ultrasound may detect a subperiosteal collection of fluid in the early stages of osteomyelitis, but it cannot distinguish between a haematoma and pus.

Radioscintigrapby with 99mTc-HDP reveals increased activity in both the perfusion phase and the bone phase.. It has relatively low specificity and other inflammatory lesions can show similar changes. In doubtful cases, scanning with Ga-citrate or In labelled leucocytes may be more revealing. MRI is extremely sensitive, even in the early phase of bone infection, and can help to differentiate between soft-tissue infection and osteomyelitis. The most typical feature is a reduced intensity signal in T1-weighted images.

INVESTIGATIONS
The most certain way to confirm the clinical diagnosis is to aspirate pus from the metaphyseal subperiosteal abscess or the adjacent joint. The white cell count and C-reactive protein values are usually high and the haemoglobin concentration diminished; the ESR also rises but it may take several days to do so and it often remains elevated even after the infection subsides. Blood culture is positive in only about half the cases of proven infection.

DIFFERENTIAL DIAGNOSIS
Cellulitis Streptococcal necrotizing myositis Acute suppurative arthritis Acute rheumatism Sickle-cell crisis Gaucher's disease

TREATMENT
Supportive treatment for pain and dehydration; Splintage of the affected part; Antibiotic therapy 3 6 weeks; and Surgical drainage

ANTIBIOTIK TREATMENT

Older children and fit adult : Staphylococcus group

Flucloxacillin and fusidic acid i.v 1 2 weeks Orally antibiotics 3 6 weeks

Children < 4 years ; Haemophilus group and gram negatife organisms

Cephalosporins (cefuroxime or cefotaxime) i.v or orally Amoxicillin-clavulanic acid combination (co-amoxiclav, a -lactamase inhibitor)

SUBACUTE OSTEOMYELITIS
Relative mildness The organism being less virulent (Staphylococcus aureusor ) and the patient more resistance (or both); More variable in skeletal distribution than acute osteomyelitis The Distal femur and the proximal and distal tibia are favorite sites.

PATHOLOGY
Well defined cavity in cancellous bone glairy seropurulent fluid (rare pus) Cavity is lined by granulation tissue of mixture of acute and chronic inflammatory cells. The surrounding bone trabeculae are often thickened

CLINICAL FEATURES
The patient : child or adolescent Pain near one of the larger joints for several weeks or even months A limp or slight swelling, muscle wasting and local tenderness Normal temperature to slight higher White cell count may be normal but ESR is raised

IMAGING

Plain X-Ray

A circumscribed, oval or round cavity 1 2 cm in diameter on tibia or femoral metaphysis or in epiphysis or in cuboidal bone (calcaneus) Cavity surrounded by halo of sclerosis (the classic Brodies abscess) Metaphysis lesion little or no periosteal reaction Diaphysial lesion periosteal new bone formation and cortical thickening

Radioisotope scan

DIAGNOSIS
Differential diagnosis : Osteoid osteoma with appearance as malignant bone tumour Certain examination by Biopsy for bacteriological culture.

TREATMENT
Conservative Immobilization and antibiotics (flucloxacillin and fusidic acid) for 6 weeks than thereafter for 6 12 months Curretage; indicate for lesion after biopsy and also for the case with no healing with conservative treatment. Antibiotics

CHRONIC OSTEOMYELITIS
The usual organisms (and with time there is always a mixed infection) are Staph. aureus, E. coti, S. pyogenes, Proteus and Pseudomonas; In the presence of foreign implants Staph. cpidermidis, which is normally non-pathogenic, is the commonest of all.

PATHOLOGY
Bone is destroyed or devitalized in a discrete area at the focus of infection or more diffusely along the surface of a foreign implant. Cavities containing pus and pieces of dead bone (sequestra) are surrounded by vascular tissue, and beyond that by areas of sclerosis -the result of chronic reactive new bone formation. The sequestra act as substrates The histological picture is one of chronic inflammatory cell infiltration around areas of acellular bone or microscopic sequestra.

CHRONIC OSTEOMYELITIS CHRONIC BONE INFECTION, WITH A PERSISTENT SEQUESTRUM, MAY BE A SEQUEL TO ACUTE OSTEOMYELITIS (A). MORE OFTEN IT FOLLOWS AN OPEN FRACTURE OR OPERATION (B). OCCASIONALLY IT PRESENTS AS A BRODIE'S ABSCESS (C).

CLINICAL FEATURES
The patient presents because pain, pyrexia, redness and tenderness have recurred (a 'flare'), or with a discharging sinus. In long-standing cases the tissues are thickened and often puckered or folded in where a scar or sinus is attached to the underlying bone. There may be a sero-purulent discharge and excoriation of the surrounding skin. In post-traumatic osteomyelitis the bone may be deformed or non-united.

IMAGING

X-ray examination
Bone resorption with thickening and sclerosis of surrounding bone, loss of trabeculation, area osteoporosis, periosteal thickening, sequestra, or the bone crudely thickened and misshapen

Radioisotope scintigraphy
Sensitive but not specific. Using 99m Tc-HDP for showing increased activity of perfusion and bone phase and 67 GaCitrate or In-labelled leucocytes for showing hidden foci of infection

CT and MRI
Show the extent of bone destruction and reactive edema, hidden abscess and sequestra

INVESTIGATIONS
ESR and blood white cell count may be increased; are helpful in assessing the progress of bone infection but they are not for diagnostic. Organisms cultured from discharging sinuses should be tested repeatedly for antibiotic sensitivity; with time, they often change their characteristics and become resistant to treatment.

TREATMENT
Antibiotics ; Fucidic acid, clindamycin and cephalosporins Local treatment : incision and drainage Operation

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