MINISTRY OF HEALTH- ETHIOPIA

NATIONAL
INTEGRATED EMERGENCY
MEDICINE TRAINING

Participants manual

JANUARY 2020
ADDIS ABABA, ETHIOPIA
 Acknowledgement

Ministry of Health would like to acknowledge Emergency Medicine and critical Care
physicians as well asnurses for their immense technical and academic support.TheMOH
would like to acknowledge the following individuals for their participation on updating the
second Integrated Emergency Medicine participants training manual.

No Name Profession Email Affiliation

1 Dr. Alegneta Assistant Professor [email protected] FMOH

G/Eyesus of Emergency
medicine and Critical
Care

2 Dr. Muluwork Tefera Associate Professor [email protected] AAU

of Pediatrics and
Critical Care

3 Dr. AntenehMitiku Assistant Professor [email protected] Yekatit 12

of Emergency HMC
medicine and Critical
Care

4 Dr. TesfayeGetachew Assistant Professor [email protected] SPHMMC

of Emergency
medicine and Critical
Care

5 Dr. SofiyaKebede Assistant Professor [email protected] AAU

of Emergency
medicine and Critical
Care

6 Dr. AyalewZewdie Assistant Professor [email protected] SPHMMC

of Emergency
medicine and Critical
Care
7 Dr. Rediet Selemon Assistant Professor [email protected] SPHMMC
of Emergency
medicine and Critical
Care

8 Dr. TigistTesfaye Assistant Professor [email protected] SPSH

of Emergency
medicine and Critical
Care

9 Mr. Lecturer Emergency [email protected] FMOH

HaimanotGeremew and Critical Care

10 Mr. KibatuGebre Lecturer Emergency [email protected] AAU

and Critical Care

11 Ms. Nejat Ibrahim. MPH [email protected] FMOH

12 ECCD

First edition authors:

 Acronyms

AAU – Addis Ababa University

ABC- Airway Breathing Circulation
ACEIs- Angiotensin converting enzyme inhibitors
ACLS -Advanced cardiac Life support.
AFB- Acid fast bacilli
AMS-Altered Mental Status
BLS-Basic Life Support,
BP- Blood pressure
BPM- Beats Per Minute
BUN- Blood urea nitrogen
C/I- Contraindication
CPR- Cardio pulmonary resuscitation
CSF-Cerebrospinal fluid
CVA-Cerbro Vascular Accident,
DDX- Differential diagnosis
DKA-Diabetic Ketoacidosis,
Dx- Diagnosis
ECG-Electrocardiogram
ED- Emergency Department
EMCC-Emergency Medicine and Critical Care
EMS- Emergency medical service
EMT- Emergency Medical Technician
ETT- endotracheal tube
GCS- Glasgow coma scale
GFR- Glomerular filtration rate
Hct-Hematocrit
Hgb-Hemoglobulin
HHS -Hyperglycemic Hyperosmolar State
Hx- History
ICP- intra cranial pressure
IM- Intra muscular
INR- International normalized ratio
IV- Intra venous
JVP-Jugular vein pressure
LFTs-Liver function tests
LMWH - Low Molecular weight Heparin
MAP-Mean arterial pressure
MDI- metered dose inhaler
MI - Myocardial Infarction,
Mx - Management
NSAIDs - Non-Steroidalanti Inflammatory Drugs
OFT- Organ Function Test
P/E- Physical examination
PEF-peak expiratory flow
PO - per Os
PT - Prothrombin time
PTE- Pulmonary Thrombo Embolism
RBS- Random blood sugar
RHB-Regional Health Bureau
RR - Respiratory rate
Rx- Treatment
SABA-Short Acting Beta Agonist
SC- Subcutaneous
SIRS - Systemic Inflammatory Response syndrome
Sn - Sign
SPHMMC – St. Paul Hospital Millinium Medical College
SPSH – St. Peter Specialized Hospital
Sx - Symptom
TBI – Traumatic Brain Injury
TTC- Tetracycline
U/A-Urine analysis
UFH- Unfractionated Heparin
URT- Upper respiratory tract
UTI -Urinary tract infection
WBCs-White blood cell
Yekatit 12 HMC – Yekatit 12 Hospital Medical College
Contents
Forward ................................................................................................... Error! Bookmark not defined.
Acknowledgement.................................................................................................................................. 3
Acronyms ................................................................................................................................................ 5
INTRODUCTION ...................................................................................................................................... 9
Training/Learning Methods .................................................................................................................. 10
CHAPTER ONE: EMERGENCY MEDICALSERVICE SYSTEM ..................................................................... 16
1.1 Pre-hospital EMS ....................................................................................................................... 20
1.2 In Hospital Components of EMSS ............................................................................................. 23
1.3 ED/ER Work Flow ..................................................................................................................... 25
1.4 Communication in ED ................................................................................................................ 27
CHATER TWO: ADULT TRIAGE .............................................................................................................. 29
CHAPTER THREE: APPROACH TO CRITICALLY ILL PATIENT ................................................................... 35
3.1 The ABCDE approach:............................................................................................................... 37
CHAPTER FOUR: AIRWAY AND BREATHING ASSESSMENT AND MANAGEMENT ................................. 46
CHAPTER FIVE: COMMON ARRHYTHMIASAND CARDIAC RESUSCITATION .......................................... 66
5.1 Introduction to basic ECG .......................................................................................................... 67
5.2. Cardiac arrest resuscitation........................................................................................................ 82
5.3. Arrhythmia / Dysrhythmia ........................................................................................................ 92
CHAPTER SIX: EMERGENCY APPROACH TO SHOCK ............................................................................ 105
6.1 Definition.................................................................................................................................. 105
6.2 Clinical presentation ................................................................................................................. 106
6.3 Management of Shock .............................................................................................................. 108
CHAPTER SEVEN: ALTERED MENTAL STATUS ..................................................................................... 111
7.1 Altered Mental Status ............................................................................................................... 111
7.2 Direct CNS Trauma .................................................................................................................. 113
7.3 Seizure ..................................................................................................................................... 115
7.4 Status Epilepticus ................................................................................................................... 119
CHAPTER EIGHT: COMMON CARDIO-RESPIRATORY EMERGENCY ..................................................... 122
8.1.Heart Failure ............................................................................................................................. 122
8.2. Pulmonary edema .................................................................................................................... 130
8.3Acute Coronary Syndrome ........................................................................................................ 132
8.4 Emergency approach to Asthma ............................................................................................... 137
CHAPTER NINE: COMMON ENDOCRINE EMERGENCIES .................................................................... 142
8.1. Diabetic ketoacidosis (DKA) .................................................................................................. 142
8.2. Emergency management of hypoglycemia.............................................................................. 147
CHAPTER-TEN: APPROCH TO A POISONED PATIENT .......................................................................... 151
CHAPTER ELEVEN: ASSESSMENT AND MANAGEMENT OF TRAUMA ................................................. 157
11.2 Chest trauma ........................................................................................................................... 167
11.3 Abdominal and pelvic trauma .............................................................................................. 174
11.5 Head Trauma ........................................................................................................................ 182
11.6 Management of Burns ............................................................................................................ 187
CHAPTER TWELVE: Common pediatrics emergencies........................................................................ 192
12.1 Pediatric Triage ..................................................................................................................... 192
12.2 Pediatrics Airway .................................................................................................................. 195
12.3 Pediatric Breathing ................................................................................................................. 198
12.4 Pediatrics Circulation ............................................................................................................. 202
12.5 Basic life support .................................................................................................................... 206
12.6 Management of Pediatrics Burn ............................................................................................. 211
12.7 Pediatrics Snake bite and poisoning ....................................................................................... 214
12.8 Pediatrics POISONING .......................................................................................................... 216
12.9 Newborn Resuscitation .......................................................................................................... 219
Chapter 13: OBSTETRIC EMERGENCIES .............................................................................................. 223
13.1 HYPERTENSIVE DISORDER OF PREGNACY ............................................................. 223
13.2 Vaginal bleeding during pregnancy....................................................................................... 233
13.3 Post Partum Hemorrhage (PPH) ............................................................................................. 243
13.4 Trauma during Pregnancy ...................................................................................................... 246
REFERANCE ............................................................................................ Error! Bookmark not defined.
Annex ....................................................................................................... Error! Bookmark not defined.
INTRODUCTION

Emergency patient care is a comprehensive and continuous care provided for those
who are sick, injured or presented with obstetric emergencies.
According to WHO, 52% of the mortality is caused by non-communicable diseases
including injuries. Ethiopia is one of the countries with high burden of road traffic accident,
which is more than 56 deaths per 10,000 vehicles. This is causing increased morbidity and
mortality in economically active group leading to high socioeconomic impact in the country.
After the due attention given to Emergency Care, MOH established Emergency and Critical
Care Directorate (ECCD) in 2015 G.C which has previously been an emergency and referral
team under medical service. The ECCD, MOH has identified various gaps regarding system
management, human resource, capacity building, infrastructure, documentation and
communication on emergency care nationwide.
Ministry of Health (MOH) is currently working on strengthening the continuum of
emergency care at pre-facility, facility and referral system by developing guidelines and
protocols. Therefore, it’s being considered as a priority to implement a short-term trainings
(TOT) for health professionals on emergency care. This training manual will be used by both
participants and trainers as a reference guide. Once the health professionals had short course
training on national integrated emergency manual, they will be able to train other health
professionals who are working at Emergency room/ departments.
The Manual has thirteen Chapters:
 Chapter One; Emergency Medical Service System
 Chapter Two - Adult triage
 Chapter Three - Approach to Critically ill Patients
 Chapter Four – Airway and breathing assessment and management
 Chapter Five – Common arrhythmias and cardiac resuscitation
 Chapter Six – Approach to shock
 Chapter Seven – Approach to altered mental status
 Chapter Eight - Common Cardiac Emergencies
 Chapter Nine - Common endocrine emergencies
 Chapter Ten– Approach to a poisoned patient
 Chapter Eleven – Trauma
 Chapter Twelve- Common Pediatric Emergencies
 Chapter Thirteen - Common Obstetrics Emergencies

Course Syllabus
Course Description
This National Integrated Emergency Medicine training/course is designed to train physicians, nurses
and health officers, on the basic emergency care,knowledge, attitude and skills, they need to use to
save lives and limbs in hospital settings with availableresources.
Course Goal
To improve knowledge and skill of health professionals on emergency patients’ assessment and
management of critically sick/injured patients.
Course Objectives
At the end of this course participants will be able to:

 Describe EMS structure and functions

 Recognize adult triage and categorize emergent patients based on their acuity level.
 Explain how to approach critically ill patients.
 Assess and manage airway and breathing problems
 Identify and manage common arrhythmias and cardiac arrest
 Assess and manage patient with shock
 Assess and manage patient with altered mental status.
 Assess and manage patient with cardiorespiratory emergencies
 Assess and manage patient with common endocrine emergencies
 Describe approach to a poisoned patient
 Assess patients with trauma
 Identify common gynecological and obstetric emergencies
 List common pediatric emergencies

Course Evaluation
Each day’s courses will be evaluated based on the developed format addressing the provided
documents, training contents, instructors, facilities, time and interactions. Feedbacks will be given
based on the given comments immediately at end of training session.Course evaluation format will be
used to assess the overall effectiveness of the course as perceived by the trainees.

Course Duration
6 days with a total of 48hours courses with:

 Emergency Medical Service System –01hour

 Adult triage - 01 hour
 Approach to Critically Ill Patients - 01hour
 Airway and breathing assessment and management– 03hours
 Common arrhythmias and cardiac resuscitation - 06 hours
 Approach to shock - 01:30 hours
 Approach to altered mental status 01:30 hours
 Common Cardiac Emergencies - 02 hours
 Common endocrine emergencies – 02hours
 Approach to a poisoned patient - 01:30 hours
 Trauma – 06 hours
 Common Pediatric Emergencies - 07 hours
 Common Obstetrics Emergencies - 03 hours

Training/Learning Methods
 Interactive lectures
 Demonstration
  Brainstorming
 Small group discussions
 Individual and group exercise
 Role-plays and simulations
 Videotapes and discussions

Instructional materials, supplies and equipment needed in the training

 Ethiopian Hospital Reform Implementation Guideline

 National Integrated Emergency Medicine Training Participant Manual
 National integrated Emergency Medicine Training Facilitator Guide
 Case study booklet
 Power point slides
 Training videotapes
 Class rooms should include a space for the lecture presentations and a room for
skill stations
 Mannequins and other trauma care equipment’s
 Pediatrics, neonatal and obstetric mannequins and supplies
 Laptop and LCD projectors for lecture presentations
 Flip chart, markers, pen, note books

Target audience

 Health professional (physicians, nurses, Heath officers and other health workers)
working in healthcare facilities.
Trainer selection criteria

Instructors will be selected from manual developers, and health professionals who passed
TOT and certified on National Integrated Emergency Medicine training course. The NIEM
trainer must have experience using the master learning approach to provide the training,
which is conducted according to adult learning principles- learning is participatory, relevant,
and practical-and uses behavior modeling, is competency-based, and incorporates humanistic
training techniques.
Facilitator’s (organizer’s) responsibilities

 Assign trainers
 Schedule a daily meeting of all trainers at the close of each day to review progress,
 solve problems, and to plan for the following day.
 Conduct pre and posttest
 Develop norms on how to behave during the training period
 Encourage active participation of trainee
 At the end of the training course conduct training evaluation using pre prepared
evaluation questioner

Trainees’ assessment, qualification and criteria for certification

 All the trainees will be assessed at the start and end of the course by pretest and
posttest respectively and will be certified with >70 % of posttest result and 100%
of attendance.
Core competencies

The followings are core competencies that will be achieved after this training.
 Patient care:
 Triage patients
 Access and manage critically ill/injured patients in all age groups and
obstetric emergencies
 Utilize emergency drugs and equipment’s
 System development
 Emergency medical service system
 Organize Emergency room
Schedule of National Integrated Emergency Medicine Training

Day 1 Time Activity Duration

8:30-8:45 Registration 5 minutes 15 minutes
8:45-9:00 Welcome and introduction 15 minute
9:00- 9:15 Participants introduce each other and 15 minutes
expectations
9:15-9:45 Pre Test 30 minute
9:45-10:45 Introduction to Emergency medical 1 hour
service system/EMS
10:45-11:00 Tea Break
11:00-12:00 Adult triage 1 hour
12:00-12;30 Group Exercise on triaging 30 minutes

12.30- 1.30 Lunch

1.30- 2:30 Approach to Critically Ill Patient 1 hour
2:30-3:00 Approach to Critically Ill Patient 30 minuts
discussions
3:00 – 3:30 Tea break Organizers
3:30-4.30 Airway and breathing assessment 1 hour

4:30 – 5:00 General discussion and rap up & daily 30 minuts

evaluation
Day 2 8:30-9:00 Recap Trainees
9:00- 10.00 Practical session 1 hour
Airway and breathing
10:00-10-30 Practical session 1 hour
Airway and breathing
10:30 :11:00 Tea break Organizers
11:00- Approach to Basic ECG 1:30 hours
12.30

12.30- 1.30 Lunch

1:30-2.30 Common Arrhythmia 1 hour

 2:30-3:00 Common Arrhythmia discussion 30 minutes

3.00-3:15 Tea break Organizers

3.15-4:15 Cardiac Arrest 1 hour

4:15 – 5:00 General discussion and rap up & daily 45 minuts

evaluation

8.30- 9:00 Recap Trainees

Day 9:00 -10:45 Video show and 1 :45 hour
Three
Practice on CPR

10.45- 11.00 Tea break Organizers

11.00- ACS- Heart Failure and Pulmonary 1:30 hors
12:30 Edema

12.30- 1.30 Lunch

1.30- 3:00 Approach to shock 1:30 hrs

3.00- 3.15 Tea break Organizers

3.15- 4:45 1:30 hrs
Altered Mental Status

4:45 - 5:0 General discussion and rap up & daily 30 mnts

evaluation
Recap Trainees

8.30- 9.00
Day 9:00-10:45 DKA & Hypoglycemia 1:45 hrs
Four

10.45-11:00 Tea Break Organizers

11:00-12:30 Poisoning 1:30 hrs

12.30- 1.30 Lunch

1.30-3.00 Gyn/obs 1:30 hrs

3.00-3.15 Tea Break Organizers

 3:15- 4:30 Practice on Obs, 1:30 hrs

4:30-11:00 General discussion and rap up & daily 30 mints

evaluation
8.30- 9.00 Recap All trainees
Day five 9.00- 10.30 Approach to Trauma 1:30 hrs
10.30-10.45 Tea Break Organizers
10:45-12:30 Chest trauma, 2:45 hrs
Practice on trauma
12.30- 1.30 Lunch
1.30- 3.00 Abdomen and Pelvic trauma 1:30 hurs
3.00- 3.15 Tea Break Organizers
3:15 – 5.00 Head trauma,
Burn
5:00- 5:30 General discussion and rap up & daily 30 mits
evaluation
Day six 8:30 – 9:00 Recap All trainees
9.00- 10.30 Pediatrics Emergency 1:30 hrs

10.30-10.45 Tea Break

10:45-12:30 Pediatrics Emergency 1:45 hrs

12.30- 1.30 Lunch

1.30- 3.15 Pediatrics Emergency 1:45 hrs
3:15-3:30 Tea Break
3:30- 5:00 Pediatrics Emergency 1 hour
5:00-5:30 Post test,Evaluation,discustion, 1 hour
Certification,closing.
 CHAPTER ONE: EMERGENCY MEDICALSERVICE
SYSTEM

Duration - 01hr

Learning objectives
At the end of this session participants will be able to
 Describe different level, structure, and organization of EMSS
 Describe the organization of emergency units and their function
 Describe organization of pre facility and facility emergency service
organization.

1. Emergency Medical Services System (EMSS)

A network of services and resources coordinated to provide aid and medical assistance from
primary response to definitive care, involving personnel trained in the rescue, stabilization,
transportation, and advanced treatment of traumatic, obstetric and medical emergencies.

1.1 Historical background

Emergency medical care has developed from the days when the local funeral home was the
ambulance provider and patient care did not begin until arrival at the hospital. By contrast,
the modern, sophisticated EMS system (Emergency Medical Service system) permits patient
care to begin at the scene of injury or illness, and EMS is part of a continuum of patient care
that extends from the time of injury or illness until rehabilitation or discharge. Today when a
person becomes ill or suffers an injury, he has easy access to EMS by telephone, gets a
prompt response, and can depend on getting high-quality prehospital emergency care from
trained professional.

What happens to an injured person before he reaches a hospital is of critical importance?

Wars helped to teach us this lesson. During the Korean and Vietnam conflicts, for example, it
becomes obvious that injured soldiers benefited from emergency care in the field prior to
transport. This realization helped the civilian EMS system evolve from a load, go operation
to a system that provides professional care Department of Transportation at the scene, and
enroot to the hospital.
The modern EMS system has evolved from its beginning in the 1960’s. During that decade,
the National Academy of Sciences Research Counsel advocated professional training for
prehospital emergency personnel. More significantly, the Federal government and the
American Heart Association made two important contributions.
 The National Highway Safety act charged with developing an Emergency Medical
Services (EMS) system and upgrading prehospital care. The Emergency Medical
technician programs now available have gradually evolved from the charge.
 The American Heart Association began to teach cardiopulmonary resuscitation (CPR)
and basic life support to the public. Completion of a CPR course is now a prerequisite
to the EMT Basic course.

Advances continue to be made in emergency medical services, equipment design, research

and the education of EMTs. Many lives have been saved and unnecessary disabilities avoided
because the EMS system extends the services of the hospital in to the community

1.2 Rationale of Emergency care development in Ethiopia

Ethiopian health policy states that all Citizens will have access to Emergency Care. Using
this policy framework the federal ministry of health is working by giving special emphases to
Emergency Care. It is evident that Ethiopia drives development of Emergency Service, as the
country is second population in a sub-Saharan Africa.
In addition to the traditional communicable diseases, emerging diseases like trauma and other
non-communicable diseases are on the rise. This means similar to other developing countries
there is double burden of diseases. Ethiopian population is relatively young with high
growth rate and there is large material mortality and infant mortality, which can be
improved if timely care is available.
Considering these facts federal ministry of health has designed Emergency care
strategy in to facility based (hospital) or pre-hospital Care. In the hospital care,
Emergency directorate is one of the three directorates in addition to inpatient and outpatient
ones.Pre-hospital care in Ethiopia is a new approach, which has come in to attention in the
past few years. Until few years ago, Red Cross and hospital/health center ambulances have
been giving patient transfer from place to place but with no medical care in the ambulance.
EMS in Ethiopia formal pre-hospital care or hospital based Emergency department (ED)
development is a recent phenomenon. Emergency Medicine task force (EMTF) has been
established in Addis Ababa University (AAU) school of Medicine (SOM) in June 2006 and
the taskforce has closely worked with Federal Ministry of Health (FMOH) and Addis Ababa
city council Health Bureau (AACCHB). In addition to the main actors, many partners have
contributed significantly to this initiative. Some of the developments were establishment of
emergency departments in TikurAnbessa Specialized Hospital (TASH) and the restructuring
of EM service by FMOH. Emergency care has been considered as a crucial service in
hospitals' service along with outpatient and inpatient services.

The Federal Ministry of health in this historic moment is determined to set up pre-
hospital care to all woredas, which is the smallest district in Ethiopia with somewhat
100,000 people living. To achieve this goal, the Ministry is supplying over 800 ambulances
to woredas, one each. For this operation ambulance standard and ambulance management
guideline is developed. Moreover, stakeholders have reached in to consensus that Emergency
Medical technicians at level II that will have 6 months training after completing high School
will operate ambulances. At present this year (2019), St Paul’shospital Millennium
University developed a 2 years’ curriculum for EMT-Paramedics at masters’ level. The first
batch is on roll and will be graduated in 2020/2021 in the academic calendar year.

Major activities of EMSs/ECCS: It encompasses a wide variety of activities, including

 Prevention of injury and acute illness (public education and public health activities)
 Recognition of the event by bystanders
 Activation of the EMS system,
 Bystander care (ideally with telephone instructions from the EMS dispatcher),
 Arrival of First Responders, who might be Fire/rescue personnel (paid or volunteer),
Law enforcement personnel, Industrial response teams, arrival of additional EMS
resources, which may include EMT-Basics, Intermediates, or Paramedics, according
to the level of services designed by the service provider,
 Emergency care at the scene,
 Transport to the receiving facility (hospital) and In-hospital care.

Components of EMS, current standards include:

  Regulation and policy, each state must have lows, regulations, policies and
procedures that govern its EMS system.
 Resource management, each state must have central control of EMS recourse, so
that each locality and all patients have equal access to acceptable emergency care.
 Human resources and training, all personnel who staff ambulance and transport
patients must be trained to at least the EMT-Basic level.
 Transportation, Patients must be provided with safe reliable transportation by
ground or air ambulance.
 Facilities (different level of health facilities), each seriously ill or injured patient must
be delivered in a timely manner to an appropriate medical facility.
 Communications, a system of communications must be in place to provide public
access to the system and communication among dispatcher, EMS personnel and
hospital.
 Public information and education, EMS Personnel should participate in program
designed to educate the public in the prevention of injuries and how to properly and
appropriately access the EMS system.
 Medical oversight (physician involvement), Each EMS system must have an
emergency physician oversees patient care and delegate appropriate medical practice
to EMT basics and other EMS personnel.
 Trauma systems (organized network of resources and procedures for providing care
to critically injured patients), each state must develop a system of specialized care for
trauma patients, including one or more trauma centers and rehabilitation programs,
plus systems for assigning and transporting patient to those facilities.
 Evaluation (quality assurance/quality improvement processes). Each state/country
must have a quality improvement system for the continuing evaluation and upgrading
of the system.

1.3 EMSS Structure

1.1 Pre-hospital EMS
The type of medical care provided at the scene of a medical emergency, which includes
better communication and coordination with the ultimate goal of emergency medical
services, is to transport the victim with appropriate care and support to the health facilities. It
includes the following six steps:

1. Detection – The first rescuers on the scene, usually untrained civilians or those
Involved in the incident, observe the scene, understand the problem, identify the
Dangers to themselves and the others, and take appropriate measures to ensure their
Safety on the scene (environmental, electricity, chemicals, radiations, etc.).
2. Reporting – The call for professional help is made and dispatch is connected with
The victims, providing emergency medical dispatch.
3. Response – The first rescuers provide First AID immediate care to the extent of
Their capabilities.
4. On scene care – The EMS personnel arrive and provide immediate care to the
Extent of their capabilities on-scene.
5. Care in Transit – The EMS personnel proceed to transfer the patient to a hospital
Via an ambulance for specialized care. They provide medical care during the
Transportation.

Ambulance: is used to transport and to render care for sick or injured people appropriate to
the medical care needs. A pre hospital emergency medical services provider attends to the
sick or injured occupant during transportation.
Fig.1. Standard ambulance with internal compartment.

Dispatch center and Ambulance stations: The public must be able to notify the EMS
system in a timely manner in order for the EMS system to be of value. The most efficient
way to do so is through 3-digit system in which trained dispatchers collect information from
the caller and activate the appropriate level of response. In a system, there should be one call
or dispatch center, but many ambulance stations in order the ambulance will reach to the
caller or scene in short period of time acceptable to save life.

Fig.2 Dispatch center

Prehospital Levels of EMS/ECCS Trainings
There are Four Internationally accepted levels of prehospital emergency medical training.

First responder: The first responder is typically the first EMS-trained provider to arrive on
the scene. First Responders are trained at the most basic level to provide initial emergency
care at the scene until more highly trained personnel arrive. Ideally, in a system, there will be
a high number of First Responders may be a police officer or firefighter, industrial health
officer, truck driver, school teacher or volunteer associated with the community emergency
care system, located throughout the community in order to arrive at the scene of the
emergency quickly.

EMT Basics: The basic course prepares an EMT Basics to function in three
Areas
 Control life treating situations, including main training an open air way, provide
artificial ventilation, delivering semi-automated defibrillation,
 Controlling severe bleeding, administering a limited number of medications and
treating shock.
 Stabilizing non-life threatening situations including dressing and bandaging wounds,
splinting injured extremities, delivering and caring for infants, and dealing with the
psychological stress of the patient, family members, neighbors, and colleagues.
 Using non-medical skills such as driving, maintaining supplies, and equipment in
proper order, using good communication skills, keeping good records, knowing
proper extrication techniques and coping with related legal issues.

EMT-Intermediates
Are EMT-Basics who have acquired additional training to provide care that is more
complicated to patients?
 The training includes human system, Emergency pharmacology, venous access and
medication administration, patient assessment, medical condition, traumatic injuries,
obstetrics, neonatal resuscitation, pediatrics and geriatric. Additional skill includes
intravenous therapy, manual defibrillation, medication administration, endotracheal
intubation and use of alternative advanced airway devices, and ECG interpretation.
  These higher-level skills are referred to as advanced life support (ALS) and include
starting IVs and giving some medications.

EMT-Paramedics
 Are the most highly trained pre-hospital care providers in the EMS system.
Paramedics are EMT-Basics with extensive additional training and education that
have a wider scope of knowledge of disease processes and provide advanced life
support for patients with a variety of problems.
 One of the responsibilities of an EMT-Paramedic is providing patient education and
community injury and illness prevention activities.

1.2 In Hospital Components of EMSS

The patient’s third contact with the EMS system occurs in the hospital, primarily in the
emergency department. After being treated at the scene, the patient is transported to an
appropriate hospital, where definitive treatment can be provided.

Fig.3. EMSstructure.

It may be necessary for the patient to be transported to the closest appropriate medical
facility first, for stabilization, and then to a hospital that provides specialized treatment.
Specialized treatment facilities include trauma centers, stroke centers, burn centers, pediatric
centers, poison control centers, and prenatal centers.
In our context, a coordinated Emergency medical support is provided at health facility level
with standard triage system and definitive care. The emergency department (ED) or the
emergency room (ER) is a hospital or primary care department that provides initial treatment
to patients with a broad spectrum of illnesses and injuries, which could be life-threatening
and requiring immediate attention.

A typical emergency department has several different areas; each specialized for patients
with particular severities or types of illness.

1. The triage area, patients are seen by a triage nurse who completes a preliminary
evaluation, and treatment as necessary, before transferring care to another area of the ED or a
different department in the hospital. Patients with life or limb-threatening conditions may
bypass triage and to be seen directly by a physician. The triage nurse has to go to
resuscitation area and complete the triage form, and patients relatively stable can be sent to
waiting area while re triaging and reassurance is maintained.

2. The resuscitation area is a key area with full resuscitation materials and drugs of an
emergency department. It usually contains several individual resuscitation inlets, usually with
one specially equipped for pediatric resuscitation. Each bay is equipped with a defibrillator,
monitors, advanced airway equipment, oxygen, intravenous seats and fluids, and emergency
drugs. Resuscitation areas also have ECG machines, and portable X-ray facilities to perform
chest and pelvis films. Other equipment may include non-invasive ventilation (NIV), fast
intubation equipment and portable ultrasound devices.

3. The observation and treatment area is an area for patient to be kept after
resuscitation/stabilization and for stable patients who still need to be confined to bed or an
area to keep patients for 24hrs until transfer to respective wards or transferred/referred to
other health institutions.

4. Procedure room: where different interventional activities are undertaken

5. Other area: Such as stores, dispensary for emergency drugs, isolation rooms and
Decontamination rooms have to be considered.
1.3 ED/ER Work Flow
Patients arrive at emergency departments in two main ways: by ambulance (ground or air) or
independently. The ambulance crew notifies the hospital beforehand of the patient's
condition and begins Basic Life Support measures as needed. Depending on the patient's
condition, the emergency department physician may direct the ambulance crew to begin
specific interventions while still en route. These patients are taken to the emergency
department's resuscitation area, where a team with the expertise to deal with the patients’
conditions meets them. For example, a trauma team consisting of emergency physicians and
nurses and other relevant workers sees patients with major trauma.

Patients arriving independently or by ambulance are typically triaged by Emergency

Medicine Critical Care Specialized MSc Nurse or trained Nurse in emergency medicine and
Critical care. Patients are seen in order of medical urgency, not in order of arrival. Patients
are triaged to the resuscitation area, observation and treatment area, or minor’s area. When
patient arrives, the ED porters will take to the triage officers and the process will be
triggered. In our context /setup, the triage officer will be Emergency Medicine Critical Care
Specialized MSc Nurse or emergency medicine and Critical care trained BSC nurses, health
officers or other relevant workers trained in Basic Emergency Care in the hospital setup and
any nurse who is trained in Basic Emergency Care can led this process in the health centers.

Emergency Department Human resource

The structural units available in the department are triage room including porters/runners,
registration and recording room, procedures and resuscitation room, observation and
treatment rooms, minor emergency OR, diagnostic, stores and ambulance units.

Physicians
Different categories of physicians depending on the hospital level. It includes emergency
Medicine physician, general practitioner trained in Basic Emergency Care or residents in
teaching institutes. In rural and regional hospitals, Emergency Medicine Critical Care
Specialized MSc Nurse or emergency medicine and Critical care trained BSC nurses, and
health officers trained in Basic Emergency Care would take the responsibility.

ED/ER Nurses
Emergency Nurse Initiates care according to the urgency in ED, consult doctors in difficulty
and so they are integral part of the management Process.

Runners/Porters
They transport only stable patients from ambulance to ED, move Patients from place to place
for diagnostic and treatment procedures and to other hospitals in referrals. It is suggested that
these workers are primary emergency health care workers, emergency medical technicians,
or individuals who has BLS training to handle patients professionally and even assist nurses
in delivering care.

Environment keeping/Cleaners
New categories of patients constantly visit emergency rooms and environment should be kept
clean regularly. Therefore, cleaners should work in team with health care workers and to this
goal, training and frequent sensitization is needed.

Guards
Crowding and security issues are threats to emergency care in number of ways and as a result
cooperative team of security workers are needed in the ER.

Registration Rooms and officers

Registration and recording room must be adjacent and easily accessible. The system must be
designed in modern way so that information can easily be retrieved and analyzed. Any
patient should get privilege to be registered and evaluated in emergency, regardless of
payment.

ED Service
• In higher level where space is not problem Majority of service should be available in
the same place
• Basic laboratory, portable X ray and other necessities should be available in the
emergency department if possible.
• Emergency drugs and supplies should always be available and accessible, emergency
drug box/crash carts should always filled with resuscitation and essential drugs.
• Checklist of such items must be available with periodic revision and refilling.
 • There must be standard of ED equipment has and drugs to each levels and specialties,
this must also be worked out and annexed.

1.4 Communication in ED
ED of hospitals needs to communicate with Dispatch center, pre-hospital care, and other
health facility, RHB
 There should be vertical communication -with dispatch center and ambulances if
needed and also inpatient structures such as OR, ICU and wards.
 Horizontal communications should be in place with House staff (health professionals
and non-professionals) to facilitate patient care

Efficient emergency care plays a critical role in reducing mortality and morbidity/disability
resulting from obstetric and medical or surgical emergencies or injuries sustained during an
automobile accident, fire or any natural or manmade disasters. The survival of emergency
patients depends on the quick and efficient emergency pre hospital care delivered at the scene
and during transportation to both public and private health facilities (health centers and
hospitals).

The Federal Ministry of Health has a plan to overcome problem faced in delivering the right
service to the community in all case including EMS by establishing emergency care in all
health institutions and strengthen pre hospital care, which are on progress.
Some of the important prioritized areas to improve and strengthening EMS are:

 Organize to have a task force which involves University hospitals, Reginald health
burrow, City administration health office and other stake holders in some selected
module cities to:
- Establish common platform for the development of city pre-hospital system
and for Community 1st responder
- Establish modern/technology-assisted Ambulance dispatch system
- Initiating GPS tracking system in some ambulances in Addis Ababa
 Emergency and Critical Directorate is organizing each hospital to develop written
protocols for the referral of patients (receiving into the hospital and referring outside
of the hospital).
- To initiate higher facility hospitals to provide outreach and mentoring
 - Service on emergency for other facility?
- Providing technical support for 70 hospitals for facility based disaster
- Support emergency trainings (DMAT, ICU, NIEM, Community prehospital
care/firs aid etc.)

References
1. Mistovich. Hafen. Karren Prehospital Emergency Care, (2004), 7th ed. Pearson
Education Inc.
2. Shade. Rothenberg. wertz. Jones. Mosby’s EMT-Intermediate Textbook , 1997 Ed.
3. Emergency Medical Responder 5th ed. 2011, © by Jones and Bartlett & Learning
LLC.
4. Federal Ministry of Health, National Integrated Emergency Medicine Training, 2015,
Ethiopia.
5. Emergency medicine and its development in Ethiopia with emphasis on the role of
Addis Ababa university, school of medicine, emergency medicine department,
Ethiopian, med j, 2014, Supp 2
6. 2019/2O ECCD Annual BSC Plan
7. Health Sector Transformation Plan II, Situational analysis report,EMCCD
feedback,oct/2019.
 CHATER TWO: ADULT TRIAGE

Duration - 01 hour

Objectives
At the end of this session, trainees will be able to:
 Describe triage during different situations
 List organization and sequence of patient evaluation (triage)
 Categorizing emergency patients during different situations
 Develop skill on triage documentation

2. Triage
The term “Triage” comes from the French word “Trier” meaning to “sort” or “choose. It is a
method of ranking sick or injured people according to the severity of their sickness or injury
in order to ensure that medical and nursing staff facilities are used most efficiently.
In triage, patients with the greatest need are helped first.

2.1 Types

Patient to triage:
When a patient appears relatively stable and is able to mobilize him/herself to the designated
triage area. This will be the type of triage used in most of the cases.

Triage to patient
Here the patient is usually unstable. The patient is unable to mobilize him/herself to the
designated triage area and should be referred directly to the resuscitation room. Triage should
be performed at the bedside and documented in retrospect. This type of triage is used in
critical patients.

Triaging involves
 Controlling the flow of patients through the emergency department
 Rapidly gather sufficient information to determine triage acuity
 Provide first aid or send directly for resuscitation

2.2 Benefits of triage

 Speed up the delivery of critical treatment timely for patients with life and limb
threatening conditions
 Ensure that all people requiring emergency care are appropriately categorized
according to their clinical condition
 Improve patient flow
 Improve patient satisfaction
 Decrease the patient’s overall length of stay
 Facilitate streaming of less urgent patients

2.3 Organization and sequence of emergency patient

Evaluation (triage)
 The triage nurse should be available at the triage area all the time, organize his/her
working area with necessary supplies (emergency drugs, basic airway and splinting
equipment, BVM, oxygen with administrative devices, infection prevention materials
etc). He/she needs to be attentive to pick up the critical patient on arrival.
 All unconscious patients should be evaluated for ABCD before any history and taking
vital sign
 Critical patients transferred immediately to the resuscitation area while the triage
nurses can do their triage documentation at bed side
 Whenever critical patient or injured patient is evaluated, complete undressing is
important to minimize pitfall
 During assessment / triage of critical patients, conduct primary assessment: ABCD,
vital signs, short history about the course of illness or mechanism of injury
  After the evaluation, score the patient's condition using the Triage Early warning
Score (TEWS) (table 1)
 Then add your findings and categorize the patient according to the Emergent Severity
Index (ESI) (table 2)
 According to the color code, distribute patients to the respective treatment/assessment
area

2.4 Clinical Activities of Triage

Quick look for two or more patients’ assessment at triage office

 All arriving patients receive a “quick look” to determine ABCD stability and “Sick”
 Emergent patients go immediately to the treatment area
 The rest are prioritized for the more thorough triage history and assessment
 Use the simplest method to see the stability of ABC in primary survey by using
 30 - 2 - CAN DO methods
- If an adult patients’ respiration is less than 30 (RR < 30)
- Knows their name and where they are (2)
- Follow verbal command (CAN DO)
* All of these indicate the patients may have adequate initial oxygenation
And perfusion
Conduct the appropriate focused history and physical examination
o Triage physical assessment
o General appearance
o ABC stability
o Focused P/E
o Pain assessment

Triage history should include

o Chief complaint
o Pain assessment
o Medications
o Allergies
o Past medical history
Investigations at triage
o Finger prick RBS

Treatment
o Follow the triage protocol
o Secure iv line, start fluid, oxygen administration as indicated
o Medication administration as indicated

Communication
For seriously injured/critically ill patient
 When communicating with the receiving area a brief verbal communication should be
made with the treating team.
 Patient should be accompanied by triage officer to resuscitation area.

2.5 Triage Acuity Level/ Category

ESI - is a five level triage algorithm that categorizes ER patients by evaluating both patient
acuity and resource needs
Acuity is determined by the stability of vital functions and the potential threat to life or limb

2.5.1 Triage Scale (TS) or Emergent Severity Index (ESI)

ESI - RED
Immediately life threatening - disposed to resuscitation

ESI- Orange
Potentially life threatening - disposed to resuscitation within 10-15 minutes

ESI - Yellow
Less urgent, potentially serious, could be delayed up to 60 minutes disposed to treatment and
observation area

ESI - Green
Non-urgent, can be delayed up to 240 minutes and can be sent to nearby health institution,
regular OPDs or can be kept at the waiting area.
ESI -Black/Blue
Death on arrival

TEWS ESI
≥7 Red
5-6 Orange
3-4 Yellow
0-2 Green

Table1: TEWS (Triage Early Warning Score)

Table2- ESI (Emergency Severity Index)

Exercise (See at triage appendix)

References
1. Manual of Emergency, prepared by AAU Emergency Department task force,
December 2009
2. Emergency and critical care Lecture documents on triage
3. Federal Ministry of Health, National Integrated Emergency Medicine Training,
2015, Ethiopia
4. ED Unit protocol, Addis Ababa University, Department of Emergency Medicine,
TikurAnbessa Specialized Hospital
5. Adult ED triage sheet, TASH
 CHAPTER THREE: APPROACH TO CRITICALLY ILL
PATIENT

Duration- 01 hour

Learning Objectives:
At the end of this session, Participants will be able to:
 Describe aims of ABCDE approach to critically ill patient
 Identify critically ill patient
 Explain ABCDE assessment
 Explain management approach to critically ill patient

3.1 Introduction
The Airway, Breathing, Circulation, Disability, Exposure (ABCDE) approach is a
Systematic approach to the immediate assessment and treatment of critically ill or
Injured patients. It can be used in the street without any equipment or, in a more advanced
form, upon arrival of emergency medical services, in emergency rooms, in general wards of
hospitals, or in intensive care units
.
The aims of the ABCDE approach are:
 To provide life-saving treatment
 To break down complex clinical situations into more manageable parts
 To serve as an assessment and treatment algorithm
 To establish common situational awareness among all treatment providers
 To buy time to establish a final diagnosis and treatment.
Fig.1: The ABCDE approach to critically ill patient.

3.2 Identifying a Critically Ill Patient

Triage is a reliable method to quickly select from a large group of waiting patients, those
who may have a potential illness requiring time-critical management to save a life or the
brain. As a standard structure, currently, all modern emergency departments have a triage
unit to prioritize the patients. It aims to select patients that are more critical as early as
possible and create an appropriate patient flow in the emergency department. However, triage
can be done in the field by EMS staff, and patients may directly bring to the resuscitation
room.
Potential critically ill patients may present with:
 Altered mental status (unresponsive or confused/agitated)
 Noisy respiration (gurgling, stridor, wheezing)
 Inability to speak normally (acute hoarseness or inability to articulate words)
 Respiratory distress (rapid/deep or slow/shallow/agonal respirations)
 Acute weakness or inability to ambulate (diffuse/focal muscle weakness or light-
headedness/syncope)
 Acute torso discomfort (may be associated with radiation to jaw, anterior neck or
shoulder/medial upper arms) suggestive of an MI/cardiovascular problem.
  Severe acute headache
 Intractable seizure (may not show muscular signs after a period of time)
 History of significant trauma, drug ingestion, exposure, suicidal/homicidal ideation
 Significant vital signs abnormalities (age-dependent)

3.1 The ABCDE approach:

 Each letter represents a crucial body system that if significantly disrupted and left
untreated over hours rather than minutes, can result in death or brain damage.
 The order is performed sequentially to avoid skipping crucial steps and generally to
manage the most serious first
 Sequence can and should be performed simultaneously (horizontal approach) in those
with multiple life-threatening conditions if there are enough team members.
 Because management may need to be simultaneous, the team approach is crucial in
successfully resuscitating any critically ill patient.
 It is also important to emphasize that the availability of various treatment modalities
at each medical facility.
 For each letter or body system:
 Obtain a brief, focused history and exam
 Obtain available point-of-care testing to aid in the evaluation/management
 Initiate management for any acute life or brain threatening condition
 Then, proceed to the next letter and repeat, if no intervention is needed, quickly
proceed through the sequence.

A – Airway with C-spine Control

 Focused clinical assessment for impending/actual airway compromise:
 Noisy respirations (gurgling, stridor, choking sounds) with or without retractions
 Drooling, inability to swallow secretions, leaning forward in a tripod position
 Throat swelling sensation with or without pain
 Change in voice associated with symptoms of bacterial infection or allergy
(hoarseness, “hot potato” voice)
 Active retching or vomiting with an inability to turn or move to protect from
aspiration
 Oral exposure to fire/steam inhalation, chemicals, acids/alkali
  Neck trauma with crepitus over larynx or expanding hematoma

Management Algorithm for Critical Airway Problems

 Possible c-spine injury – employ the second person to immobilize c-spine. Only jaw
thrust maneuver is allowed in this situation
 Tongue obstructs airway in an obtunded patient – perform either head tilt, chin lift, or
use jaw thrust maneuvers if possible.
 Obtunded, without trauma – position patient on the side to avoid tongue obstruction
 Patient unable to be positioned – place nasal or oral airway. Avoid oral airway if
partially awake since may cause gagging/vomiting. Avoid nasal airway if midface
trauma.
 Pharyngeal secretions, blood, and/or vomitus – suction
 Obstructing foreign body – perform abdominal thrusts/chest compressions per BLS or
if visible, attempt to retrieve with McGill forceps.
 laryngeal edema; likely anaphylaxis – administer IV/IM Epinephrine.
 Signs of imminent or complete airway obstruction, unrelieved from above – attempt
intubation with the most appropriate device by the most experienced provider.
 May attempt BVM ventilation first, especially in children with epiglottis, as a
temporizing measure.
 Unable to intubate or BVM – immediately perform cricothryoidotomy
 The airway is always associated with the phrase, “with c-spine control”.
 Before performing any airway procedures, one must quickly assess the likelihood of a
c-spine injury.
 If there is a possibility of an injury in an unresponsive patient, i.e. found at the bottom
of the stairs, or on the side of the road, unconscious, then assume an injury and
protect the c-spine by simply immobilizing as best possible.
 Typically, a C-collar is slide under the back of the neck while someone immobilizes
the head.
 If airway management is required, the front of the collar can be opened or removed,
as needed, while someone stabilizes the head in relation to the torso. Nothing further
needs to be done in the primary survey to evaluate the c-spine.

Conditions causing airway compromise

  Unresponsive patient with tongue blocking the airway
 An unresponsive patient who is unable to protect from aspiration of blood/vomitus,
etc.
 Infections, i.e. epiglottis, retropharyngeal abscess, etc.
 Allergic reactions/anaphylaxis, airway burns, i.e. steam, chemicals, alkali/acids, etc.
 Airway burns, i.e. steam, chemicals, alkali/acids, etc.
 other causes of edema, i.e. ACE inhibitors, hereditary angioneurotic edema, laryngeal
cartilage fractures secondary to trauma
 Laryngeal cartilage fractures secondary to trauma
 Expanding paratracheal hematoma
 Tracheomalacia
 Pharyngeal malignancies

B – Breathing Disorders
 Focused clinical assessment for evidence respiratory failure
o Cyanosis, inability to speak full sentences without needing a breath,
o confused/agitated or unresponsive with:
o Rate: too slow, shallow, agonal, gasping (age-dependent, generally rates <10
in an adult are abnormal)
o Rate: too fast and/or deep (again age-dependent but >20 in a resting adult is
abnormal, and > 30 is significantly abnormal)
o Abnormal lung sounds:
o Unilateral decreased breath sounds (either dull or hyper-resonant)
o Wheezing or poor air movement
o Rales (fine crepitations) or rhonchi
o Chest wall abnormalities affecting breathing dynamics – flail chest/open
punctures
o Obtain as much focused history/exam as able to help define the need for a
particular emergent treatment strategy for the common causes of critical
respiratory conditions. For example, two common causes of severe respiratory
distress are pulmonary edema and COPD. Both may present with wheezing
(“cardiac asthma” in CHF), pedal edema and/or JVD, making the decision for
which type of emergent management strategy difficult. Obtain as much focused
 history/exam in a brief period of time, i.e. family states heavy smoker with similar
episodes in the past, all resolved with inhaler therapy or the patient has a history
of recent ECHO with very poor ejection fraction, etc. to help make a decision
about treatment.
o If still not clear as to a management strategy, add point-of-care testing, i.e., lung
sonography or upright portable CXR.

Management Algorithm for Acute Respiratory Disorders

 Fix all upper airway critical issues first
 Slow, agonal respirations or significant respiratory acidosis on ABG – provide BVM
ventilation till Intubation is achieved
 Rapid breathing with hypoxia – provide supplemental O2 by the non-rebreather mask
to keep O2 saturation greater than 94%.
 Sucking chest wound – seal with an occlusive dressing (3 sides only)
 Tension pneumothorax – place a 14 gauge needle, immediately followed by a chest
tube
 Massive hemothorax/pleural effusion – drain fluid, contact trauma surgeon since may
need transfusion/transfer to OR for massive hemothorax
 Signs of obstructive pulmonary disease (COPD/asthma) – administer inhalational
beta agonist. Consider additional therapy (i.e., ipratropium, Prednisone, Magnesium,
epinephrine, etc.).
 Signs of acute pulmonary edema with adequate BP – administer repetitive or
continuous doses of Nitroglycerin SL, spray or IV. Consider additional drug therapy
(i.e. Furosemide, etc.)
 Respiratory distress unresponsive to above therapy – intubate and mechanically
ventilate

Conditions Associated with Respiratory Failure

 Pulmonary edema
 COPD/asthma
 severe pneumonia
 ALI/ARDS from any cause (drugs, aspiration, etc.)
 tension pneumothorax
  chest wall dysfunction, (flail chest, muscular weakness, open sucking wound)
 Respiratory depressants (narcotic OD, sedative OD)
 pulmonary embolus, air/amniotic fluid/fat embolus
 Massive hemothorax or massive pleural effusion
 Exhaustion from prolonged hyperventilation

C – Circulation Disorders
 Clinically assess for poor perfusion associated with
o Tachycardia: > 100 abnormal in adults, > 150 frequently clinically
o Symptomatic.
o Bradycardia: < 60 abnormal, < 30 frequently clinically symptomatic.
o Hypotension: systolic < 90
o Perfusion and cardiovascular assessment may include
o Skin – i.e., cool, diaphoresis, pale, poor capillary refill, hives, erythema
o Mental status changes – i.e., confusion, slow responses, agitation
o Rhythm/quality of pulses in all four extremities
o Assessment for hidden blood loss, i.e., rectal for melena, pelvic instability,
pulsatile abdominal mass
o history: internal/external bleeding/trauma, vomiting/diarrhea, oral intake/urine
output, fever, diabetes/renal insufficiency/cardiac failure, medications, drug
abuse/OD, last menses
 Clinically assess for hypertension associated with:
o signs of end-organ damage/involvement, i.e., encephalopathy and/or
papilledema, pulmonary edema, cardiac ischemia, renal impairment, and/or
neurological abnormalities
o pregnancy (generally 3rd trimester/first weeks postpartum); any new elevation
of BP >140/90, particularly associated with a headache, abdominal pain,
jaundice, shortness of breath and/or visual disturbances

Management Algorithm for Critical Circulatory Disorders

 Management of Poor Perfusion
 place two large bore IV’s and attach telemetry monitor to all (may collect
 various labs including blood cultures, but should send type and cross match
 now)
 evidence of external bleeding, unstable pelvis – apply pressure/ binder; in rare
cases tourniquet
 patient in the 3rd trimester of pregnancy – displace uterus to left/wedge under
right flankunable to start IV – attempt IO (intraosseous) with 300 mmHg
pressure cuff over the fluid bag to increase flow rate (Central line sheaths, if
unable to start IO).
 Unable to start IV – attempt IO (intraosseous) with 300-mmHg pressure cuff
over the fluid bag to increase flow rate (Central line sheaths, if unable to start
IO).
 If no evidence of cardiac failure – administer bolus 10-20cc/kg 0.9%
NS/Ringers solution. (Further fluid administration determined by clinical/sono
evaluation, risk/benefit, i.e., permissive hypotension and clinical response,
i.e., urine output).
 Evidence of unstoppable internal bleeding – immediate consultation with
appropriate specialty, i.e., surgery, OB, GI, etc.
 Severe blood loss and/or persistent unstoppable bleeding – transfuse O-
negative units until type specific or fully cross-matched blood available
 Unstable tachydysrhythmia (not sinus, multifocal atrial tachycardia,
junctional) – cardiovertion per ACLS
 Unstable bradydysrhythmia – administer meds (i.e., Atropine, etc.)/place
external pacemaker per ACLS

 Management Algorithm for Severe Hypertension associated with

 Evidence of end-organ damage (ischemia, heart failure, encephalopathy, etc.) –
administer IV antihypertensive (Labetalol, Nitroprusside, etc.) Avoid pure beta-
blockers if suspect cocaine overdose.
 Evidence of hemorrhagic stroke, thrombotic stroke, subarachnoid hemorrhage
(See Disability Section)
 Pregnancy and new elevation of BP >140/90 – re-evaluate in 15 minutes
 Pregnancy with evidence of pre-eclampsia/eclampsia (i.e., headache,
nausea/vomiting, abdominal pain, visual disturbances, shortness of breath,
hyperreflexia, seizures – with or without proteinuria) – or severe hypertension BP
 160/110 – administer MgSO4 and initiate antihypertensive, (i.e., Hydralazine,
Labetalol, or Nifedipine), immediate OB consult.

D – Disability
 Clinically assess for
 Depressed consciousness (lethargic, confused, comatose) (may use GCS to
assess the degree of unresponsiveness)
 Pupil size, symmetry, and reactivity
 Agitation, delirium (waxing and waning level of consciousness associated
with confusion/disorientation and/or hallucinations – typically, visual/tactile)
 Acute focal weakness/paralysis, or inability to speak
 Signs of status epilepticus, including subtle seizure-like activity (i.e.,
twitching eyelids, stiffness, persistent unresponsiveness after obvious seizure-
like activity)

Management Algorithm for Disability problems

 Fix the airway, breathing and circulation conditions first
 Check finger stick glucose – if low administer bolus or drip of D50/D 40 or D10
depending on patient age. May give IM Glucagon if unable to start IV and patient
cannot swallow.
 IF GCS < 9 after ABC resuscitation – the patient likely requires intubation to protect
from aspiration – prepare equipment
 History acute fever, headache, without focal neurological signs, recent seizure history
or impaired immunity and exam/sono shows no papilledema – check malaria smear,
rapid HIV test, perform LP, initiate empiric antibiotic treatment (possible steroids
first), based on age/likely etiology.
 Before any meds given attempt to quickly determine if allergic, from family, old
records, etc.
 History acute fever, headache, with focal neurological signs or seizures, impaired
immunity and/or exam/sono shows papilledema – do not perform immediate LP –
check malaria smear, rapid HIV test, initiate empiric antibiotic treatment , based on
age/likely etiology.
 Before any meds given, attempt to determine if allergic, from family, old records, etc.
 Follow with CT and possible LP, ASAP.
 Consider status epilepticus in all non-responsive patients, (motor signs may be
minimal) or if not awakening between seizures:
 check electrolytes – if hyponatremic administer 2cc/kg over 10 min of 3% NaCl(max
100cc)
 Third trimester/post delivery – administer MgSO4/consult OB
 Likely INH OD or neonatal dependency – administer Pyridoxine.
 all others – start with Benzodiazepines, consult neurology
 If no improvement with above – obtain head CT and treat accordingly

E – Exposure
 Clinically evaluate
 areas hidden by clothing/body position for missed lesions
(rashes/stab/gunshot wounds) by undressing and logrolling.
 The body for evidence of self/child/elder/domestic abuse and evidence of IV
drug abuse.
 For possible contaminated clothing/skin: substances absorbed through the skin
(i.e., hydrocarbon pesticides), caustics, radiation or objects causing continued
burns, etc.

 Management Algorithm for Exposure Disorders

 signs of child or self-abuse – provide safe location and separate from abusers
 evidence of hidden bleeding – manage as per Section C
 evidence of clothes/skin contamination – decontaminate, according to toxicity and
protect self and others in the process (self-protection should be implemented at
the onset of patient evaluation)
 re-dress patient in a gown to prevent cooling and provide privacy
 After the sequence is completed, quickly re-evaluate the patient to see if
intervention(s) resulted in improvement.
 Then follow the ABC’s with:
 Evaluation of past medical history, medication history, and allergy history, if not
already performed
  Perform the secondary survey (i.e., detailed history and a complete exam)
 Further Investigation based on presumptive diagnosis which we can get from
Primary and secondary assessment.

Summary

 The Airway, Breathing, Circulation, Disability, Exposure (ABCDE) approach is a

Systematic approach to the immediate assessment and treatment of critically ill or
injured patients.
 Each letter represents a crucial body system that if significantly disrupted and left
untreated over hours rather than minutes, can result in death or brain damage.
 The order is performed sequentially to avoid skipping crucial steps and generally to
manage the most serious first
 Sequence can and should be performed simultaneously (horizontal approach) in those
with multiple life-threatening conditions if there are enough team members.
 Because management may need to be simultaneous, the team approach is crucial in
successfully resuscitating any critically ill patient.
Self-assessment questions

1. How do you identify critically ill patient among patients presented to ED?
2. List the aims of ABCDE assessment
3. List some of the causes which resulting respiratory failure

References
1. https://iem-student.org/abc-approach-critically-ill/
2. https://www.researchgate.net/signup.SignUp.htm
3. Rosen’s Emergency Medicine, 8th edition
4. Tintinalli Emergency Medicine, 8th edition
 CHAPTER FOUR: AIRWAY AND BREATHING
ASSESSMENT AND MANAGEMENT

Duration -3 hrs

Learning objectives
At the end of this session, participants will be able to:
1. Perform proper air way assessment and Identify potential air way problems

2. Use adjuvant equipment properly

3. Detect signs and symptoms of emergency breathing problems

4. Use adjuvant equipment’s to rescue breath and oxygen administration

5. Use NIPPV appropriately

4.1: Airway assessment and Management

The airway conducts gases between the atmosphere and the alveoli. Therefore, competence
in airway management is a critical skill for safe emergency airway problem management and
to play a key role in cardio pulmonary resuscitation.
 Maintaining the airway patent is a fundamental medical skill and Airway
management is a process of ensuring:
1. There is an open pathway between a patient’s lungs and the atmosphere.

2. The lungs are safe from aspiration

4.1.1 Airway Emergencies, which need immediate intervention

I. Causes upper airway obstruction include:
a) The patient's tongue, in patients with impaired consciousness
b) Secretions in patients who are unconscious with suppressed airway reflexes
c) Foreign body
d) Swelling (Anaphylaxis)
e) Infection ( e.g. Epiglottitis)
f) Facial trauma or burn etc
 II. Airway assessment in conscious patients
 The patient’s airway history should be evaluated to determine whether there are any
medical, surgical, factors that have implications for airway management.

 If the patient is sitting up and talking normally, he/she have an adequate airway AT
THAT TIME, Reassess regularly;

o Look for dyspnea;

o Hoarseness or weakness of the patient’s voice,

o Stridor: an abnormal, high pitched sound produced by turbulent airflow

through a partially obstructed upper air way during inspiratory phase

III. Airway assessment in unconscious patient

General approach
 If Cervical Spine Injury is suspected (major trauma, unconscious patient, head
injury), either, apply rigid cervical collar or Maintain in-line stabilization manually,
while attempting airway maneuvers.

 Left lateral position in unconscious patient with adequate spontaneous breathing

(unless suspected cervical spine injury)

 Left lateral position (or wedge) in 3rd trimester of pregnancy

 Remember that patients with a GCS ≤ 8 are unable to protect their airway, due to the
absence of coughs, swallowing and gage reflexes.

IV. Steps in Airway Management: Basic Airway Skills

 Open the airway using head tilt chin lift maneuver in non trauma patient and jaw
thrust for trauma patients, and See for the following findings and treat as you find

1. Presence of any foreign body or secretions –suction or remove manually if the

foreign body is reachable

2. See Whether the tong is falling back to obstruct the airway- apply head tilt
chin lift of jaw thrust maneuvers and if patient is not maintaining patent
airway insert oropharyngeal or nasopharyngeal airway
 3. For any facial bone deformity, progressive soft tissue swelling and with signs
of airway obstruction- consider definitive airway management (intubations,
crico-thyrotomy) consult colleagues with such skill

V. Airway Opening Maneuvers(techniques)

A. Head tilt/Chin lift
 Used for lifting the tongue from the back of the throat.

 Contraindicated in pts with suspicion of cervical spine injury

 While tilting the head see for chest movement and air is coming in and out

 If no chest movement lift the chin see for any foreign body or secretions and
manage accordingly

 If patient has adequate breathing with this maneuver, position patient in left
lateral position and administer oxygen

 If there is no effort of breath deliver TWO RESCUE BREATH

Figure 2: Head tilt and Chin lift maneuver

 Jaw thrust

 The jaw thrust is a technique used on patients with a suspected cervical spinal
injury and is used on a supine patient.
  The practitioner uses their thumbs to physically push the posterior (back) aspects
of the mandible upwards –

 When the mandible is displaced forward, it pulls the tongue forward and prevents
it from occluding (blocking) the entrance to the trachea, helping to ensure a
patent (open) airway.
 While maintaining this maneuver see for chest movement or breathing effort ;If
no see for foreign body or secretions and manage

 If no effort give TWO FESCUE BREATH

Figure 3: Jaw thrust Maneuver

Recovery position
 Unconscious patients who have adequate breathing effort should turn into the
recovery position, (left lateral position) as this allows prevent tongue from falling
back and occluding the airway, and the drainage of fluids, secretions out of the
mouth instead of down to the trachea.
 Therefore, all unconscious patients with breathing effort have to be in left lateral
position if no contraindications.
 Figure 5: Recovery Position

4.1.2 Airway adjuncts

Oropharyngeal Airway (OPA)

 A curved piece of plastic inserted over the tongue that creates an air passageway
between the mouth and the posterior pharyngeal wall.
 Useful in unconscious patients with GCS of less than 8
 Technique of insertion: insert the oral airway upside down until the soft palate is
reached and rotate the device 180 degrees and slip it over the tongue.
 Be sure not to use the airway to push the tongue backward and block, rather than
clear, the airway.
 Make sure proper size to the patient is used (measure from the angle of the mouth to
the angle of mandible).

Oropharyngeal airway
 Nasopharyngeal airway
 Is inserted through one nostril to create an air passage between the nose and the
nasopharynx.
 The NPA is preferred to the OPA in semi conscious patients because it is more
tolerated and less likely to induce a gag reflex.
 The length of the nasal airway can be estimated as the distance from the nostrils to the
meatus of the ears and is usually 2-4 cm longer than the oral airway.
 Any tube inserted through the nose should be well lubricated and advanced at an
angle perpendicular to the face.
 NPA are contraindicated in patients who are on anti- coagulant, patients with basilar
skull fractures, and with nasal infections and deformities

Laryngeal Mask Airway (LMA)

 The LMA is an effective alternative when the ETT fails because the vocal cords
cannot be visualized in situations of a difficult intubation, airway masses, or cervical
pathology
 LMA is a wide bore tube, with a connector at its proximal end (that can be connected
to a breathing circuit) and with an elliptical cuff at its distal end. When inflated, the
elliptical cuff forms a low-pressure seal around the entrance into the larynx.
 The LMA comes in a variety of pediatric and adult sizes and successful insertion
requires appropriate size selection.

Figure 6: Laryngeal mask airway

4.1.3 Advanced Airway Management

I. Intubation
 Intubation it is an invasive method of airway management by insertion of ETT in
to the trachea to facilitate ventilation and it is a definitive airway management.
 There are three types of intubation
a. Rapid sequence intubation is the preferred method of intubation in
emergency situation, because patients NPO time is not known and due to
their acute illness, they have increased sympathetic flow that makes slow GI
motility.
b. Crush intubation is indicated for a patient who is unconscious and apneic
because such type of patients requires with immediate BVM ventilation and
intubation without delay
c. Elective or ordinary intubation: for patients with stable condition and at least
fasting for >4hrs or empty stomach
 Intubation in ED is more complicated than done in Operation Theater and found
associated with severe hypoxia and even cardiac arrest due to:
o patients in the ED are physiologically unstable,
o the airway is not well assessed,
o Patient’s response for preoxygenation is not adequate.

 Although many techniques are available for intubation of the emergency

patient, four methods are most common, with RSI being the most frequently
used in non arrested patient

 RSI is the cornerstone of modern emergency airway management and is

defined as the virtually simultaneous administration of a potent sedative
(induction) agent and an NMBA, usually Succinylcholine, for the purpose of
endotracheal intubation.

 This approach provides optimal intubating conditions and has long been
believed to minimize the risk of aspiration of gastric contents.

Indication for intubation:

I. Respiratory arrest or failure
II. Inability to protect airway
III. Inability to oxygenate/ventilate
IV. Anticipated deterioration
Preparation for intubation
 Prepare equipment, personal Airway experts and more assistants present) equipment
and drugs.
 Equipment can be remembered by the acronym SOAP ME
o S: Suction,
o O: Oxygen,
o A: Airway equipment includes
 Endo tracheal tube appropriate sized stylet, 3 different size ETT
(female 6.5-7.5size, male 7.0-8.00cm) for adult and for
 Children ETT size:2kg-2.5mm, 2-4kg-3.0mm, term neonate 3.5mm,
3mo-1year-4.0mm, over 2years use the formula-
 Uncuffed tubes- choose [age (yr.)/4] + 4 or Cuffed tubes [age (yr.)/4]
+ 3.5at least one size smaller and 1 size larger tube. Tube length in cm
can be calculated= age/2+12 cm, or tube size x 3. Simply tube size in
children can be approximated to the size of the little finger or diameter
of the nostril
 Laryngoscope and its blades: Though either curved or straight
laryngoscope blades can be used for all patients based on the users
choice .For young children- use of Straight laryngoscope blades
(Miller) is preferred. Mackintosh or curved for adult and older
children. The advantage is it can directly lift the large epiglottis and
displace the large tongue. Make sure the light on the blade is working
before you put the patient sleep.
 Stylet, bougie, Magill forceps (for forceps for foreign body removal),
different size Facemask, for Bag valve mask ventilation, 10ml syringe
Oral airway, Nasopharyngeal airway, laryngeal mask airway.
o P: prepare pharmacy
1. Sedatives (ketamine 1-2mg/kg, or thiopental 3-4mg/kg, or propofol
1-1.5mg/kg) Anti-cholinergic (atropine 0.4-1mg, or 0.01mg/kg)
2. Muscle relaxant (suxamethonium 100-150mg, or 0.5-1mg/kg).
Succinylcholine is contraindicated
 If there is hyperkalemia,severe acidosis, acute or chronic
Neuromuscular disease, burn patient with more than 48 hrs and
Spinal cord trauma
 The alternative drug is cysatracurium or vecronium. Large bore
(18G) IV line secured, and checked for functionality and loading
dose fluid (isotonic saline 500 ml in adults) and (20 mL/kg normal
saline IV/IO) for pediatrics given in absence of contraindication.
o ME: Monitoring equipment: ECG monitors, pulse oximeter

Confirm the ETT placement with the following

 Immediate confirmation of tube placement using check for fogging of the tube, direct
visualization of tube passing the cords ,bilateral chest auscultation on the mid
axillary line, observation of bilateral chest movement during bag valve ventilation,
feeling of tracheal cartilages while the tube is passing the trachea, and if available
using capnography, and when necessary chest x ray

Post-intubation:
 Mark the depth of the ETT to avoid single lung intubation by multiplying the size of the
ETT by 3. The product of these two is where the ETT marking should be at the angle of
the mouth.
 Secure the ETT together with an oral airway to prevent dislodging of the tube and ETT
being chewed by the patient.ETT is secured with adhesive plaster and bandage
 Put on mechanical ventilator with appropriate settings for patient condition.
 There should be a good ETT care by immobilizing the head and neck in the neutral
position and avoid hyperextension and flexion. Head flexion can cause displacement of
the tube into right main stem bronchus with head extension can cause displacement of
the tube into the oral pharynx.

II. Cricothryoidotomy
The cricothyroid membrane joins the thyroid with the adjacent cricoids cartilage. It is close
to the skin, relatively avascular, and the widest gap between the cartilage of the larynx and
trachea, so it provides the best access for per-cutaneous (cricothyrotomy) airway rescue
techniques.
This technique is used in emergency condition when intubation and ventilation are
impossible with the usual methods.
Figure 7: anatomic location of Cricothyroid membrane

Indications
• emergency airway not able to be secured by other means
• cannot intubate / cannot ventilate = Failed intubation, oxygenation unable to be
maintained by bag- mask ventilation

Contraindications
• Children < 8 years old - Needle cricothryoidotomy with jet insufflations is preferred.

Complications
• Immediate: Hemorrhage, Creation of a false passage into the tissues, Hematoma
formation, Laceration of the esophagus, Laceration of the trachea,
• Longer term: Sub glottic stenosis, Laryngeal stenosis, Vocal cord paralysis
hoarseness
Figure 8: procedures shows needle cricothryoidotomy

Surgically prepare the neck, using antiseptic swabs.

 Palpate the cricothyroid membrane, anteriorly, between the thyroid cartilage and
cricoid cartilage. Stabilize the trachea with the thumb and forefinger of one hand to
prevent lateral movement of the trachea during the procedure.
 Local anesthetic down to cricothyroid membrane if patient is conscious.
 Puncture the skin in the midline with a 14 - 16 gauge cannula attached to a syringe,
directly over the cricothyroid membrane (i.e., midsagittal).
 Direct the needle at a 45-degree angle caudally, while applying negative pressure to
the syringe.
 Carefully insert the needle through the lower half of the cricothyroid membrane,
aspirating as the needle is advanced.
 Aspiration of air signifies entry into the tracheal lumen.
 Remove the syringe, and needle then widen the puncture size with scalpel and insert a
tube to facilitate breathing or use for jet insufflations
4.2 Assessment of Breathing and Management

Assessment of Breathing
 Respiratory Rate and breathing pattern
 Increase due to lower respiratory or airway problem, pyrexia and
metabolic acidosis
 Decrease due to fatigue: over dose of sedation drugs or opiods ,
exhaustion, poisoning
 Use of accessory muscles
 Sternocleidomastoid, Intercostals, sub costal, sternal recession
 Sounds of breathing
 Stridor: upper airway obstruction
 Wheeze: lower airway obstruction
 Grunting: sign of severe respiratory distress, characteristically in infants
 Degree of chest expansion
 Breath sounds on auscultation - beware the silent chest
 Heart rate
 Color
 Mental state
 Pulse oximeter

Management of breathing difficulty

 The primary problem in airway management is an inability to oxygenate, ventilate,
prevent aspiration, or a combination of these factors.

 Effective ventilation requires both a face-tight mask fit and a patent airway. In
unconscious patients following opening of the airway using hand maneuvers and
airway adjutants if the breathing is inadequate or no breathing start assist/rescue
breath mouth to mouth or with bag valve mask.

The bag-valve masks (BVM) ventilation:

 BVM device is used to manually deliver positive pressure through an applied
facemask, extraglottic/LMA device or endotracheal tube.

 The former would be an initial step in an apneic or hypo ventilating patient, and is
usually indicated prior to, or during intubation of an ill patient.
  The clinician should be intimately familiar with the workings of the BVM device, as
it has a number of valves, and needs proper assembly to work. Also

 These devices incorporate a self-inflating bag, a one-way bag inlet valve, and a no
rebreathing patient valve.

Indications
 Patients with inadequate ventilation BVM is meant to simply provide positive
pressure ventilation.

Technique
 Select appropriate mask size that fits comfortably over the mouth and nose.

 Place the mask strap beneath the occiput. Use the C and E method (see the picture
below)

 Apply the mask’s nasal groove to the low point of the nasal bridge to avoid pressure
on the eyes.

 Grip the left mandible with the third and fourth fingers of the left hand
  Lower the mask so that its inferior rim contacts the face between the lower lip and the
mental prominence.
 If there is a leak between the mask and the cheeks, consolidate the seal by dragging
mobile tissue of the left cheek toward and under the mask cushion, stabilizing the
tissue with the ulnar margin of the left hand.

 Bracing the mentum against the mask, pull the mandible up and forward with the
third through fifth fingers, while the thumb and index finger grip the mask above and
below the connector... C&E method

 Maintaining the left-sided seal, tilt the mask toward the right cheek, consolidating the
seal by dragging the mobile tissue forward to the cushion and by keeping it there with
one limb of the mask strap.

Figure 9:One-person bag-valve mask ventilation

 Figure 10: Two-handed mask seal BVM

Predictors of difficult mask ventilation

o Age >55yr
o Body mass index > 26kg/m2
o History of snoring
o Beards
o Absence of teeth (the presence of two of the above factors has >70%sensitivity and
specificity)
o Facial abnormalities
o Receding jaw
o Obstructive sleep apnea

Laryngeal Mask Airway (LMA)

 The LMA is an effective alternative when the ETT fails because the vocal cords cannot be
visualized in situations of a difficult intubation, airway masses, or cervical pathology
 LMA is a wide bore tube, with a connector at its proximal end (that can be connected
to a breathing circuit) and with an elliptical cuff at its distal end. When inflated, the
elliptical cuff forms a low-pressure seal around the entrance into the larynx.
 The LMA comes in a variety of pediatric and adult sizes and successful insertion
requires appropriate size selection.
4.2.1 Oxygen therapy
 Oxygen is a life saving treatment. It should be treated like any other drug; it should be
prescribed in writing, with the required flow rate and the method of delivery clearly
specified.
 Failure to correct hypoxemia (PaO2>60mmHg or s02>90%) for fear of causing
hypoventilation and carbon dioxide retention is unacceptable clinical practice.
 Careful monitoring of treatment is essential and will detect those patients at risk.
 Intermittent oxygen therapy is particularly dangerous since the increased alveolar
CO2 concentration which may then occur, results in an even lower O2 concentration
when the patient breaths air (o2 supply is discontinued).
 The amount can be adjusted and regulated according to the results of pulseoximetry
and arterial blood gas analysis if available

Causes of tissue hypoxia

1. Arterial hypoxemia
o Low inspired oxygen partial pressure (high altitude)
o Alveolar hypoventilation respiratory rate decreased (sleep apnea, opiate overdose)
o Ventilation-perfusion mismatches (acute asthma, atelectatic lung zones, ARDS
2. Failure of oxygen-hemoglobin transport system
o Inadequate tissue perfusion,(shock), Low hemoglobin concentration
(anemia),Abnormal oxygen dissociation curve (hemoglobinopathies, high
carboxyhemoglobin),Histotoxic poisoning of intracellular enzymes (cyanide
poisoning, carbon monoxide poisoning septicemia,

Recommendations for instituting oxygen therapy

o Cardiac and respiratory arrest
o Hypoxia with pulse oximeter measurement (saturation of oxygen
o <93%)
o Hypotension (systolic blood pressure <100 mm Hg)
o Low cardiac output and metabolic acidosis (bicarbonate<18 mmol/l)
o Respiratory distress (respiratory rate >24/min)in adult
Technique of Oxygen administration:
1. Nasal prongs or catheter-
o Suitable and better tolerated.
o Oxygen administration via nasal prongs range from 1-litter -5litter/minute.
o Rises inspired oxygen concentration to 30-40 percent.
o A humidifier should be used.
o If a flow rate greater than this amount is used it results on irritation to the nose
and it does not increase the oxygen delivery to the patient rather it is wastage.
o If the patient has fast breathing and the oxygen, saturation is not improving
change to face mask.

2. Face mask-
There are different types of facemasks.
o They could be with reservoir or without.
o A flow rate of 6-10 liters/minute provides a rise in inspired oxygen concentration
to 60-70 percent with simple face mask
o On re-breathing face mask 10-15L/min increase FiO2 80%-85%, with no mixing
in expiration
o If you decide patient is hypoxic start from the higher flow suitable to the device
and titrate down ward according the patients response.
 N.B: If patients oxygenation and general conditions is not improving and signs of
hypoxia or hypercarbia are persisting consider the next technique of oxygen
administration, non invasive respiratory support (CPAP) or invasive (intubation
and ventilation with mechanical ventilator) respiratory support according the
patient’s condition

4.2.2 Non-invasive positive pressure ventilation

 Noninvasive positive pressure ventilation (NIPPV) refers to positive pressure
ventilation delivered through a noninvasive interface (nasal mask, facemask, or nasal
plugs), rather than an invasive interface (endotracheal tube, tracheotomy). Its use has
become more common as its benefits are increasingly recognized.
Indications
Conditions known to respond to NIPPV include:
  Exacerbations of chronic obstructive pulmonary disease (COPD) that are complicated
by hypercapnic acidosis (arterial carbon dioxide tension [PaCO2] >45 mmHg or pH
<7.30)
 Cardiogenic pulmonary edema
 Acute hypoxemic respiratory failure
 NIPPV may also be helpful for preventing post-extubation respiratory failure

Pre-requisite to use NIPPV

 Patients must be conscious
 Cooperative
 Able to breathe spontaneously
 Able to protect their airway
 Have good air way reflexes

Contraindications
The need for emergent intubation is an absolute contraindication to NIPPV:
 Cardiac or respiratory arrest
 Inability to cooperate, protect the airway, or clear secretions
 Severely impaired consciousness ( GCS<10)
 Non respiratory organ failure that is acutely life threatening
 Facial surgery, trauma, or deformity
 High aspiration risk
 Prolonged duration of mechanical ventilation anticipated
Figure 11:- Non-Invasive positive pressure ventilation

Types of Positive pressure Ventilation

1. Continuos Positive Airways Pressure Ventilation (NIV- CPAP)

 constant pressure on inspiration and expiration
2. Biphasé positive Airways pressure ventilation (NIV- BiPAP)
 Pressure varies during inspiration and expiration
 N.B: NPPV works by augments ventilation by delivering pressurized air through a
facial or nasal mask using tight fitting mask

Application of NIPPV
 Oxygen flow - A gas flow of 6-10 L/min
 For C PAP-set the default pressure at 4-10 cm H 2O
 For BiPAP- the initial IPAP settings is 10-12 cm H 2 O pressure and EPAP settings
of 5-7 cm H 2 O

Monitoring of patient who is on NIPPV

 Close monitoring of all vital signs, & saturation
 Pattern and rate of breathing
 consciousness level
  When patient is getting fatigue

Advantages of NIPPV
• It prevents alveolar collapse; facilitates Oxygen delivery to pulmonary capillaries.
• Increases the Functional Residual Capacity (FRC) and opens collapsed alveoli
• Enhances gas exchange and oxygenation
• Reduce the work of breathing

Potential harms of NIPPV

• NIPPV is generally safe.
• Most complications due to NIV are local and related to the tightly fitting mask:
• Modest mask leaks
• Eye irritation, sinus pain, or sinus congestion
• Mild gastric distention

Summary
 The commonest cause of pharyngeal/airway obstruction in unconscious patients is
tongue falling back and secretions
 Recovery position (left lateral) is used in unconscious patients who have breathing
effort. This technique prevents aspiration and airway obstruction by the falling back
tongue
 Avoid head tilt chin lift in trauma patients with suspicion of C- spine injury
 The jaw-thrust maneuver moves the mandible and attached relaxed soft tissue
structures anteriorly which helps to make airway patent mainly used in trauma
patients to minimize C-spine manipulations
 Oro-pharyngeal airway is used in patients with depressed (absent) gag, swallowing
reflexes or GCS of less than 8.
 Patients with GCS less than 8 are considered as depressed gag, swallowing and cough
reflexes therefore during insertion of Oropharyngeal airway they tolerate without
complications or vomiting will not induced
 Nasopharyngeal airway is used for all types of patients who are prone for airway
obstruction and facilitates suctioning of the airway
  Laryngeal Mask Airway is a rescue device where mask ventilation is difficult or
attempts to intubate is failed
 The cricothyroid membraneis close to the skin, relatively avascular, and the widest
gap between the cartilage of the larynx and trachea, so it provides the best access for
percutaneous (cricothyrotomy) airway rescue techniques. This technique is used in
emergency condition when intubation and ventilation are impossible with the usual
methods.

Self-assessment questions
1. Describe the commonest cause of airway obstruction in unconscious patients

2. Describe the different techniques of manual maneuvers of airway management

3. Describe the difference and function of oro-pharyngeal and naso-pharyngeal

Airways

4. Describe the anatomy, indications and technique of cricothyrotomy

References
1. Tintinalli Emergency Medicine, 8th edition
2. Rosen’s Emergency medicine, 8the edition
3. Roberts and hedges’ Clinical procedures in Emergency Medicine, 5th edition
4. Integrated Emergency Participants manual, first edition
5. Manuals of Emergency Airway management, 3rd edition

CHAPTER FIVE: COMMON ARRHYTHMIASAND

CARDIAC RESUSCITATION
Duration – 06 hours
Duration - 03 hours
Objectives
At the end of this session, participants will be able to
 Know normal electrical conduction of the heart
 Learn ECG leads proper placement
 Develop skill to Interpret ECG

5.1 Introduction to basic ECG

ECG records and electrical activity of the heart.

Cardiac Physiology: The Pacemakers

Fig.1: Electrical conduction pathway starting from SA node to AV node then

bundles

• SA node
- Intrinsic rate 60-100 bpm
 - Supplied by RCA (55%)
- Supplied by L Circumflex artery (45%)
• AV node
- Intrinsic rate 40-60 bpm
- Supplied by RCA (90%)
- Supplied by L Circumflex artery (10%)
- Slow conduction velocity and long refractory period
• Slow conduction velocity of AV node allows for ‘atrial kick’ (increased stroke volume)
.Long refractory period protects ventricles from overly rapid stimulation (causing
decreased diastolic filling time and therefore decreased cardiac output)

Figure 2: Electrical conduction starting from AV node

Fig. 3:Normal electrical conduction system

Cardiac electrical activity

Fig.4: Cardiac electrical activity depicted on ECG

- Ordinary ECG has 12 leads
-6 limb leads (“standard leads”): 3 Bipolar: I, II, III and 3 unipolar: aVR, aVL and
AVF
-6 precordial (chest) leads: V1-V6
• V1 - R sternal margin, 4th intercostals space
• V2 - Left sternal margin, 4th intercostals space
• V3 - midpoint between V2 and V4
• V4 - Left midclavicular line, 5th intercostal space
• V5 - Anterioaxiallary line, 5th interconstal space
• V6 - Midaxillary line, 5th intercostal space

Leads

Fig.5: ECG lead placement sites with ECG Display

• The contraction and relaxation of cardiac muscle result from the depolarization and
repolarization of myocardial cells. These electrical changes are recorded via
electrodes placed on the limbs and chest wall .Depolarization vector travels towards
or away from a lead. These changes are transcribed on to graph paper to produce an
ECG
• ECG tracing is recorded on a graph where the horizontal axis represents time and
Vertical axis represents voltage.
 Voltage

Time

Fig. 6: ECG paper (X axis shows Time, Y –axis shows Voltage)

The ECG is recorded on to standard paper travelling at a rate of 25 mm/s. The paper is
divided into large squares, each measuring 5 mm wide and equivalent to 0.2 s. Each large
square is five small squares in width, and each small square is 1 mm wide and equivalent to
0.04 s.

Fig.7: ECG paper in detail (Small box, larger box, paper speed)
The Normal ECG

Waves –Upward or downward deflections: P, QRS complex, T, U wave

Segments-Flat Lines: ST, PR, TP Segments

Intervals –Waves plus segments: PR interval, QT interval

Fig. 8: Normal ECG

Waves:

• P wave: represents atrial depolarization. Normal duration is <0.12 sec or < 3 small
squares. Amplitude is <0.25mv(<2.5mm).P wave represents the summation of the
depolarization of the right and left atrium

 The first represents the right atrium

 The second part the left atrium

Fig.9: P wave (Blue-right atrial, Red –left atrial)

 QRS complex: represents ventricular depolarization. Duration is <0.12 sec.

o Q is the initial downward deflection
o R is the first positive deflection
 o S wave is the negative deflection following the R wave
 Not all QRS complexes have all three components
 T wave: represents ventricular repolarization. Polarity is similar to preceding QRS
 U wave sometimes follows the T wave - origin of it is uncertain

o PR interval: represents conduction delay in the AV node. Duration is 0.12-

0.2 sec
o QT interval :Represents Duration of ventricular depolarization and
repolarization
– The END on T wave should be less than halfway between RR
– Normally it is < 0.44 sec

 ST segment: begins with J point. Usually isoelectric with reference to TP segment.

Fig.10: ST segment (red), J point (Green)

Anatomical relations of leads in a standard 12 lead ECG

-II, III, and aVF: inferior surface of the heart
-V1 to V4: anterior surface
-I, aVL, V5, and V6: lateral surface

Approach to ECG

Follow the following step to interpret ECG

1. Rhythm
2. Rate
3. Axis
4. Look waves
5. Look segments
6. Look intervals
7. Summarize

Step 1: Rhythm
Look for rhythm strip (Lead II, or V1)
Ask 4 questions:
1. Are normal P waves present?
2. Are the QRS complexes narrow or wide?
3. What is the relationship between the P waves and the QRS complexes?
4. Is the rhythm regular or irregular?

Normal sinus rhythm:

1. There are normal P waves.
2. The QRS complexes are narrow.
3. There is one P wave for every QRS complex.
4. The rhythm is essentially regular.
If it is not sinus rhythm ,it is arrhythmia /dysrhythmia.
Example -If No P wave,Narrow QRS , and irregular –Atrial fibrillation
-If No P wave ,Wide QRS and regular –Ventricular rhythm

Step 2:Rate
When the rhythm is regular and the paper speed is running at the standard rate of 25 mm/s,
the heart rate can be calculated by counting the number of large squares between two
consecutive R waves, and dividing this number into 300. Alternatively, the number of small
squares between two consecutive R waves may be divided into 1500.
• Normal is 60-100 beats per minute
Fig.11: ECG rate calculation regular rhythm (5 large box ,regular ;Rate
=300/5=60 beats/min)

When an irregular rhythm is present, the heart rate may be calculated from the rhythm strip (
lead II).
The heart rate per minute can be calculated by counting the number of intervals between
QRS complexes in 10 seconds (namely, 25 cm of recording paper) and multiplying by six.

Fig.12: ECG rate calculation irregular rhythm(5 Intervals:5x6=30bpm)

Step 3:Axis
• Axis is the direction of the mean QRS vector (or direction of depolarization)
• Look I and aVF
Lead I Lead aVF Axis

Positive Positive Normal

Positive Negative Left Axis deviation

Negative Positive Right Axis Deviation

Negative Negative Extreme axis deviation

Tab.2:Axis determination

What is the axis of the following ECG?

Answer: right

Step 4:Waves
Assess the duration and voltage of different waves: P, QRS, T

Step 4.1: P wave

P wave will help to assess atrial enlargement.
Right atrial enlargement will give peaked P wave (P Pulmonale) while left atrial enlargement
makes P wave to be wider (P mitrale )

Fig.13: Normal P wave versus large P wave in Right atrial enlargement

Fig.14:Pmitrale (wide P wave showing left atrial enlargement)

Step 4.2 QRS

Assess duration and Voltage of QRS complex.
QRS is wide when the duration is >0.12 sec.Some of the causes for Wide QRS are:
• BBB bundle branch block
• VT-Ventricular tachycardia
• Hyper-kalemia
• IVCD-interventricular conduction delay
• Drug toxicity-TCA
Left ventricular hypertrophy
• When ventricle enlarges - the vector shifts in that direction
VOLTAGE CRITERIA for LVH
• S in V1 + R in V5 (or V6) > 35 mm
• R in aVL> 11 mm
• REPOLARIZATION CHANGES
• “Strain pattern”
• ST depression and asymmetric T inversion in leads with prominent R waves
• OTHER
• +/- LAD
• Widened QRS
• LAE

Fig.15:ECG showing LVH(Based on voltage criteria)

Right ventricular hypertrophy /RVH/ ECG criteria

• RAD
• Ratio of R to S wave in V1 > 1 (R > 15 mm in RBBB or > 10 in incomplete RBBB)
• Right Atrial Enlargement
• REPOLARIZATION CHANGES
• ST depression and inverted T waves in leads with prominent R waves ( (V1,
III, aVF)
Fig.16: ECG showing RVH (Prominent R wave in V1,ST depression with T wave
inversion V1-3,RAD)

Low voltage criteria

• R+S<5 limb leads
• R+S<10 pericardial leads
• I+II+III<15
• V1+V2+V3<30
 CAUSES
 Obesity
 Pericardial effusion
 Myxedema
 COPD

Step 4.3 T wave

• Is T wave peaked, inverted? Read on the causes.

Step 4.4 U wave

• Is it present?
• If so ,could be because of hypokalemia

Step 5 Segments
• Look for ST /PR segment elevation or depression in reference to TP segment.
• Causes of ST segment elevation
 • Myocardial infarction
• Acute pericarditis
• LVH
• LBBB
• RBBB

Step 6 : Interval

PR Interval

 Prolonged PR interval is caused by AV blocks

 First degree

 Second degree Mobitz type 1

 Second degree Mobitz type 2

 Third degree

QT interval
• 0.35- 0.45 s,
• Should not be more than half of the interval between adjacent R waves (R-R
interval).
 PROLONGED QT is caused by Hypokalemia ,hypocalcemia,hypothermia
- Prolonged QT has risk of degeneration to Torsade de pointes

Fig.17:Nowmalvs. Prolonged QT interval

Step 7:Summary
Summarize step 1 to 6 AND also look for special features

Exercise
1)How do you interpret the following ECGs?
A)

B)

Summary
 ECG shows electrical activity of the heart
 Systematic approach to interpret ECG is required not to miss abnormalities
 References
1.ECG for Emergency physicians ,AmalMatu
2.The only EKG book,MalcomeThaler
3.Pocket ECG interpretation Guide ,AyalewZewdie

5.2. Cardiac arrest resuscitation

Learning objectives
At the end of this session, participants will be able to
 Describe Chain of survival
 Identify Cardiac arrest algorithms
 Demonstrate the steps for approach of cardiac arrest
 Perform high quality CPR

Cardiac arrest is defined as abrupt cessation of cardiac pump function which may be
reversible by prompt intervention but will lead to death in its absence.There will be no
central pulse (carotid or femoral pulse)

Chain of survival
Chain of survival’ is what reduces mortality, morbidity in cardiac arrest
Out of Hospital cardiac arrest/OHCA/ Chain of survival includes the following
 Immediate recognition and activation of EMS
 Early high quality CPR
 Early defibrillation
 Advanced cardiac resuscitation
 Post cardiac arrest care
 Fig. 17:Chain of survival for out of hospital cardiac arrest(OHCA)

In hospital cardiac arrest chain of survival/IHCA/ includes the following

 Surveillance and monitoring
 Activation of Code team
 Early high quality CPR
 Early defibrillation
 Post cardiac arrest care

Figure 18: Chain of survival for inhospital cardiac arrest(IHCA)

Core Advanced cardiac resuscitation Concepts
• The BRAIN must be kept perfused
• The PATIENT requires frequent reassessment
• BLS to post-resuscitation care important
• Survival decreases as arrest time prolonged
• Timely treatment of underlying cause is key

What has led to increased survival?

• Training of rescuers
• Planned and practiced response
• Prompt recognition of cardiac arrest
• Prompt provision of CPR
• Early defibrillation (within 5 minutes)

Cardiac arrest algorithms

There are 2 main type of cardiac arrest algorithms .These are Shockable rhythm and the non
shockable rhythms .Ventricular fibrillation and pulseless ventricular tachycardia are
shockable rhythms whereas asystole and pulseless electrical activity /PEA/ are nonshockable
rhythms.

Pulseless electrical activity /PEA/ is an organized rhythm without central pulse .It requires
high quality CPR and Adrenaline.

Asystole is cardiac arrest rhythm without discernible cardiac electrical activity ,also known
as flat line . You should validate flat line is not operator error(missing leads, no power )

Fig. 19: Asystole

  The only class one recommendation for cardiac arrest is effective high
quality CPR and early defibrillation .Most important contributor to
increased survival is time to defibrillation

Figure 20: Adult cardiac arrest algorithm

Systematic approach for cardiac arrest

The three main components during advanced cardiac arrest resuscitation are the following
1. Basic life support /BLS/ Assessment
2. Primary Assessment –ABCDE
3. Secondary Assessment (SAMPLE history, H’s and T’s)

1. Basic life support /BLS/ Assessment

a. Check responsiveness
b. Shout for help to get AED/Defibrillator
c. Check for breathing and pulse (Carotid or femoral)
d. Start high quality CPR
e. Defibrillation
Figure 21: Sequential approach of BLS

Cardiopulmonary resuscitation /CPR/

is a skill, which includes artificial respiration to provide oxygen to the lungs and artificial
circulation to maintain blood flow through the body enough to give a person a chance for
survival.
Proper position for chest compression is at the center of the chest, midsternum.

Figure 21: Proper position of chest compression

Characteristics ofHigh quality CPR

• Push hard –depth at least 5 inch
• Push fast-Rate 100 to 120 per min
• Minimize interruption
• Allow adequate chest recoil
• Avoid excessive ventilation
• Switch compressor every 2 min or earlier if fatigued
 Figure 22: Hemodynamic response to ‘ideal’ chest compressions.

1. Primary assessment during cardiac arrest

A-airway assessment and Management
Ask the following questions
- Is the air way patent ?
- Is advanced air way indicated?
Maintain open airway with maneuvers and devices.
B-Breathing assessment and management
Are ventilation and oxygenation adequate ?
 For cardiac arrest administer 100 % oxygen
 Avoid excessive ventilation
 30 chest compressions to 2 ventilations if no definitive airway
 Ventilations at a rate of 1 breath every 6 to 8 seconds (8 to 10 ventilations
per minute) should be performed
 Deliver each rescue breath over 1 sec.
 Give a sufficient tidal volume to produce visible chest rise
C-Circulatory assessment
- Is chest compression adequate ?
- What is the rhythm?
• Check pulse every 2 min
• Monitor CPR Quality
• Attach monitor
• Ready to defibrillate if needed
 • Secure iv/IO access
D-disability assessment
• GCS/AVPU assessment
- Pupillary function

E-Exposure
● Remove clothing to do physical exams
• Look for signs of trauma
• Look for burn
• Look for unusual marks
• Look for medical alert bracelets
1. Secondary assessment
• SAMPLE History
- Sign and symptoms
- Allergy
- Medication
- Past medical history
- Last meal
- Events

• Look for 5 H’S and 5 T’S- Causes for PEA and Asystole
5H ‘S 5T’S
Hypoxia Tension pneumothorax
Hypotension Tamponade cardiac
Hypo/hyperkalemia Thrombosis-coronary
Hydrogen ion/acidosis Thrombosis-pulmonary
Hypothermia Toxins
Figure 23 :Full cardiac arrest algorithm
Figure 24: Reversible causes of cardiac arrest and therapies
Post cardiac arrest care
• After ROSC –return of spontaneous circulation
- Advanced air way and ventilation
- Improve perfusion –consider vasopressors
- Therapeutic hypothermia
- Treat underlying cause

Figure 25: Post cardiac arrest algorithm

Team Dynamics
• Team with team leader
• Clear roles and responsibilities
• Mutual respect
• Knowledge sharing
• Closed loop communication
• Clear message
Terminating resuscitation
• Consider factors:
- Time from collapse to CPR
- Time from collapse to first defibrillation
- Comorbid condition
- Pre-arrest state
- Initial arrest rhythm
Stop when your team determines higher certainty that the patient will not respond for further
resuscitation

Summary
 Well organized chain of survival improve survival in cardiac arrest
 Systematic approach for cardiac arrest involves primary assessment with ABCD
followed by secondary assessment SAMPLE History and 5H’s and 5 T’s evaluation
and management
 Terminating resuscitation should consider different factors.

References
1. Tintinall’is Text book of Emergency Medicine
2. AHA ACLS provider course manual,2015
3. AHA BLS provider course manual,2015
4. Rosen’s Text book of Emergency Medicine

5.3. Arrhythmia / Dysrhythmia

Learning objectives
At the end of this session participants are expected to
 Describe the classification of arrhythmia
 Describe the mechanisms of arrhythmia
 Identify different arrhythmias
 Discuss treatment options of different arrhythmias
Arrhythmia /Dysrhythmia is any rhythm that is not normal sinus rhythm with normal
atrioventricular (AV) conduction.
What is normal sinus rhythm? discussion

Classification of arrhythmia
• Tachyarrhythmia:arrhythmia with rate >100
• Brady-arrhythmia :arrhythmia with rate <60

Tachyarrhythmia
Mechanisms of Tachyarythmias
• Increased automaticity
- Normal or ectopic site
- Gradual onset and offset
• Re-entry
- Normal or accessory pathway
- Abrupt onset and offset
• After-depolarization causing triggered rhythms
- Rate-related
- Abrupt onset and offset

Approach to Tachyarrhythmia:
The following 4 KEY QUESTIONS should be asked.
1. Is my patient stable or unstable?
2. Is the rhythm narrow or wide?
3. Is the rhythm regular or irregular?
4. Is there a potential to degenerate to a more dangerous rhythm?

Stable patients are ~ asymptomatic

Unstable patients exhibit signs and symptoms of hypoperfusion/circulatory compromise
• Altered mental status
• Ongoing chest pain
• Dyspnea/Tachypnea
• Hypotension
Rate-related symptoms uncommon <150 bpm
Unstable patients require electrical therapy but stable patients need medical therapy .

Is the Rhythm Narrow or Wide?

Narrow complex (QRS<120 msec ATRIAL origin
- PSVT
- Junctional tachycardia
- Atrial fibrillation
- Atrial flutter
- Multifocal atrial tachycardia
Wide complex (QRS>=120 msec) VENTRICULAR origin
- Ventricular Tachycardia
- Ventricular fibrillation
Is the Rhythm Regular or Irregular?
Narrow Complex
• Regular
- SVT
- A flutter with 2:1 block
- Junctional tachycardia
• Irregular
- Atrial Fibrillation
- Multifocal Atrial Tachycardia
Wide Complex
• Regular
- Ventricular tachycardia
• Irregular
-Ventricular fibrillation
-Torsades de Pointe
Figure 26: Classification of tachyarrhythmia

PSVT-Paroxysmal supraventricular tachycardia

• Characteristics
- No P wave
- Regular
- Narrow QRS
- Rate >150

Figure 27: ParoxysmalSVT(No visible P wave, narrow QRS,Rate of 150)

Atrial flutter
• Characteristics
- P wave-saw toothed appearance, flutter waves
- QRS –Narrow
- 2:1- Regular

Figure 28 :Atrial flutter(Saw toothed P wave,narrow QRS)

Atrial fibrillation
• Characteristics
- P wave-not clearly seen ,fibrillatory
- Narrow QRS
- Irregular

Figure 29: Atrial fibrillation (No well defined P wave, Narrow QRS, Irregular)

Ventricular tachycardia
• Characteristics
- No P wave
- Wide QRS
- Regular
Figure 30: Ventricular tachycardia (No P wave,regular,wide QRS)

Ventricular fibrillation
• Characteristics
- No P wave
- Wide QRS
- Irregular,fibrillatory QRS
- Arrest rhythm-always without pulse

Figure 31: Ventricular fibrillation (No P wave ,irregular ,wide QRS)

Treatment of tachyarrhythmia
Treatment depends on whether patient Stable or unstable
• What are the unstablity signs?
• What is the therapy for unstable tachyarythmias?
Figure 32: Tachyarrhythmiaunstability signs and management

Pulse less Ventricular tachycardia and ventricular fibrillation require early CPR and
defibrillation.

Stable narrow complex Tachyarythmias

• Iv access, put on monitor ,give oxygen
• Vagal maneuvers-valsalva, carotidmassage ,eyeballmassage, water immersion
• Adenosine -6mg then 12 mg then 12 mg iv push ,follow with flush
• Beta blockers
• Calcium blockers

Stable wide complex tachyarrhythmia

• IV access, put on monitor, give oxygen
• Amiodarone -150 mg over 10 min, then 1mg/min
• Procainamide -25-50 mg /min
• Lidocaine

Exercise
• Case 1:25 years old female lady presented with paliptation of 2 hours
duration.She has no SOB.She is communicative ,chest clear .BP-100/60 .On
the monitor you saw the following .What is the rhythm and therapy?
What are the 4 things we should ask here ?
1.Stable /unstable Stable
2.Narrow /wide Narrow
3.Regular /irregular Regular
4.Potential to deteriorate ? No
Therapy :IV ,O2 ,Monitor
medical-vagal manuever,adenosine ,BB

• Case 2.The above lady after she was given adenosine converted to sinus rhythm. 3O
minutes later she complained SOB,but still communicating BP=80/50 ,SP02=80%
.The rhythm is shown below. What should be done?

Fig.33: Brady-arrhythmia

Definition:Rate<60 , symptomatic usually when below 50bpm

• Causes ‘DIE’
- Drugs
- Electrolyte abnormality
- Ischemia
• Hypoxemia is commonest cause
Look for signs of respiratory distress, pulse oxymetry reading
Classification
• Sinus bradycardia:Sinus rhythm with Rate <60

Figure34:Sinus bradycardia

 AV Blocks
• First degree AV block:PR Prolonged >0.2 ,Defect in AV node

Figure 35:First degree AV Block

• Second Degree AV block Type 1:Progressively prolonged PR interval until there is a
P with no QRS complex, Defect in AV node

Figure 36: Second degree mobitz type 1

 o Second Degree AV Block Type 2:QRS follows P wave at normal speed then
develops sudden unexpected loss of P-wave conduction and the QRS is
missing, Defect in His-purkinji system

Figure 37: second degree mobitz type 2

o Third Degree AV block:P waves are not coordinated with the QRS complex;–
Dissociated ,Complete heart block between atria and ventricles

Figure 34: :3rd degree AV Block

Approach to Brady Arrhythmia

Ask the following questions?
1-Stable or unstable
2-Look PR interval
3-Think causes-DIE
4-Treat the patient not the number
– Slow or very slow –differentiate from normal physiologic change like athletes
Figure 35: Approach tobradyarrhyhmia

Treatment Unstable bradyarrhyhmia

• Atropine 0.5 mg Q 3-5 mn –total 3 mg
• Dopamine 2-10 mic /kg/mn
• Adrenaline 2-10 mic/mn
• Pacemaker

Exercise
What is the finding?
 Answer

The ECG Shows SECOND degree AV Block Mobitz type 1

Answer
It shows AV dissociation which is feature of third degree AV block.

Summary
• Arrhythmia is abnormal rhythm which is not sinus
• Management to patient with arrhythmia depends on presence or absence of unstability
signs
• Unstable tachyarrhythmias require electrical therapy
• Think of ‘DIE’ for patients with bradycardia
References
1. Tintinalli Text book of Emergency Medicine
2. AHA ACLS provider course manual,2015
3. Rosen’s Text book of Emergency Medicine
 CHAPTER SIX: EMERGENCY APPROACH TO SHOCK

Time:

Learning Objective:

At the end of the session participants will:

 Explain how to approach shock in the Emergency room

 Identify the causes and classification of shock
 Identify different types of shock
 Recognize the signs of shock clinically
 Management Principle of different types of shock
 Recognize types of vasopressors and their use

Shock
6.1 Definition: - physiologic state characterized by a significant reduction in systemic tissue
perfusion, resulting in decreased oxygen delivery to the tissues, which creates an imbalance
between oxygen delivery and oxygen consumption. In Adults
 Systolic BP < 90 mmHg, or
 MAP < /= 60 mmHg
 Reduction of systolic BP > 30 mm Hg from the patient’s baseline
 Physiologic determinants
 Systemic vascular resistance(SVR): Vessel length, Blood viscosity, Vessel diameter
Cardiac output (CO): - Heart rate(HR), stroke volume (preload, myocardial contractility,
after load)

Stages of shock:

The overall goal of therapy is to reverse tissue hypo perfusion as quickly as possible in order
to preserve organ function.
 Pre-shock (warm/compensated shock): regulatory mechanisms compensate for
 diminished perfusion
o Tachycardia, warm extremity, low/normal BP
 Shock: overwhelmed compensatory mechanisms. E.g. with loss of 20 – 5% of
effective blood volume.
 End organ damage: irreversible state due to untreated shock.

Types of Shock

 Hypovolemic: Causes- hemorrhage, vomiting, diarrhea, third-space loss, burns,

 Cardiogenic: due to abnormality in cardiac function, resulting in pump failure
and decreased cardiac output
o Causes: cardiomyopathies, arrhythmias, mechanical causes, extra
cardiac/obstructive
 Distributive: sepsis, anaphylactic, acute adrenal insufficiency, neurogenic,
resulting mainly in decreased systemic vascular resistance
 Obstructive: cardiac tamponade, tension pneumothorax, massive pulmonary
embolus, etc... resulting in decreased CO and increased SVR

6.2 Clinical presentation

 Varies according to the type of shock, its cause, and its stage of presentation. Several
features are common among all types of shock (cardinal features), while others may
suggest a particular type of shock

Cardinal findings

1. Hypotension(absolute/relative)
2. Oliguria,
3. Abnormal mental status (the continuum of agitation confusion, delirium andcoma
4. Metabolic acidosis (decreased clearance of lactate by the liver, kidneys,
andskeletalmuscle
5. Cool and clammy skin
Suggestive findings:

Hypovolemic shock:
History: - hematemesis, hematochesia, vomiting, diarrhea, or abdominal pain,
blunt/penetrating trauma
P/E: - decreased skin turgor, dry skin, dry axillae, tongue/ buccal mucosa, postural
 hypotension, decreased JVP

Cardiogenic shock:
History: - Dyspnea, chest pain, or palpitation
o P/E: - diffuse crackles on lung
examination, new murmur, elevated jugular and central venous pressures
Investigations: -
evidence of pulmonary congestion/edema on CXR, evidence of
old/recent ischemia on ECG, elevated cardiac enzymes

Distributive shock:
History: - dyspnea, productive cough, dysuria, hematuria, chills, myalgia, rashes,
fatigue, etc
P/E: - fever, tachypnea, tachycardia, leukocytosis, abnormal mental status, flushing
Diagnostic approach

Diagnostic evaluation should occur at the same time as resuscitation. Resuscitative efforts
should not be delayed for Hx, P/E, and lab.
History: - baseline medical status, recent complaints and recent activities, food
and medical allergies, etc

Physical exam: - neither sensitive nor specific, should be directed to uncover the
type, severity, and cause of the shock
Laboratory: -

 To identify the cause and early organ failure.

 Especially performed early in undifferentiated shock.
 CBC, Basic chemistry- Na, K, Cl, serum bicarbonate, BUN, creatinine, LFTs,
amylase, lipase, PT, INR, PTT, fibrinogen, ABG, Type and cross-match, CXR,
abdominal x-ray, CT/MRI,
Empiric criteria for diagnosis of circulatory shock:

 Ill appearance or altered mental status (AMS)

 HR > 100 beats/minute
 RR >22bpm, or PaCO2 < 32 mmHg
 Arterial base deficit <-5 mEq/L or lactate >4 mM/L
 Urine output <0.5 mL/kg/hr.
 Hypotension> 20minutes duration
 Regardless of the cause, 4 criteria should be met

6.3 Management of Shock

Hemorrhagic shock
a. Ensure adequate ventilation/oxygenation
b. Provide immediate control of hemorrhage, when possible (e.g., traction for long
bone fracture, direct pressure)
c. Initiate judicious infusion of Normal Saline or lactated ringer’s solution (10-20
ml/kg)
d. With evidence of poor organ perfusion and 30-minutes anticipated delay to
hemorrhage control, begin PRBC infusion (5-10 ml/kg)
e. Adjunctive therapy
 Rewarming techniques (e.g. warm fluids, blankets, radiant lamps, head covers)- as
hypothermia is a common consequence of massive blood transfusion that
cancontribute to cardiac dysfunction and coagulation abnormalities.
 Antibiotics: when open dirty or contaminated wounds are present to prevent and treat
bacterial infections.

Cardiogenic shock
a. Put the patient on cardiac and pulse oximetry monitoring
b. Ameliorate increased work of breathing: provide oxygen; pain control, e.g.
Morphine for acute MI; PEEP for pulmonary edema
c. Preload augmentation: give fluid: 250ml of NS
d. Begin inotropic support: dobutamine (5micro gm/kg/min) is common empiric
agent for a border line BP (SBP between 90 – 100 mmHg), dopamine/
norepinephrine are choices for significantly reduced BP (SBP < 80 mmHg). If
no option, epinephrine can be considered. The most important part is titration of
the dose of inotropes and vasopressors based on patient’s response.
e. Diuresis after inotropic support if there are signs and symptoms of pulmonary
edema
f. Reverse the underlying pathology (e.g. treatment of arrhythmias, MI etc.)

Septic shock
a. Remove work of breathing - Ensure adequate oxygenation by giving oxygen via

face mask, if possible or through nasal catheter or nasal prongs..

b. Administer 30 ml/kg of IV crystalloid as bolus within first 3 hours, and titrate

infusion to adequate urine output, up to 5 -6 liters, until you see evidence of lung

congestion. MAP >= 65mmHg

c. Initiate broad spectrum antibiotic therapy early within one hour, usually based the

possible focus of infection/septic focus.

d. Source control intervention or surgical drainage/debridement of an abscess or dead

and necrotized tissue.

d. If volume restoration fails to improve organ perfusion, begin vasopressor support:

Vasopressors: Norepinephrine as the first – choose vasopressor; norepinephrine, infused at

0.5-1mcg/min, and titrated based on response, others include dopamine, infused at 5-
15mcg/kg/min and titrated every 10 – 15 min until response is achieved. f. Corticosteroid
administration- for refractory vasopressor-dependent shock.

g. Blood transfusion only when hemoglobin concentration decrease to less than 7g/dl

or if HCT is < 30% to keep adequate O2 saturation

h. Mechanical ventilation using target tidal volume of 6ml/kg predicted body weight.

Maintain plateau pressure less than 30cm H2O

i. Glucose control: maintain glucose <= 180mg/dl Update Hour – 1 bundle
 Measure lactate level, re-measure if initial lactate >2mmol/L
 Obtain blood cultures prior to administration of antibiotics
 Administer broad spectrum antibiotic
 Begin rapid administration of 30ml/Kg crystalloid for hypotension or
lactate>=4mmol/L
 Apply vasopressors if patient is hypotension during or after resuscitation to maintain
MAP >=65mmHg.
Anaphylactic shock
a. Control airway and ventilation
 Put the patient on monitor and give oxygen via high pressured face mask
 Consider Early definitive airway control for those evidence of significant airway
edemaor if you fail to correct oxygenation with face mask.
b. Secure bilateral wide bore needle IV lines and administer 20ml/kg of crystalloids
as fast as possible.
c. Administer Epinephrine for control of acute symptoms.
 0.3 -0.5 mg of adrenaline The dose is epinephrine, 0.3 to 0.5 milligram (0.3 to 0.5 mL
of the 1:1000 dilution) IM repeated every 5 to 10 minutes according to response or
relapse.
 If the patient is refractory to treatment despite repeated IM epinephrine, or with signs
of cardiovascular compromise or collapse, then institute an IV infusion of
epinephrine. Initially, epinephrine, 100 micrograms (0.1 milligram) IV, should be
given as a 1: 100,000dilutions. This can be done by placing epinephrine, 0.1
milligram (0.1 mL of the 1:1000 dilution), in 10 mL of normal saline (NS) solution
and infusing it over 5 to 10 minutes (a rate of 1 to 2 mL/min)
 If the patient is refractory to the initial bolus, then an epinephrine infusion can be
started by placing epinephrine, 1 milligram (1.0 mL of the 1:1000 dilution), in 500
mL of 5% dextrose in water or NS and administering at a rate of 1 to 4
micrograms/min (0.5 to 2 mL/min), titrating to effect.
d. Administer 5-10 mg/kg of hydrocortisone or 1-2 mg/kg of methyl prednisolone
for late control of symptoms
 Don’t have any role in the control of acute symptoms.
e. H2 receptor blockers

REFERENCE
 Tintinalli’s text book of Emergency Medicine 8th Edition
 Washington manual of Emergency medicine
 CHAPTER SEVEN: ALTERED MENTAL STATUS
Time: 1 hour

Learning Objectives
After completing this session participant will be able to:
 Define common terminologies of describing altered mental status
(AMS)
 Define coma and list differential diagnosis for patients
 Learn important investigative modalities for AMS
 Outline treatment plan for common causes of AMS
 Define seizure and identify the different types
 Define status epilepticus and formulate treatment plan

7.1 Altered Mental Status

Mental status is the clinical state of emotional and intellectual functioning of an individual.
Disorders of consciousness may be divided into processes that affect either arousal or
content of consciousness, or a combination of both. Arousal behaviors include wakefulness
and basic alerting. Anatomically, neurons responsible for these arousal functions reside in the
RAS (Reticular activating system), a collection of neurons scattered through the midbrain,
Pons, and medulla. The neuronal structures responsible for the content of consciousness
reside in the cerebral cortex. Content of consciousness includes self-awareness, language,
reasoning, spatial relationship integration, emotions, and the myriad complex integration
processes that make us human.
Dementia: is failure of the content portions of the consciousness with relatively preserved
alerting functions.
Delirium: is arousal system dysfunction with the content of consciousness affected as well.
Coma: is a failure of both arousal and content functions.

Coma: Coma is a state of reduced alertness and responsiveness from which the patient
cannot be aroused. The Glasgow coma scale is widely used and also the FOUR (Full Outline
of Unresponsiveness) score is used widely in ICU and it the advantages of assessing simple
brainstem functions and respiratory patterns, as well as eye and motor responses.

Clinical feature
History
 Exploit all available historical sources (EMS personnel, caregivers, family,
witnesses, medical records, etc)
 Onset of symptoms
 Any history of fever, medication, seizure

Physical examination
 Vital signs including RBS
 Look for signs of trauma
 Neurologic examination (cranial nerves, motor examination, posturing or meningeal
signs)
The clinical features of coma vary with the depth of coma and the cause.
Based on the clinical findings the cause of coma can be categorized in to two
1. Toxic-Metabolic coma –
 characterized by diffuse CNS dysfunction and no focal neurologic findings
2. Structural Coma- characterized by focal CNS dysfunction further classified to
 Hemispheric (supratentorial)
 Progressive hemiparesis or asymmetric muscle tone and reflex on the contrary
coma without lateralizing sign may result from increased ICP

 Posterior fossa (intra tentorial)

 An expanding lesion, such as cerebellar hemorrhage or infarction, may cause
abrupt coma, abnormal extensor posturing, loss of papillary reflexes, and loss of
extraocular movements.
Investigations
 CBC, RBS, serum electrolytes, renal and liver function tests, blood film etc.
 Brain CT, CXR, ECG, Brain MRI
 Lumbar puncture
 o Contraindications- although no absolute contraindication, caution should
be taken in patients with:
 Focal neurologic deficits
 Possible raised intracranial pressure
 Thrombocytopenia
 Suspected spinal epidural abscess

Differential Diagnosis
1. Coma from causes affecting the brain diffusely
Encephalopathies;
i. Hypoxic encephalopathy

ii. Metabolic encephalopathy ( hypoglycemia, hyperosmolar state, electrolyte

abnormalities e.g. hyper/hyponatremia)

iii. Hypertensive encephalopathy

iv. Organ system failure :

 Hepatic encephalopathy, uremia/renal failure,endocrine
 Addisons disease, hypothyroidism), hypoxia, carbon dioxide narcosis)
 Toxins
 Drug reactions ( e.g neuroleptic malignant syndrome)
 Environmental causes (e.g hypothermia / hyperthermia)
 Sepsis
3. Coma from primary CNS disease or trauma

7.2 Direct CNS Trauma

i. Diffuse axonal injury

ii. Subdural hematoma

iii. Epidural hematoma
 Vascular disease
 CNS infections
 Neoplasm
 Seizures
i. non convulsive status epilepticus
 ii. postictal state

Approach to the patient

The goal of the physician is to rapidly determine if the CNS dysfunction is from diffuse
impairment of the brain or if signs point to a focal (and perhaps surgically treatable) region of
CNS dysfunction.
Treatment of coma involves identification of the cause and initiation of specific therapy
directed at the underlying cause. Evaluation for readily reversible causes of coma, such as
hypoglycemia and opioid toxicity, demands priority.

1. ABC of life
Secure airway, breathing and circulation, take vital signs including RBS, secure IV line
Indication for intubation
i. Deep coma - GCS<9

ii. Status epilepticus

iii. Anticipated clinical worsening or rapidly deteriorating GCS despite initial

management

iv. If suspected poisoning and gastric lavage is planned.

2. Immobilization of C-spine if there is any concern of trauma

3. Coma cocktail
 Thiamine 100mg IV prior to dextrose in alcoholic patients
 Dextrose 50gm IV push
 Naloxone 0.01mg/kg if opiates suspected
 Flumazenil 0.2mg IV if benzodiazepine suspected (routine use in coma of unknown
etiology is not recommended)
4. If concern for increased ICP and herniation
 Elevate head 30 degrees

 Consider mannitol 0.5-1gm/kg bolus

 If mass lesion- consider dexamethasone
5. Send lab examinations and do LP if no contraindication. If patient is febrile give empiric
antibiotic ceftriaxone 2gm IV stat with dexamethasone without waiting for result.

6. Send the patient for investigation after stabilization

Glasgow Coma Scale

7.3 Seizure
Definition:

 Seizure is an episode of abnormal, paroxysmal, excessive discharge of central

nervous system/CNS/ neurons.
 Epilepsy is recurrent seizure due to an underlying cause
Classification of seizures

1. Generalized seizures: involves brain diffusely

a. Tonic-clonic (grand mal)

b. Absence seizures (petit mal)

c. Others (myoclonic, tonic, clonic, or atonic seizures)

2. Partial or focal seizures: electrical discharges begin in a localized region of the
cortex
a. Simple partial: without impairment of consciousness

b. Complex partial: with impairment of consciousness

c. Partial with secondary generalization

Clinical features

History
 When a patient presents after the event, the first step is to determine whether the
attack was truly seizure.

 Suggestive histories include presence of preceding aura, abrupt or gradual onset,

progression of motor activity, loss of bladder or bowel control, whether the activity is
local or generalized and symmetric or not, duration of the attack

 Clinical features that help to distinguish seizure from other kinds of mimicking
attacks
1. Abrupt onset and termination. (most lasting 1 to 2 minutes)

2. Lack of recall. Except simple partial seizure

3. Purposeless movements or behavior during the attack

4. Post-ictal confusion and lethargy.

Physical Examination
 Check vital signs including RBS
 Check for injuries ( head or spine, look for posterior dislocation of the shoulder,
laceration of tongue and mouth, dental fracture and pulmonary aspiration)

 Perform detailed neurologic examination

  Todd’s paralysis is a transient focal neurologic deficit following a simple or complex
seizure which should resolve within 48 hours.

Differential diagnosis

1. Syncope

2. Pseudo seizures

3. Hyperventilation syndrome

4. Migraine headache

5. Movement disorders

6. Narcolepsy/cataplexy

Laboratory examination

 In a patient with a well-documented seizure disorder who had a single unprovoked

seizure, the only tests that may be needed are a glucose level and an anticonvulsant
level.
 In case of an adult with a first seizure or when the history is unclear more extensive
studies are needed E.g. ( RBS, electrolytes, BUN, Cr, calcium, magnesium, a
pregnancy test and toxicology studies)
 Lumbar puncture- in a febrile or immunocompromised if no contraindication.
 Lab investigations helpful in distinguishing seizure from pseudo seizure
1. Wide gap metabolic (lactic acidosis)- majority will clear within 30min

2. Serum prolactin level- may be elevated briefly 15 to 60 minutes

Treatment of uncomplicated seizures

1. Patients with active seizure

 Protect the patient from injury; do not try to restrain

 If possible, turn the patient to the side

 Do not try to insert bite block or to ventilate during seizure attack

 Once attack subsides, ensure a clear airway

  There is no indication for IV anticonvulsant medication during the course of an
uncomplicated seizure

2. Patients with a history of seizure

 Identify and treat seizure precipitants
 In the known epileptic patient non-compliance is the main cause of acute onset of
seizure so if possible send for serum drug level.
 If serum levels are very low, supplemental doses may be appropriate, and the regular
doses may be adjusted or restarted. E.g. Phenytoin 18mg/kg Po as a single dose or
divide in to three doses given every three hours will achieve therapeutic serum level
within 2 to 24 hrs.
 If serum level is normal and patient has single attack additional treatment is not
needed because even patients with well controlled seizure might have breakthrough
attacks.
 If seizures are too frequent dose adjustment, adding another antiepileptic drug or even
changing of medication should be considered but should be done in consultation with
a neurologist or primary care physician.

3. Patient with a first seizure

 In general patients with a first seizure who have a normal neurologic examination, no
acute or chronic medical comorbidities, normal diagnostic testing including normal
imaging and who have normal mental status can be discharged from the ED without
initiation of antiepileptic medication.
 Patients with secondary seizure due to an identifiable neurologic condition should
generally be treated as the risk of seizure recurrence is high.
 The ideal initial antiepileptic regimen is a single-drug therapy that controls seizure
with minimum toxicity.

Selection of antiepileptic drugs

i. Generalized tonic colonic seizure
 First line- Valproic acid, lamotrigine, topiramate

 Alternatives- Phenytoin, carbamazepine, Phenobarbital

ii. Focal seizure
 First line- carbamazepine, phenytoin, lamotrigine

 Alternative- valproic acid, Phenobarbital

iii. Absence, myoclonic, tonic, clonic
 First line- valproic acid

4. Seizures in the HIV positive patient

 Mass lesions, HIV encephalopathy and meningitis are seen more frequently.
 If there is no evidence of increased intra cranial pressure, and focal neurologic deficit
Lumbar puncture should be done
 If CT is available and cost is not an issue non-contrast head CT scan can be used
initially.
 If no explanation for seizure, a contrast-enhanced head CT or MRI should be
obtained.

7.4 Status Epilepticus

Status epilepticus is continuous or intermittent seizures for more than 5 minutes without
recovery of consciousness. The most common causes of status epilepticus include sub
therapeutic antiepileptic levels; preexisting neurologic conditions such as prior CNS
infection, trauma, hemorrhage, or stroke; acute stroke; hypoxia; metabolic abnormalities; and
alcohol or drug withdrawal.

Types of Seizure Activity

Seizure activity may be generalized tonic clonic type which is associated with higher
mortality and complications. In non-convulsive status epilepticus, the patient is comatose or
has fluctuating abnormal mental status or confusion, but no overt seizure activity or only
subtle activity and the diagnosis is made by EEG.
Epilepsiapartialis continua is a focal tonic-clonic seizure activity with normal alertness and
responsiveness.

Treatment
The goal of treatment is seizure control as soon as possible and within 30 minutes of
presentation. Examination, identification of precipitating cause, application of the ABCs and
treatment begin simultaneously.

Approach to the patient

 ABC of life

 Place the patient in semi prone or lateral position to decrease risk of aspiration.

 Large bore IV line should be established and RBS should be determined

 Thiamine 100mg Iv prior to dextrose infusion

 Dextrose 50g IV push.

Administration of anticonvulsant

 If IV line is difficult to establish give diazepam 5 to 10 mg (0.15 mg/kg) diluted in

10 ml NS per rectum.
 Phenytoin should not be mixed with any glucose containing IV fluid
 Phenytoin should be infused no faster than 25 mg/min
 An oral loading dose of phenytoin will achieve therapeutic serum concentration in 2
to 24 hours, where as IV phenytoin achieves anticonvulsant level in 1 to 2 hours.

Remember; if status epilepticus is diagnosed, the patient should be started with both
benzodiazepine and loading of phenytoin simultaneously and ideally intubation should be
considered.

Refractory Status Epilepticus:

It is defined as persistent seizure activity despite the IV administration of adequate amounts
of two antiepileptic agents.

Drug therapy of status epilepticus

1. Diazepam 5-10mg Iv stat/ lorazepam 0.1- 0.15mg over 1-2min and repeat

dose if no response after 5 min

2. Phenytoin 20mg/kg IV at 50mg/min or fosphenytoin 20mg/kg at100-150

mg/min
 3. If seizure continues repeat phenytoin 7-10mg/kg at 50mg/kg or

fosphenytoin 7-10mg/kg at150mg/min

4. If seizure continues and no ICU, Phenobarbital 20mg/kg IV at 60mg/min.

5. If no response with the first dose repeat Phenobarbital 10mg/kg IV at

60mg/kg

6. If no response general anesthesia with propofol, midazolam or pentobarbital. If the

above medications are not available ketamine 1.5mg/kg bolus then 0.01-0.05mg/kg/hr can be
infused.
 Ketamine is considered as an agent of last resort as it has neuroprotective
properties. Its major contraindication is the presence of intracranial mass
lesion.
 Valproic acid 20-40mg/kg iv at 5mg/kg/min is considered as a second line
instead of phenytoin if the patient was already on valproic acid or if the
patient cannot respond to phenytoin instead of Phenobarbital.
Note: The above medications are usually not available in the Iv form in most centers; so the
respective Po preparations with the same dose can be used.
 CHAPTER EIGHT: COMMON CARDIO-RESPIRATORY
EMERGENCY
Time:3 hours

Learning Objectives:
 To know how to approach Heart failure in the Emergency room
 To know classification of Heart failure in the Emergency room
 Management of Heart failure in the Emergency room
 To understand pulmonary edema and its management

8.1.Heart Failure
Acute decompensated Heart failure is one of the common emergency department presentations of
patients with circulatory system affection. It is part of the spectrum of the progressive. It leads to fluid
buildup in the lungs, liver, gastrointestinal tract, and the limbs and weight gain.

Heart failure can be broadly categorized as:

 systolic heart failure: (occurring when the heart is unable to pump blood) or Causes,
valvular heart disease, dilated cardiomyopathy, Ischemic heart disease, hypertensive
heart disease.
 Diastolic heart failure: (when the heart muscles are very much stiff and prevent
filling of the heart, but the contractility remains to be normal).

Causes

 Hypertrophic cardiomyopathy,
 Restrictive cardiomyopathy,
 chronic hypertension,
 Ischemic heart disease,
 diabetes.
Complex clinical syndrome of heart failure is resulting from structural and/or functional
cardiac disorders that impair systolic and/or diastolic function. The body’s neuro humoral
system tries to compensate for this state through various compensatory mechanisms initially
beneficial but later on ending up in deleterious effects.
Another schema for classifying heart failure patients is as right or left sided heart failure.
Right sided heart failure: presents with bilateral leg swelling, ascites, and
hepatomegaly
Left side heart failure: presents with pulmonary edema. In general, they occur together
though they could as well present separately.

Etiologies of heart failure

 Heart failure with depressed Ejection Fraction
o Coronary heart diseases.
o Chronic pressure overload
o Hypertension.
o Valvular obstruction.
o Chronic volume overload
o Valve Regurgitation
o Dilated cardiomyopathy.
o Toxic/drug induced
o Viral
 Heart failure with preserved Ejection Fraction
o Hypertrophic cardiomyopathy
o Hypertension
o Restrictive cardiomyopathy
 Pulmonary heart diseases
o Corpulmonale
 High output states
o Chronic anemia
o Thyrotoxicosis
 Common presentation of patients with heart failure includes:
o Progressive dyspnea, orthopnea (shortness of breath in lying position),
palpitation, Paroxysmal nocturnal dyspnea (waking up from sleep due to
severe shortness of breath)
o Swelling of the body starting from the feet progressing upwards, swollen
abdomen,cough productive of pink frothy sputum,
o Fatigue, weakness, angina, syncope.
 o Other diseases could present in a similar ways and should be considered in the
differential.
Look for evidences of other comorbidities
o E.g. Diabetes, hypertension, dyslipidemia, chronic kidney disease
Look for evidence and severity of complications

o Pulmonary edema, cardiogenic shock, acute renal failure

The severity of the dyspnea and other symptoms should be graded by the New York

Heart Association (NYHA) classification.

 Class I: symptoms* elicited only at levels of exertion that would limit normal
individuals
 Class II: symptoms elicited at ordinary exertion.
 Class III: symptoms elicited on less than ordinary exertion.
 Class IV: symptoms elicited at rest *symptoms: dyspnea/ Fatigue / palpitation /
angina pain

Physical examination.
Evaluate for any evidence of cardio respiratory distress as part of the primary survey.Look for
evidences of reduced cardiac output

 Diaphoresis,
 Resting tachycardia,
 Rarrow pulse pressure (<25mmHg),
 Rool,
 Pale and cyanotic limbs,
 Delayed capillary refill (>2 sec)

Vital signs

 Neck for any neck vein distention.

 chest - lower lung field crepitation, evidence of pleural effusion,CVS – S3 gallop,
murmurs
 Abdomen – Right upper quadrant tenderness and hepatomegaly, any sign of fluid
collection (shifting dullness, fluid thrill)
  Musculoskeletal – pitting edema in limbs, sacral area for bed ridden patient

Through apossible underlying cause and precipitating factor for the heart failure. quick
history and physical examination, we should look for evidences for the underlying cause:
Imagine the anatomy of the heart and which structures could be affected to lead to heart
failure. Common underlying causes of heart failure include:
- Valvular heart disease – commonest cause of heart disease in our set up,with
the affection of the different valves of the heart, either alone or in Combination withcardiomyopathies
(hypertrophic, dilated, restrictive cardiomyopathies)

- Ischemic heart disease – due to narrowing of small blood vessels of the heart
(coronary vessels) as a result of atherosclerosis. This results in compromised
blood and oxygen supply to the heart.
- Congenital heart disease:Examples: Atrial septal defect, Ventricular septal
defect etc.
- Pericardial diseases – Effusive pericarditis, constrictive pericarditis ,Viral
pericarditis, TB pericarditis:
Precipitating Factors: Common precipitating factors include:

Anemia, thyrotoxicosis, arrhythmia, drug discontinuation, salt intake, infection,

Spontaneous bacterial endocarditis, uncontrolled hypertension, acute myocardial infarction,
and other drugs.

Patients with a specific underlying cause of heart failure may remain asymptomatic for a long
period of time until the natural course of the disease or a precipitating cause unmasks it to
become decompensated. Identifying what precipitated the heart failure is an essential step
later guiding the management of the patient.
Patients with acute heart failure can be classified into four based on status of perfusion and
congestion.

(CO= Cardiac output, SVR = systemic vascular resistance, LV = Left ventricle)

Work up
The following investigations can be ordered to reach at a diagnosis. Work up should be
individualized.
  CBC, Urinalysis, Renal function test.
 CXR, ECG, Echocardiography.
 Serum electrolytes (potassium, sodium) .
 Other tests depending on the patient’s presentation. A quick emergency
ultrasound evaluation could help to evaluate left ventricular contractility, Inferior venacaval
distension and change of size with respiratory

movement, and pericardial effusion. Detail Echocardiography can be sent after patient
stabilizing.
Due to issues of availability of detailed echocardiographic evaluation, the emergency
practitioner needs to develop his/her skills of physical examination and performing
emergency ultrasound.

Management

Goals of management:
 Establish Diagnosis, etiology and precipitating factors.
 Treat life threatening abnormalities e.g. Oxygenation, hemodynamic stability
 Initiate therapy to rapidly provide symptom relief – revert them back to profile
In the acute setting, management of systolic and diastolic heart failure share similar
properties except for minor differences like requirement of inotropic drug in systolic failure
as opposed to diastolic failure. The general principles of management of heart failure are
mentioned here below:

1. Decision on Hospital admission

Decision on admission should be made on individual basis considering different factors. A
general guide is presented here but the emergency practitioners’ clinical judgment comes
first.

Priority of admission should be given to the following sub groups

 Evidence of severely decompensated heart failure

 Hypotension, worsening renal function, Altered mentation

 Dyspnea at rest

 Hemodynamically significant arrhythmia e.g. Atrial fibrillation with rapid ventricular

response

 Acute coronary syndromes

 A second subgroup for whom admission is recommended include

 Worsened congestion despite oral treatment even if without dyspnea

 Electrolyte disturbance.

 Concomitant comorbidities e.g. Pneumonia, DKA, stroke etc.

 Newly diagnosed patient with congestion.

2. Initial stabilization

 Assessment of the airway, oxygenation and prescription of oxygen o Oxygen support

 A decision should be made based on clinical clues of hypoxia (respiratory distress,
cyanosis) and oxygen saturation (<90%). Routine supplemental oxygen in those with
normal oxygen saturation is not recommended.
 Put the patient on Continuous cardiac monitoring.
 Elevate the head of the bed to improve comfort.
 Salt restriction <2g sodium / day
This can generally be achieved by avoiding the addition of table salt. Fluid restriction
(<2L/d) though not routinely employed for milder forms of heart failure remains an essential
component of the management of patients with concomitant heart failure and hyponatremia
and in pulmonary edema. IV fluids in general should be withheld from such patients

3. Addressing symptoms and signs related to congestion or low perfusion

a) Diuretics
A Potent diuretic, preferably parenteral loop diuretic should be initiated early to manage the
fluid overload state. Why IV route preferred over oral route?
 PO drugs have reduced absorption due to edema of gastrointestinal tract.
Dosing: The dosage of the loop diuretics e.g. Furosemide is decided based on
 The patients’ urine output response and
 The urgency of alleviating the congestion.
Unlike Peripheral congestion (ascites, limb swelling) where slow diuresis is recommended,
early aggressive diuresis in patients with pulmonary edema saves lives.
 Usual starting dose for Furosemide is 40mg IV and should be escalated
(doubled)every hour till one finds the dose that produces adequate urine
(>0.5ml/kg/hr.). That dose can be given on a twice or three times a day doses.
 If no adequate response to the loop diuretic alone
 Continuous IV infusion of the loop diuretic.
 Add a thiazide diuretic prior to the loop diuretic dose to further potentiate the action
of the loop diuretic
 Monitor for hypotension, worsening renal function, electrolyte abnormalities
 Add potassium PO or a potassium sparing diuretic or spironolactone to prevent
hypokalemia.
b) Vasodilators

 Nitrates :Improve pulmonary congestion, ↑ coronary blood flow, ↓ afterload

o Nitroglycerin: 20mg/min with 20mg/min increment every 5- 15 minutes.

Target Mean arterial pressure reduction of 10mm Hg, with systolic blood
pressure remaining above 100mm Hg.
o Unable to use after 24 hrs. due to tolerance.
o S/E: Headache, hypotension.
 Other vasodilators: Isosorbidedinitrate, Nitroprusside
o Some medications to treat chronic heart failure like Beta Blockers, and
ACEI’s have deleterious effect in the acute setting and should be discontinued
or used very cautiously.
 o NSAIDS should be avoided - they reduce efficacy of diuretics
o Approach to management of cardiogenic shock is discussed under the topic
shock.
Inotropic agentslike:Dobutamine, Dopamine are used.
The approach of management of pulmonary edema is discussed separately later in this
chapter.
4. Identification and management of precipitating factors:E.g. In atrial fibrillation with fast
ventricular response, Digoxin or low dose Beta blockers could be used for rate control.
Cardioversion can be attempted for those with new onset atrial fibrillation with
hemodynamic instability; Antibiotics for infection, etc.
5. Monitoring: - Close patient monitoring is very important for optimal outcome. Important
parameters to follow are:
 Vital signs – frequently depending on the severity of the heart failure. E.g. A patient
with cardiogenic pulmonary edema might need frequent
o V/S monitoring (every 30 minutes) to adjust the diuretic dose
o Monitoring for optimal diuresis
 Assessment of urine volume.
 Daily weight measurement – better done with the same weight scale, at
a fixed time during the day to make comparisons
 Assessing for resolution of edema – marking the upper border of the
crepitation in the lung helps to assess the response to diuretics.
 Monitoring BUN, Cr, vital signs
 Renal function test, serum electrolytes (especially potassium if high
dose diuretics are being used) – this can be done daily or even more
frequently onindividualized basis.
 Others depending on the specific underlying cause of heart failure o
Monitoring for drug side effects
 Loop diuretics, Thiazide diuretics, Worsening renal function,
hypokalemia, hypotension, hyponatremia, hypomagnesaemia
A flow sheet should be prepared for use including the most important parameters to be
followed.
Table 2. A sample flow sheet is presented as follows: follow up sheet for patient with shock
Dat Outp Insensib Daily
Vital signs Mental Diuretic
e Input ut le loss BUN Cr Weight
status dose

T
PR BP RR Sao
o
2

1. Management of the underlying cause

2. Discharge and Enroll to chronic care for Mx following principles of chronic heart
failure Mx.

8.2. Pulmonary edema

learning objective:
At the end of this course participants will be able to:
 Define approach to Pulmonary Edema
 Manage pulmonary edema in the Emergency room

Pulmonary edema occurs due to fluid leak into the interstitium of the lungs and alveoli
during severe heart failure, most frequently in left sided heart failure. Patients have profound
dyspnea and orthopnea, hemoptysis. It is a life threatening situation and timely intervention
has a great impact on the outcome.

Auscultatory findings are fine crepitation more prominent in the lower part of the chest. The
level of the upper border of the crepitation should be marked to assess for the patient’s
response to our interventions.

At times non-cardiac sources of pulmonary edema might mimic cardiogenic pulmonary

edema. They occur in situations like severe pneumonia and do not respond to the measures
done for heart failure. The role of history and physical examination cannot be over
emphasized to differentiate them.

Chest X ray feature: bilateral, perihilar, bat wing (butterfly) shaped interstitial infiltrates
more prominent in lower lung fields.

Management

 General Measures

 Admit to the emergency room

 Immediately administer oxygen via appropriate route

 Keep the patient in a propped up position with the legs dangling

 Morphine 2-4mg IV boluses for reduction of preload and anxiety

Urgent diuresis

 Parenteral loop diuretics: Furosemide are an ideal choice (venodilator reducing

preload in addition to its diuretic effect)
 Use frequent dosing provided that blood pressure, renal function permit
 There is no standing dose of furosemide that is universal for every patient and
decision on frequency and dosage must be individualized.
 Furosemide can be started at <0.5mg/kg or 40 mg IV, with 40 mg increments every
hour. The dose that gives urine output ≥0.5ml/kg/hr. should be used frequently (every
hour) with adequate monitoring. The maximum recommended dose of Furosemide as
a single IV bolus is 160-200 mg.
 in very severe pulmonary edema not responding to the above measures, the following
measures can be taken

o Addition of a thiazide diuretic e.g. Hydrochlorothiazide

o Use a perfuser to administer continuous Lasix infusion at 10- 40mg/hr. If the
urine output remains below 1ml/kg/hr., the infusion rate can be increased each
hour as necessary till a 
maximum dose of 80-160 mg/hr.
 Vasodilators, Nitrates
a. Sublingual Nitroglycerin (0.4 mg x 3 every 5 min)– first line for cardiogenic pulmonary
edema
b. If pulmonary edema persists and no evidence of shock
 IV Nitroglycerin 5-10 microgram/min infusion
Monitoring

 Resolution of symptoms (dyspnea, orthopnea)

 Vital signs, saturation
 Mark the level of upper border of crepitation to see for resolution of lung
congestion o BUN, Cr
 Serum potassium – hypokalemia is an important adverse effect of Furosemide.
o Start oral Potassium chloride, or spironolactone to prevent hypokalemia
o Management of underlying cause and precipitating factor for the heart failure
Summary:

 Heart failure and pulmonary edema is a treatable medical emergency

 If you treat the triggering factors, you can treat the Heart failure as well as
pulmonary edema
 Act fast in treating a patient in Heart failure or pulmonary edema as it may lead to
death
 Management of pulmonary edema in the ED is a step wise approach and follow up
is critical

8.3Acute Coronary Syndrome

Learning Objective:

 Define approach to Acute coronary syndrome

 List classification of Acute coronary syndrome
 Manage Acute coronary syndrome in the Emergency room

Acute chest pain;Is the recent onset of pain, pressure, or tightness in the
anterior thorax between the xiphoid, suprasternal notch, and both maxillary lines.
 Pain from visceral fibers is generally more difficult to describe and imprecisely
localized. Patients with visceral pain are more likely to use terms such as discomfort,
heaviness, pressure, tightness, or aching.
Acute coronary syndrome: Includes acute myocardial infarction and unstable angina.

Unstable angina: Is considered to be an ACS in which there is myocardial ischemia

without detectable myocardial necrosis.

 Characterized by- occurring at rest/with minimal exertion, lasting>10 min; severe &
of new onset; crescendo pattern (i.e. more severe, prolonged, or frequent than
previously).

Acute myocardial infarction: Is defined by myocardial necrosis with elevation of cardiac

biomarkers andis classified by ECG findings as:

ST-segment elevation myocardial infarction:Chest pain >20 to 30 min occurring at rest

(not relieved by nitroglycerin), serologic evidence of myonecrosis, and persistent ST segment
elevation.

Non-ST-segment elevation myocardial infarction:UA with evidence of myocardial

necrosis (elevated cardiac biomarkers)

Clinical Assessment

Risk assessment

 Patients with abnormal vital signs, concerning ECG findings (if available initially)
 History of prior coronary artery disease, multiple atherosclerotic risk factors, or any
abrupt, new, or severe chest pain or dyspnea should be quickly placed into a treatment
bed.
 Once the patient is stable, focus on history, physical exam, and laboratory findings
associated with cardiac (acute coronary syndrome) versus non cardiac chest pain
causes.

Hx

 The main symptom of ischemic heart disease is chest discomfort or pain.

 The history should characterize its severity, location, radiation, duration, and quality.
 descriptions of chest pressure, heaviness, tightness, fullness, or squeezing
 The classicpain or discomfort location is substernal or in the left chest, with radiation
to the arm (either), neck, or jaw
  The presence of associated symptoms such as nausea, vomiting, diaphoresis, dyspnea,
light-headedness, syncope, and palpitations.
 Advanced age, female gender, and a history of diabetes mellitus areassociated
with more nonclassic ACS presentations.

P/E

 May appear well, without any clinical signs of distress, or may be uncomfortable,
pale, cyanotic, or in respiratory distress.
 Pulse could be normal or display bradycardia, tachycardia, or irregular pulses.
 Bradycardic rhythms are more common with inferior wallmyocardial ischemia; in the
setting of an acute anterior wall infarction, bradycardia or new heart block is a poor
prognostic sign.
 Blood pressure can be normal, elevated (due to baseline hypertension, sympathetic
stimulation, and anxiety), or decreased (due to pump failure or inadequate preload)
 S3 gallop is present in 15% to 20% of patients with AMI; if detected, an S3may
indicate a failing myocardium.
 The presence of a new systolicmurmur is an ominous sign, because it may signify
papillary muscle dysfunction, with resultant mitralregurgitation, or a ventricular
septal defect.
 The presence of rales, with or without an S3 gallop, indicates left ventricular
dysfunction and left-sided heart failure.
 Killip class for STEMI: Class I – no HF, Class II -mild to moderate HF(S3,basal
rales,raised JVP) , Class III - overt pulmonary edema, Class IV - cardiogenic shock

Diagnosis
 The diagnosis of ST-segment elevation myocardial infarction (STEMI) depends on
the ECG in the setting of symptoms suggestive of myocardial infarction.
 The diagnosis of non-ST-segment elevation myocardial infarction (NSTEMI)
depends on abnormal elevation of cardiac biomarkers but may include ECG changes
not meeting criteria for STEMI.
  The diagnosis of unstable angina is based on history: Angina pain with at least 1 of 3
features: Occurs at rest/with minimal exertion or lasting>10 min, Severe & of
new onset or crescendo pattern (i.e. more severe, prolonged, or frequent than
previously).

1. ECG: done at presentation; repeat at 6–12 h& with any change in symptoms
UA/NSTEMI= ST depression/transient elevation or deep T inversion (>=0.3mV)
STEMI=New ST elevation in 2 contiguous leads >= 0.2 mV in men or 0.15 mV
inWomen in leads V2-3 and/or 0.1mV in other leads OR new LBBB
N.B the ECG must also be analyzed for rate, rhythm etc (look for arrhythmias)

2. Cardiac biomarkers: serial testing at presentation & 6–12 h after sx onset

 Cardiac troponins ( T&I)-rise 20 -50 Xs Upper normal limit/UNL/ in acute MI;
rise 4-8 hr after injury; may remain elevated for 7-10 days; more
Specific&Sensitive than CK-MB
 Creatine kinase (CK )-rises in 4–8 hr; normalize by 48–72 h; lacks specificity
3. Echocardiography: may show new wall motion abnormality

4. RBS, electrolytes,OFTs, lipid profiles

5. CXR: to look for pulmonary edema; R/o other DDx (PTE, pneumonia, Pneumothorax...)

6. Coronary angiography if indicated

Management of ACS:

 Should focus on stabilizing the patient's condition, relievingischemic pain, and

providing antithrombotic therapy to reduce myocardial damageand prevent further
ischemia. The goal is early revascularization.

1) General measures: Continuous ECG monitoring for arrhythmia & ST changes

 V/S: Q 2 hr until stable, then Q 4hr & as needed
 O2 (2-4 lit/min) if SaO2<90%
 Bed rest, Sedation, VTE(venous thromboembolism) prophylaxis
 NPO except for sips of water until stable; IV fluid – eg. For inferior MI
  Glycemic control-goal is RBS of 140-180mg/dl(if > 180mg/dl,give regular
Insulin-1-2IU for each 50mg/dl increase above 180mg/dl, by measuring RBS Q
6hrs)
 Treat comorbidities like DM (for both types-standing doses of lente /NPH
Insulin at A.M & P.M with correctional doses of Regular Insulin in between 6
hourly); and HTN (see Management).

2) Medications:
 Aspirin(ASA): loading:162–325 mg chewed, then 75–162 mg/d plus
 Clopidogrel-loading: 300mg Po, then 75 mg/d for at least 1 yr (but ASA lifelong)
 Nitroglycerin (NTG): sublingual 0.4 mg Q 5 min as needed or persistant chest pain
*IV NTG for persistent ischemia .C/I= low BP, sildenafil use
 Morphine sulphate: 2–5 mg IV, may be repeated Q 5–30 min as needed to relieve
Symptoms (can also use morphine syrup, pethidine or tramadol)
 Metoprolol :25–50 mg PO q 6 h* (If HTN, ongoing pain ,tachycardia: give IV over
1–2 min by 5mgincrements. If not available- use atenolol, propranolol/carvedilol.
C/I- CHF, bradycardia
 UFH: Bolus 60–70 U/kg (max. 50000 IU) IV then infusion of 12–15 U/kg/ h (initial
Maximum 1000 U/h) titrated to aPTT 50–70 s * If no per fuser, 12,500U SC BID is
possible; OR LMWH (Enoxaparin):1 mg/kg SC Q 12 h(if GFR< 30,1mg/kg once
daily)
 Statins: atorvastatin 80mg po/d is preferred. Others options are pravastatin/
Simvastatin/ lovastatin 40mg Po/day

 ACEIs: start low dose eg. Enalapril / lisinopril 2.5 to 5mg po/d OR captopril 6.25-
12.5mg TID; then escalate gradually to clinically effective dose.

Invasive therapy in ACS: for high risk patients who present early, referral to a better set up
is recommended (If the patient can afford)
 Time since onset of symptoms- 90 min for PCI / 12 hours for fibrinolysis
is this high risk STEMI?- If higher risk may manage with more invasive treatment

 Determine if fibrinolysis candidate- Meets criteria with no contraindications

 Determine if PCI candidate- Based on availability and time to balloon treatment

 STEMI: Fibrinolysis Vs PCI/CABG
Unstable angina/NSTEMI: PCI/ CABG; but fibrinolysis is not indicated.

8.4 Emergency approach to Asthma

Learning Objective:
At the end of this training participants will be able to:
 know how to approach Asthma in the Emergency room
 Identify the precipitant factor of shock
 Recognize the signs of imminent respiratory failure
 Management Principle of different types of shock

Asthma is a chronic inflammatory condition of the airways resulting in hyper

responsiveness of the airways to various stimuli. This leads to excessive
narrowing of the airways with reduced airflow and symptoms of dyspnea and
wheezing.

Triggering factors

Several stimuli trigger airway narrowing, wheezing, and dyspnea in asthmatic

patients
 Allergens, upper respiratory tract infections, exercise and
hyperventilation, chest infections (viral or bacterial), cold air, irritant
gases, sulfur dioxide, drugs (B blockers, aspirin), Stress, irritants -
household sprays, paint fumes.
 No clear precipitating factor is identified in over 30% of patients Risk
factors for severe Asthma.
Factors Increasing the risk of severe life-threatening asthma include

 Previous ventilation.
 Hospital admission for asthma in the last year.
  Heavy rescue medication use.
 >3 classes of asthma medication.
 Hepeated attendances at emergency room for asthma care
Presentation
 Characteristic symptoms are dyspnea, cough productive of whitish
sputum, chest tightness and wheezing.
 Acute attacks may build up over minutes, hours, or days and the
patientsmay deteriorate very rapidly and present as respiratory or
cardio-respiratory arrest

Initial assessment
 Patients presenting with an asthma attack may be at imminent risk of
death
 Rapid and accurate assessment of vital signs
1. Assess for signs of imminent respiratory arrest. If present start treatment
immediately
Characteristics defining a patient in imminent arrest

 Unable to walk
 Drowsy or confused
 Has paradoxical chest movements
 No wheezing
 Bradycardia
2. If no signs of imminent arrest, assess for signs of clinical distress
3. If the patient is not in imminent arrest, proceed with assessment and
treatment

Table 1: Classification of severity of an asthma attack

Imminent
Parameter Mild Moderate Severe
respiratory
 arrest
Walking
Can lie Talking
Prefers to At rest Hunched
Breathless
down sit up forward

Unable to
Talks in Sentences Phrases Words
speak

Drowsy or
Alertness May be agitated Usually agitated Always agitated
confused
increased Often > 30/min
Respiratory rate increased

Paradoxical
Accessory muscles and thoracic and
Usually not usually usually
suprasternal retractions abdominal
movements
Moderate, often
Absence of
Wheeze only end - Loud Usually loud
wheeze
expiratory
100 >120 Bradycardia
Pulse rate 100-120

<60% or (<
PEF after inhalation of >80% Impossible
60-79% 100l/min in
salbutamol to measure
adults)

*Where signs from several grades of severity are present, the highest grade of severity is
used to classify the attack, even if not all the signs for that grade are present

Acute severe asthma: Immediate therapy

Priorities of treatment
 Treat hypoxia.
 Treat bronchospasm and inflammation.
 Assess need for intensive care.
 Treat any underlying cause if present.
Severe or life threatening attack Initial treatment
 Oxygen – the highest percentage available
o Maintain O2 saturation > 92%
 Bronchodilators.
o SABA- Short acting beta agonist
 Salbutamol/Albuterol: Puff: 4-8 puffs Q 20 min for up to 4 hrs., then Q 1-4 hrs. as
needed

Technique of salbutamol puff.

 Test the inhaler: shake well and release one puff into the air
 Breathe out gently & place the mouth piece in the mouth and close lips around it.
 Tilt head slightly backwards, breathe in slowly and press down the canister to release
one dose
 Remove the inhaler and hold breath for 10 seconds and breathe out slowly
o Nebulization: 2.5-5mg every 20 mins for 3 doses then 2.5-10 mg Q 1-4 hrs.as
neede
o MDI -4 puffs every 10 mins, 8 puffs every 20 mins
 Add Iptratropium bromide 0.5 mg 4-6 hourly if initial response to B agonist is poor :
o 500 mcg via nebulizer every 20 minutes for three doses then as needed.
o Obtain IV access.
o Start steroids
 Hydrocortisone 200 mg IV, continue with either hydrocortisone 100 mg QID IV or
predinsolone 30-50mg Po daily. (IV steroid treatment is not more effective than oral
treatment)
 If no improvement:
o Add magnesium sulfate 2 gm administered over 20 minutes or
o Aminophylline
o Loading dose- 5mg/kg or 250 mg over 20 minutes (dilute with IV fluid to a
concentration of 1mg/ml) followed by continuous infusion
o Do not give loading dose in patients taking oral theopylline
FIG 1: salbutamol puff, how to inhale.

o Maintenance dose- 0.5mg/kg/hr. Q 12 hr. (increase dose in smokers & decrease in

elderly, corpulmonale, CHF& liver failure)
o Adrenaline -0.3-0.5 mg (1:1000 solution) Q 20 min for 3 doses subcutaneously
o Antibiotics – only given if there is evidence of chest infection (fever, purulent
sputum, abnormal CXR, raised WBC count).
o Adequate hydration –essential and may help prevent mucus plugging.

Management of moderate attack.

 Salbutamol 4-8 puffs every 20 minutes for the first hour .

 Oral predinsolone =40-60mg Po per day for 5-10 days (no tapering) .
 The patient is then reassessed,Complete response –disappearance of clinical
signs (and PEF> 80%)
 The patient is kept for one more hour. If stable, the patient can be discharged to
continue treatment at home

No response/incomplete response – No or incomplete disappearance of clinical signs (or

PEF<80%). After the first or second hour, the patient should be treated as for a severe attack
and be kept in the emergency room for at least 6 hours to continue treatment.

Management of mild attack

 Salbutamol 2-4 puffs every 20 minutes for the first hour

 The patient is then reassessed ;Complete response – disappearance of clinical signs
(and PEF> 80%)
  Patient is kept for one more hour. If stable, the patient is discharged to continue
treatment at home.
 No response/incomplete response – no or incomplete disappearance of clinical signs
(or PEF<80%)
 After the first or second hour, the patient should be treated as for moderate attack.

Assessment of response

Clinical improvement
 Patient is less distressed
 Decreased respiratory rate and heart rate
 Able to talk in sentences
Louder breath sounds on auscultation (may be more wheeze) Pulse oximeter- aim O2
saturation of 94-98%Monitor heart rate and Oxygen saturation continuously and measure BP
frequently

CHAPTER NINE: COMMON ENDOCRINE

EMERGENCIES
Duration: 1 hr
Learning objectives
By the end of this session, participants will be able to:
 Define diabetic ketoacidosis/DKA and Hypoglycemia
 Describe clinical features of DKA and Hypoglycemia
 Able to diagnose DKA and Hypoglycemia
 Manage DKA, Hypoglycemiaaccording to the standard protocol

8.1. Diabetic ketoacidosis (DKA)

DKA is a metabolic disorder characterized by the triad of hyperglycemia, anion gap
metabolic acidosis (increased anion gap), and ketonemia.

Precipitating factors
  The most common precipitating factors are infection and discontinuation of insulin
treatment. Other less common factors include:
o Acute major illnesses such as MI, CVA, or pancreatitis.

o New onset type 1 diabetes

o Drugs (glucocorticoids, higher dose thiazide diuretics, sympathomimetic

agents (e.g., dobutamine and terbutaline).

o Cocaine use

o Factors that may lead to insulin omission in younger patients include fear
of weight gain, fear of hypoglycemia, rebellion from authority, and the
stress of chronic disease.

o Poor compliance with the insulin regimen.

Clinical presentation

 The clinical manifestations of DKA are directly related to the three primary metabolic
derangements- hyperglycemia, volume depletion and acidosis.
 DKA usually evolves rapidly, over a 24-hour period.

Symptoms

 Nausea/vomiting ,poly symptoms(polydypsia, Polyphagia, Polyuria), Abdominal

pain, Shortness of breath

Physical Findings

 Tachycardia
 Dehydration/hypotension
 Tachypnea / Kussmaul respirations/respiratory distress
 Abdominal tenderness (may resemble acute pancreatitis or surgical abdomen)
 Lethargy/obtundation/cerebral edema/possibly coma

Lab. Abnormalities

 Serum Glucose:
o The serum glucose will be elevated(>200mg/dl)
  Serum bicarbonate
o is frequently <10 mmol/L
 Arterial PH
o ranges between 6.8 and 7.3- depending on the severity of the acidosis.
 Serum electrolyte-
o Total-body stores of sodium, chloride, phosphorus, and magnesium are
reduced in DKA but are not accurately reflected by their levels in the serum
because of dehydration and hyperglycemia.
o Renal function test- Elevated blood urea nitrogen (BUN) and serum creatinine
levels reflect intravascular volume depletion.

Treatment

 Stabilize ABC of life

 Fluid management
 Insulin
 K+ repletion
 Treatment of precipitating factors
 Monitoring
 Long term management
General measures
 Stabilize the ABC of life
 Obtain IV access
 Monitor RBS every hour ,urine ketone every 2-4 hrs
 Identify and treat Precipitating cause of DKA

Repletion of fluid deficit

 The usual fluid deficit is about 3-6 liters
 Give as much NS/RL rapidly for a patient in shock

 Fluid helps restore intravascular volume and normal tonicity, perfuse vital organs,

 Improve glomerular filtration rate

 Lower serum glucose and ketone levels

 Rehydration improves the response to low-dose insulin therapy. In general;

• The first 2 L over 0 - 2 hours

• The next 2 L over 2 - 6 hours

• And then 2 L more over 6 -12 hours.

• Change the fluid to DNS when blood sugar falls to below 200

• Replace ongoing fluid loss

Repletion of K+ deficit
 If baseline K+ is <3.3meq/L ,avoid insulin and administer 20 to 30 mEq/hour K+ IV
until [K+] is above 3.3 mEq/L.
 If base line K+ is 3.3-5.3meq/L or is unknown, administer 40meq/L to run over 4-8
hrs after confirming adequate urine output (≥50ml/hr)
 If baseline k+ is above 5.3meq/L, don’t administer k+
 The target is to keep it between 4-5meq/L
Insulin administration
 If perfuser and trained staff for monitoring of the rate of infusion is available:
 Administer short-acting insulin: IV (0.1 units/kg), then 0.1 units/kg per hour by
continuous IV infusion
 Increase two- to three fold if no response by 2–4 h.
 If the initial serum potassium is <3.3 mmol/L (3.3 meq/L), do not administer insulin
until the potassium is corrected.

 Give initial bolus of 10IU IV and 10 IU IM of regular insulin (if there is no Perfuser)
 Then give 5 IU IV every one hour until blood sugar falls below 200 and urine ketone
is twice negative
 If RBS doesn’t drop by at least 50mg/dl or is persistently above 350-400,double the
dose of insulin i.e. give 10 IU IV
o Overlap the last dose of regular insulin with the standing dose of long acting
insulin

o In Patients with known diabetes who were previously treated with insulin may
be given insulin at the dose they were receiving before the onset of DKA

o In insulin-naive patients, insulin regimen should be started at a dose of 0.5 to

0.8 U/kg per day

o Measure RBS every 4-6hrs and give correctional dose of regular insulin(1-2IU
for every 50mg/dl rise above 200mg/dl
Tab.1 :DKA follow up sheet

Disposition

 Most patients with DKA require hospital admission, often to the intensive care unit.
 Patients who have mild DKA may be discharged from ED
1. The underlying causes do not require inpatient therapy
2. Close follow-up is pursued.

8.2. Emergency management of hypoglycemia

Introduction:

 Hypoglycemia is a clinical syndrome with diverse causes in which low serum (or
plasma) glucose concentrations lead to symptoms and signs.
 In patients with diabetes, hypoglycemia symptoms and signs occur as a consequence
of therapy.

Causes of Hypoglycemia

 Drugs (Insulin or insulin secretagogue, Alcohol, quinine )

 Critical illness (Hepatic, renal or cardiac failure, Sepsis,severe malaria, Inanition)
  Hormone deficiency (Cortisol, Glucagon and epinephrine (in insulin-deficient
diabetes))
 Non–islet cell tumor
 Endogenous hyperinsulinism (Insulinoma), Functional beta-cell disorders
(nesidioblastosis), Non-insulinomapancreatogenoushypoglycemia,Post–gastric bypass
hypoglycemia, Insulin autoimmune hypoglycemia, Antibody to insulin,Antibody to
insulin receptors
 Accidental, surreptitious or malicious hypoglycemia
Clinical manifestations

Symptoms:
 Hypoglycemia causes neurogenic (autonomic) and neuroglycopenic symptoms.
 Neuroglycopenic symptoms are those caused by CNS glucose deprivation and include
behavioral changes, confusion, fatigue, seizure, loss of consciousness, and, if
hypoglycemia is severe and prolonged, death.
 The neurogenic symptoms include tremor, palpitations, and anxiety/arousal
(catecholamine-mediated, adrenergic) and sweating, hunger, and paresthesias
(acetylcholine-mediated, cholinergic). They are the results of the perception of
physiologic changes caused by the CNS-mediated sympathoadrenal discharge
triggered by hypoglycemia.
 Diaphoresis and pallor are the commonest signs of hypoglycemia. Tachycardia and
systolic blood pressure elevations also occur.
 Occasionally, transient focal neurologic deficits may be seen. Permanent neurologic
deficit may occur in patients with diabetes mellitus or prolonged hypoglycemia.
Diagnosis

 It should be considered in any patient with episodes of confusion, an altered level of

consciousness, or a seizure.
Whipple’s triad
 symptoms consistent with hypoglycemia,
 a low plasma glucose concentration measured with a precise method (not a glucose
monitor), and
 relief of those symptoms after the plasma glucose level is raised.
 The lower limit of the normal fasting plasma glucose value is typically 70 mg/dL
(3.9 mmol/L).
  Glucose levels <55 mg/dL (3.0 mmol/L) with symptoms that are relieved promptly
after the glucose level is raised document hypoglycemia. 124
Treatment

 Oral treatment with glucose tablets or glucose-containing fluids, candy, or food is

appropriate if the patient is able and willing to take these. A reasonable initial dose is
20 g of glucose.
 If the patient is unable or unwilling, because of neuroglycopenia, to take
carbohydrates orally, Initial management is administration of 1g/kg dextrose as 50%
dextrose in water followed by the infusion of 10% dextrose at a rate to maintain the
serum glucose above 100mg/dl.
 Repeat bedside glucose determination should be done Q 30 minutes for the first 2 hrs
to detect rebound hypoglycemia.
 If intravenous therapy is not practical and glucagon is available, subcutaneous or
intramuscular glucagon (1.0 mg in adults) can be used, particularly in patients with
Type 1 Diabetes. Because it acts by stimulating glycogenolysis, glucagon is
ineffective in glycogen-depleted individuals (e.g., those with alcohol-induced
hypoglycemia)
Disposition

 Type 1 diabetic patients with brief episodes of hypoglycemia uncomplicated by other

disease may be discharged from the ED if a cause of the hypoglycemia can be
identified and corrected by instruction or medication.
 All patients should be given a meal before discharge to ensure their ability to tolerate
oral feedings and to begin to replenish glycogen stores in glycogen-deficient patients.
 Patients who are discharged should receive short-term follow-up for ongoing
evaluation. Patients with hypoglycemia caused by oral agents should be observed in
the hospital because of the high likelihood of recurrent hypoglycemia.
Summary

 DKA is a metabolic disorder characterized by the triad of hyperglycemia, anion gap

metabolic acidosis (increased anion gap), and ketonemia.
 The most common precipitating factors for DKA are infection and discontinuation of
insulin treatment
 The main principles of DKA management are fluid replacement, correction of
electrolyte abnormalities, Insulin administration and treating the precipitating factors
  Close monitoring hemodynamic condition, RBS, monitoring the response for
treatment is very important for DKA patients
 Hypoglycemia is a clinical syndrome with diverse causes in which low serum (or
plasma) glucose concentrations lead to symptoms and signs; It should be considered
in any patient with episodes of confusion, an altered level of consciousness, or a
seizure.
 PO glucose or glucose containing food is reasonable in conscious patient and IV 40%
or 50 % glucose or IM glucagon administration is prudent is un conscious patient
depending on the underlying cause and patient condition
Self-assessment questions:

1. Define DKA
2. Mention common precipitation factors of DKA
3. Explain management principles of DKA
4. Describe Whipple’s triad for the Diagnosis of hypoglycemia
5. Outline the management of hypoglycemia
References:

 Tintinallis Emergency Medicine 8th edition

 Rosen’s Emergency Medicine 8 the edition
 National Integrated Emergency Manual 1st edition
 CHAPTER-TEN: APPROCH TO A POISONED PATIENT

Time:

Objectives
After completing this session participant will be able to
 Understand the burden of poisoning
 Learn portals of entry and settings of poisoning
 Recognize the sign and symptom of common poisoning
 Learn decontamination techniques
 Learn the common antidotes

General approach to the poisoned patients

Poisoning is a worldwide problem but the burden of serious poisoning is carried by the
developing world. Poisoned patients are usually directly brought to the emergency
department. The route of exposure is commonly by ingestion, other routes include inhalation,
insufflations, cutaneous and mucous membrane as well as injection.

After any exposure presenting to the ER, the first step is to determine the risk analysis. Some
exposures have minimal risk and the criteria used to determine whether the exposure is non
toxic are:

a. An unintentional exposure to a clearly identified substance

b. An estimate of the dose is known
c. A recognized information source (e.g a poison control center) confirms the
substance as nontoxic in the reported dose.

Asymptomatic patients with nontoxic exposure may be discharged after a short period of
observation, with advice of any danger signs and provided that they have access to a nearby
health center and further consultation.

The most commonly implicated poisoning exposures were due to analgesics (Especially in
the developed nations), pesticides, cleaning substances, cosmetics, sedative – hypnotics and
antipsychotics, cough & cold preparations.
Fatalities most commonly result from carbon monoxide poisoning, ingestion of analgesics,
sedative – hypnotics and organophosphate compounds.

We will see the general approach to poisoned patient subsequently,

General approach
 We should have a consistent and systematic approach to evaluation and management
of poisoned patients. Diagnosis and resuscitation proceed simultaneously.

 Attempts to identify the poison should never delay life-saving supportive care.

 First patient has to be stabilized, then we needs to consider how to minimize the
bioavailability of toxin not yet absorbed,

 which antidotes (if any) to administer, and if other measures to enhance elimination
are necessary

 The first priorities are always the ABCs ( Airway, Breathing & Circulation)

 Once the airway and respiratory status are secured abnormalities of blood pressure,
pulse, temperature, oxygen saturation and hypoglycemia must be corrected. Vital
Signs, mental status and pupillary size should be briefly assessed.

 Four possible etiologies of altered mentation in such patients can be corrected easily,
Hypoxia, Opioid intoxication, hypoglycemia, and Wernick`s
encephalopathy. Supplemental oxygen, Naloxone ( for symptoms of opioid toxicity),
50 ml of D50W and 100 mg of thiamine known as the `coma cocktail` should be
administered.

 Identify the substance ideally through obtaining the original toxic substance
container; ask detail history about the type of exposure and amount of substance and
route of exposure. ( getting accurate history may be difficult)

 Plasma concentration, when available is essential for paracetamol, salicylates,

carboxyhemoglobin for carbon monoxide poisoning, lithium, Digoxin and the likes.

 Useful investigations in most poisonings other than routine CBC and U/A, include
serum electrolyte, blood glucose, arterial blood gas, liver and kidney function tests,
INRs, urinalysis and an ECG.
Decontamination
 We should start decontaminating poisoned patients as soon as possible to decrease
exposure with the substance to themselves as well as health care providers. We
should start from external and move to internal decontamination.
 Remove all contaminated cloths from the patient and dispose it.

 Wash skin and hair with soap and water while wearing gloves

 Eye exposure: irrigate with copious amounts of water or saline for 30-40 minutes.

Gastric lavage
 Indicated for ingestion of large amounts of tablets and capsules with a high inherent
toxicity within 2hrs
Method:
 insert a large bore orogastric tube, 32-40 F in adults & 24-28F in children. ( these are
very large tubes and should be inserted orally).

 Place patient in left lateral decubitus position

 Aspirate fluid from stomach prior to fluid lavage

 Install water or saline 200 – 300 ml in to stomach for adults, 10ml/kg in children.

 Aspirate fluid back, repeat lavage until aspirate clear of debris or pill fragments.

Contraindications:
 Patients with decreased Level of Consciousness/LOC/, unprotected airway,
ingestions of corrosive agents, hydrocarbons, and patients at risk of gastrointestinal
hemorrhage.

Activated Charcoal;
 Minimizes systemic absorption from the Gastro Intestinal Track
 Consider use if within 1hr of ingestion of the poisonous substance

 Given orally or via NG tube, 1-1.5g/kg as slurry in 400-800 ml of water.

Pediatric dose:
 Less than 6 years, 10g in 50-100 ml water, older children, 20-50g in 200- 300ml
water.
 Always shake vigorously to ensure adequate dispersion of charcoal

 Has no value in strong acids, alkali, corrosives, heavy metals, lithium,

organophosphate, paraffin, methanol and ethylene glycol ingestion.

Contraindication:

 decreased LOC or unprotected airway.

Multidose activated charcoal

 Charcoal is usually given as a single dose as mentioned above. But there are
circumstances when we use the multiple dosing.

 Multiple doses can enhance elimination of drugs already absorbed into the
body by interrupting enterohepatic circulation of drugs excreted into the bile.

 After first dose of activated charcoal, follow up dose of 25g every 2 hours, or
50g every 4hrs until clinical condition improves.

 E.g. ingestion of life threatening amounts of carbamazepine, dapsone, quinine,

phenobarbitone, Digoxin & sustained release formulations.

Whole bowel irrigation

 Uses a laxative agent such as polyethylene glycol to fully flush the bowel of
stool and unabsorbed xenobiotics.
 Contraindicated in ileus, bowel obstruction or perforation, and in patients with
hemodynamic instability.
 May be considered for substantial ingestions of iron, sustained release
products, enteric coated products and lead poisoning.
 Urinary alkalinzation

 Infusion of sodium bicarbonate to raise urinary pH to enhance clearance of

toxins excreted by kidneys
 1-2 mEq/kg NaHCO3 IV push
 3 ampules of NaHCO3 in 850 cc of D5W at 1.5X maintenance fluid rate
 Target urinary pH 7.5-8.5
 Monitor electrolytes
 Useful for weak bases like amphetamines, chlorophenoxy herbicides (2,4, D),
phenobarbitone and Salicylates.

Contraindications

 Preexisting fluid overload

 Renal impairment
 Uncorrected hypokalemia

Expected complications include: hypokalemia, fluid overload, alkalemia and mild

hypocalcemia.

Extracorporal Removal:
 Techniques, including hemodialysis, hemoperfusion, and continuous renal
replacement therapies, have limited indications in poisoned patients.
 These procedures require a critical care setting, are expensive and invasive, are not
always available, and have numerous complications.

Hemodialysis

 Toxin requirements include, Low volume of distribution, low protein binding,

low endogenous clearance and low molecular weight
 Less effective when toxin has large volume of distribution (>1 L/kg), has
large molecular weight, or highly protein bound.
 Life threatening ingestions of Acetone, Barbiturates, Bromide, Ethanol,
Ethylene glycol, Salicylates, Lithium are some of the indications.
 Contraindications: hemodynamic instability, poor vascular access, significant
coagulopathy and infants (generally)

Antidotes

 Although most poisonings are managed primarily with appropriate supportive care,
there are several specific antidote agents that may be employed

Table 11: commonly used poisoning antidotes.

Agent Antidote

Paracetamol N-acetylcysteine

Cardiac glycosides Digoxin immune Fab

Cyanide Hydroxycobalamin

Iron Desfroxamine

Lead Succimer, Dimercaprol, Ca.EDTA

Methemoglobinemia Methylene blue

Opioids Naloxone

Sulfonyl ureas Glucose/Octeoride

Benzodiazepines Flumazenil

Beta blockers Glucagon

Ethylene glycol, Methanol Fomepizole

Isoniazid Pyridoxine

Monomethylhydrazine mushrooms Pyridoxine

Organophosphates Atropine/Pralidoxime
 CHAPTER ELEVEN:
ASSESSMENT AND MANAGEMENT OF TRAUMA

11.1 Approach to trauma patient

Learning Objectives

Learn the basics of Primary survey

Identify life threatening condition in trauma

Manage life threatening emergencies in trauma

Introduction

The ATLS method is still considered the foundation of critical care, with initial assessment
running from ‘A’ to ‘B’ to ‘C’ and so forth, with ongoing re-assessment (returning to ‘A’)
after any interventions/treatments or any changes in the patient’s condition.

Airway maintenance with restriction of cervical spine motion (A)

While assessing and securing the airway, all patients should have immobilization of their
cervical spine until a complete clinical or radiological evaluation has excluded injury to
prevent secondary injury to the spinal cord or worsening of an injury already present. This
can be achieved by neck collar or sand bags if collar is not available or manually restricts
motion of the cervical spine.

The simplest initial assessment of the airway in a conscious patient is to ask them their name
and what happened. An appropriate response suggests that there is no major airway
compromise (ability to speak clearly), breathing is not severely compromised (ability to
generate air movement to permit speech); however, repeated assessment of airway patency is
prudent.
If the patient cannot talk normally do the following assessments:

- Look to see if the chest wall is moving and listen to see if there is air movement from
the mouth or nose.
- Listen for abnormal sounds (such as stridor, grunting, or snoring) or a hoarse or raspy
voice that indicates a partially obstructed airway.
- Look and listen for fluid (such as blood, vomit) in the airway.
- Look for foreign body or abnormal swelling around the airway, and altered mental
status.
- Check if the patient is able to swallow saliva or is drooling
If the patient is unconscious and not breathing normally do the following immediate
managements:

- NO TRAUMA: open the airway using the head-tilt and chin-lift maneuver. This
maneuver can correct airway obstruction due to tongue drop.
- CONCERN FOR TRAUMA: maintain cervical spine immobilization and open the
airway using the jaw thrust maneuver (don’t use chin lift maneuver)
- Place an oropharyngeal or nasopharyngeal airway to maintain the airway in patients
with a decreased level of consciousness to maintain the air way and prevent tongue
drop.
 Figure - Chin lift (A) and Jaw trust and maneuvers (B)
If a foreign body is suspected:

- If the object is visible, remove it with finger or spongy/Majil forceps

- If the patient is able to cough or make noises, keep the patient calm and encourage
coughing.
- If the patient is choking (unable to cough, not making sounds) use age-appropriate
chest thrusts/abdominal thrusts/back blows.
- If the patient becomes unconscious while choking, follow relevant CPR protocols.
If secretions or vomit are present, suction the airway.

In a Patients with severe head injuries who have an altered level of consciousness or a
Glasgow Coma Scale (GCS) score of 8 or lower and patients who are unable to maintain a
patent airway or provide adequate oxygenation usually require the placement of a definitive
airway (i.e., cuffed, secured tube in the trachea – Endotracheal tube).

This is other indications for definitive air away: Severe maxillofacial fractures, Risk for
aspiration from bleeding and/or vomiting, Inadequate respiratory efforts, Neck hematoma,
Laryngeal or tracheal injury, Inhalation injury from burns and facial burns.

If intubation is unsuccessful or contraindicated, in patients with upper air way obstruction a

surgical airway is required. The options are crichothyroidectomy (needle cricothyroidotomy
in children less than 12 years) and tracheostomy depending on the available expertise and
resources.

Breathing and ventilation (B)

Look chest movement, listen to the breath sounds, and feel the air flow to see if the patient is
breathing. Then assess if breathing is very fast, very slow, or very shallow. Look for signs of
increased work of breathing (such as accessory muscle use, chest indrawing/retractions, nasal
flaring) or abnormal chest wall movement. Listen for abnormal/decreased breath sounds.
Check for dull sounds with percussion on one side (large pleural effusion or hemothorax). If
there are no breath sounds on one side, and hypotension, check for distended neck veins or a
shifted trachea (tension pneumothorax). Check oxygen saturation with a pulse oximeter when
available.

If the patient is unconscious with abnormal breathing, start bag-valve-mask ventilation and
follow relevant CPR protocols.

If the patient is not breathing adequately (too slow for age or too shallow), begin bag-valve-
mask ventilation with oxygen. If oxygen is not immediately available, DO NOT DELAY
ventilation. Start bag-valve-mask ventilation while oxygen is being prepared.

If breathing fast or hypoxic, give oxygen.

If concern for tension pneumothorax, perform needle decompression at the 2nd intercostal
space at the MCL line immediately and give IV fluids and oxygen. Then perform chest tube
insertion as fast as possible.

Sucking chest wounds are important to recognize because they can rapidly cause a tension
pneumothorax. So if a patient has penetrating chest wounds give oxygen, place a three-sided
dressing that allows air to leave with exhalation but prevents air from entering when the
person inhales and insert chest tube as fast as possible. There is a danger of the dressing
becoming stuck to the chest wall with clotted blood and causing a tension pneumothorax, so
after applying a three-sided dressing the patient should be observed continuously.
Figure – Three way valve dressing for sucking chest wound

If concern for hemothorax (decreased breath sounds, dull sounds with percussion), give
oxygen and plan for chest tube insertion.

Part of chest wall moving in the opposite direction of the rest of the chest when breathing
indicates flail chest segments (three or more contiguous ribs are fractured in at least two
locations). Without connection to the chest wall, the flail segment will move abnormally with
breathing and prevent part of the lung from expanding. Flail chest is also usually associated
with damage to underlying lung tissue (pulmonary contusion). Oxygen and pain control are
crucial for this patients. Since there is a very high risk of developing difficulty in breathing
and hypoxia, plan for rapid handover/transfer to a provider capable of chest tube placement,
advanced airway placement and ventilation.

Injuries that reduce ventilation and require prompt identification and intervention are tension
pneumothorax, open pneumothorax, massive hemothorax and tracheal/bronchial injuries.
These injuries should be identified during the primary survey and often require immediate
attention to ensure effective ventilation.

Every injured patient should receive supplemental oxygen. If the patient is not intubated,
oxygen should be delivered by a mask-reservoir device to achieve optimal oxygenation. Use
a pulse oximeter to monitor adequacy of hemoglobin oxygen saturation. Simple
pneumothorax, simple hemothorax, fractured ribs, flail chest, and pulmonary contusion can
compromise ventilation to a lesser degree and are usually identified during the secondary
survey.
Circulation with Hemorrhage Control

Hemorrhage is the predominant cause of preventable deaths after injury. Identifying, quickly
controlling hemorrhage, and initiating resuscitation are therefore crucial steps in assessing
and managing such patients. Once tension pneumothorax has been excluded as a cause of
shock, consider that hypotension following injury is due to blood loss until proven otherwise.
Rapid and accurate assessment of an injured patient’s hemodynamic status is essential.

Look and feel for signs of poor perfusion (cool, moist extremities, delayed capillary refill
greater than 3 seconds, low blood pressure < 90/60mmHg, tachypnea, tachycardia,
absent/feeble pulses).

Look for both external AND internal bleeding, including bleeding into chest, abdomen,
pelvic or femur fracture, wounds.

Look for hypotension, distended neck veins and muffled heart sounds that might indicate
pericardial tamponade.

For cardiopulmonary arrest, follow relevant CPR protocols (see BLS portion of the module).

If there are signs of poor perfusion, give IV fluids and oxygen (see below)

Identify the source of bleeding as external or internal. External hemorrhage is identified and
controlled during the primary survey. Rapid, external blood loss is managed by direct manual
pressure on the wound. Tourniquets are effective in massive exsanguination from an
extremity but carry a risk of ischemic injury to that extremity. Use a tourniquet only when
direct pressure is not effective and the patient’s life is threatened. Blind clamping can result
in damage to nerves and veins. Other means of control is to elevate the limb,
ligation/clamping of the bleeding vessel and proximal compression of the feeding artery.
Figure - Ways of controlling bleeding. A) Direct manual pressure on the wound. B)
Tourniquet

The major areas of internal hemorrhage are the chest, abdomen, retroperitoneum, pelvis, and
long bones. The source of this bleedings are usually identified by physical examination and
imaging (e.g., chest x-ray, pelvic x-ray, focused assessment with sonography for trauma
[FAST], or diagnostic peritoneal lavage [DPL]). Immediate management may include chest
decompression, and application of a pelvic stabilizing device and/or extremity splints.
Definitive management may require surgical or interventional radiologic treatment and pelvic
and long-bone stabilization. Initiate surgical consultation or transfer for procedures early in
these patients.

Definitive bleeding control is essential, along with appropriate replacement of intravascular

volume. Vascular access must be established; typically two large-bore peripheral venous
catheters are placed to administer fluid (isotonic crystalloids – Normal saline or Ringers
lactate), blood, and plasma. Blood samples for baseline hematologic studies are obtained,
including a pregnancy test for all females of childbearing age and blood type and cross
matching. To assess the presence and degree of shock, blood gases and/or lactate level are
obtained if available. When peripheral sites cannot be accessed, intraosseous infusion (for
children less than 6 years), central venous access, or venous cut down may be used
depending on the patient’s injuries and the clinician’s skill level.

Aggressive and continued volume resuscitation is not a substitute for definitive control of
hemorrhage. Shock associated with injury is most often hypovolemic in origin. In such cases,
initiate IV fluid therapy with crystalloids. All IV solutions should be warmed either by
storage in a warm environment (i.e., 37°C to 40°C. A bolus of 1 L of an isotonic solution
may be required to achieve an appropriate response in an adult patient. If a patient is
unresponsive to initial crystalloid therapy, he or she should receive a blood transfusion.
Fluids are administered judiciously, as aggressive resuscitation before control of bleeding has
been demonstrated to increase mortality and morbidity.

The same signs and symptoms of inadequate perfusion that are used to diagnose shock help
determine the patient’s response to therapy. The return of normal blood pressure, pulse
pressure, pulse rate and urine output (>0.5ml/kg/hr in adults />1ml/kg/hr in children) are
signs that perfusion is returning to normal. After resuscitation there are three forms of
response. Responders (responds for our resuscitation), Transient responders (respond to the
initial fluid bolus, but they begin to show deterioration of perfusion) and non-responders
(Failure to respond to crystalloid and blood administration). Transnet responders and non-
responders have ongoing loss and that should be secured as fast as possible.

Severely injured trauma patients are at risk for coagulopathy, which can be further fueled by
resuscitative measures. This condition potentially establishes a cycle of ongoing bleeding and
further resuscitation, which can be mitigated by use of massive transfusion protocols with
blood components administered at predefined low ratios.

Disability (Neurologic Evaluation)

A rapid neurologic evaluation establishes the patient’s level of consciousness and pupillary
size and reaction; identifies the presence of lateralizing signs; and determines spinal cord
injury level, if present.

The GCS is a quick, simple, and objective method of determining the level of consciousness.
The motor score of the GCS correlates with outcome. A decrease in a patient’s level of
consciousness may indicate decreased cerebral oxygenation and/or perfusion, or it may be
caused by direct cerebral injury. An altered level of consciousness indicates the need to
immediately reevaluate the patient’s oxygenation, ventilation, and perfusion status.
Hypoglycemia, alcohol, narcotics, and other drugs can also alter a patient’s level of
consciousness. Until proven otherwise, always presume that changes in level of
consciousness are a result of central nervous system injury. Remember that drug or alcohol
intoxication can accompany traumatic brain injury.

Primary brain injury results from the structural effect of the injury to the brain. Prevention of
secondary brain injury by maintaining adequate oxygenation and perfusion are the main
goals of initial management.

Because evidence of brain injury can be absent or minimal at the time of initial evaluation, it
is crucial to repeat the examination. When resources to care for these patients are not
available arrangements for transfer should begin as soon as this condition is recognized.

Exposure and Environmental Control

During the primary survey, completely undress the patient, usually by cutting off his or her
garments to facilitate a thorough examination and assessment including hidden areas (back,
perineum), log roll maneuver to examine the back. After completing the assessment, cover
the patient with warm blankets or an external warming device to prevent him or her from
developing hypothermia in the trauma receiving area. Warm intravenous fluids before
infusing them, and maintain a warm environment.

Hypothermia can be present when the patient arrives, or it may develop quickly in the ED if
the patient is uncovered and undergoes rapid administration of room-temperature fluids or
refrigerated blood. Because hypothermia is a potentially lethal complication in injured
patients, take aggressive measures to prevent the loss of body heat and restore body
temperature to normal.

Adjuncts of the primary survey

Adjuncts used during the primary survey include continuous electrocardiography, pulse
oximetry, carbon dioxide (CO2) monitoring, and assessment of ventilatory rate, and arterial
blood gas (ABG) measurement. In addition, urinary catheters can be placed to monitor urine
output and assess for hematuria. Gastric catheters decompress distention and assess for
evidence of blood. Other helpful tests include blood lactate, x-ray examinations (e.g., chest,
Cervical and pelvis), FAST, extended focused assessment with sonography for trauma
(eFAST), and DPL.

Physiologic parameters such as pulse rate, blood pressure, pulse pressure, ventilatory rate,
ABG levels, body temperature, and urinary output are assessable measures that reflect the
adequacy of resuscitation. Values for these parameters should be obtained as soon as is
practical during or after completing the primary survey, and reevaluated periodically.

Secondary Survey

The secondary survey does not begin until the primary survey (ABCDEs) is completed,
resuscitative efforts are underway, and the normalization of vital functions has been
demonstrated.
The secondary survey is a head-to-toe evaluation of the trauma patient, that is, a complete
historyand physical examination, including reassessment of all vital signs. Each region of the
body is completely examined. The potential for missing an injury or failure to appreciate the
significance of an injury is great, especially in an unresponsive or unstable patient.

Every complete medical assessment includes a history of the mechanism of injury. Often,
such a history cannot be obtained from a patient who has sustained trauma; therefore,
prehospital personnel and family must be consulted to obtain information that can enhance
the understanding of the patient’s physiologic state.
 The AMPLE history is a useful mnemonic for this purpose:
 Allergies
 Medications currently used
 Past illnesses/Pregnancy
 Last meal
 Events/Environment related to the injury

Definitive Care
Ultimate disposition is dictated by a number of factors, including the patient’s condition, the
nature of the injury, and the availability of surgeons, subspecialists, and anesthesiologists.
Possible dispositions include transfer to the operating room, admission to the surgical
service, limited observation in the emergency department, or transfer to another hospital. The
level of care and monitoring established in the emergency department should be maintained
throughout patients transfer.

Definitive Care

11.2 Chest trauma

Time: 1 hour

Learning Objective
At the end of this course participants will be able to:

 Identify common life threatening chest injuries

 Manage life threatening chest injuries

Introduction

Chest injuries account for up to one fourth of all injury deaths. Initial resuscitation and
airway management should be performed according to established principles of Advanced
Trauma life support.
Life-threatening pulmonary injuries

Specific life-threatening pulmonary injuries should be suspected, diagnosed, and treated

during the primary survey. These include tension pneumothorax, massive hemothorax, open
pneumothorax, and flail chest.

Tension Pneumothorax

The diagnosis of tension pneumothorax should be made clinically. The classic presentation
includes distended neck veins, hypotension or evidence of hypoperfusion, diminished or
absent breath sounds on the affected side, and tracheal deviation to the contralateral side.
However, one or more of these elements may be absent. Tracheal deviation and distention of
the neck veins are late signs, and veins may remain flat in the presence of hypovolemia.

If a tension pneumothorax is suspected, immediate needle decompression is indicated.

The most common approach is to introduce a 14-gauge IV needle and catheter into the
pleural space through the chest wall in the midclavicular line just above the rib at the second
intercostal space. A midclavicular approach is very important because the internal mammary
vessels are located approximately 3 cm away from the sternal border.4 A rush of air exiting
the pleural space may be audible and is diagnostic of a pneumothorax. This procedure
converts the tension pneumothorax into an open pneumothorax. Once the tension
pneumothorax is decompressed the patient's perfusion often improves immediately. A needle
decompression is a temporary measure only and should be followed promptly by the
insertion of a large-bore chest tube (tube thoracostomy) on the side of the tension
pneumothorax.

An important consideration when performing either a needle decompression or a tube

thoracostomy is that although the mean chest wall thickness is 3.5 cm, up to 20% of patients
may have chest wall thicknesses that exceed 4.5 cm.5 Therefore, longer needles and careful
consideration of equipment may be necessary for effective needle decompression and tube
thoracostomy for tension pneumothorax in obese patients.

If the patient fails to improve following decompression, other causes of hypoperfusion

should be immediately considered. For example, persistent neck vein distention may indicate
the presence of pericardial tamponade.
Fig.1:Massive Hemo -thorax

Common causes of massive hemothorax include injury to the lung parenchyma, intercostal
artery, or internal mammary artery. Each hemithorax can potentially hold approximately 40%
of a patient's circulating blood volume. A massive hemothorax is defined in the adult as at
least 1500 mL, or approximately two thirds of the available space in the hemithorax. Massive
hemothorax is life threatening by three mechanisms. First, acute hypovolemia does not allow
for sufficient preload to sustain left ventricular function and adequate cardiac output. Second,
the collapsed lung promotes hypoxia by creating alveolar hypoventilation, ventilation–
perfusion mismatch, and anatomic shunting. Third, the hydrostatic pressure of the
hemothorax compresses the vena cava and the pulmonary parenchyma, further impairing
preload and raising pulmonary vascular resistance, respectively. Although the clinical signs
and symptoms of hemothorax in the chest trauma patient can vary, findings that should
prompt the clinician to suspect hemothorax include: decreased or absent breath sounds on the
affected hemithorax; no chest movement with respiratory effort; and dullness with percussion
on the affected side.
The diagnosis of massive hemothorax can be made by plain chest radiography when a
hemithorax is completely opacified. As an alternative to chest radiography in the unstable
patient, bedside ultrasonography performed by a skilled operator may reveal a layer of fluid
between the chest wall and lung.

Tube thoracostomy is both diagnostic and therapeutic in the patient with massive
hemothorax. Evacuation of >1500 mL of blood immediately after tube thoracostomy or
200 mL of blood per hour for 4 hours are generally recognized definitions of massive
hemothorax and are indications for operative management. Even in patients not meeting
these criteria, evidence of ongoing hemorrhage or rebleeding may warrant consideration of
an operative intervention.

Because massive hemothorax is, by definition, associated with accumulation and subsequent
drainage of large volumes of potentially uncontaminated blood, it is desirable to collect the
chest tube output into a device compatible with later autotransfusion.

Open Pneumothorax

Open pneumothorax is a communication between the pleural space and surrounding

atmospheric pressure. This may be apparent on inspection of the chest,if there is an obvious
violation of the outer chest wall and communication with the pleural space (sometimes
referred to as "sucking chest wound") or may be due to small rents in the parietal pleura or
small air passages without penetrating injury. Respiratory distress is due to lung collapse and
subsequent inability to ventilate the affected lung. Air entry and breath sounds are often
diminished on the affected side, and chest wall motion can be impaired. The injury may also
be associated with a hemothorax. In the case of a sucking chest wound, the initial
therapeutic maneuver is to cover the wound with a three-sided dressing so that air can
escape but not enter through the wound. Care should be taken to avoid complete
occlusion, which may convert the injury into a tension pneumothorax.

Flail Chest
Fig 2.Flail chest.

Segmental fractures (in two or more locations on the same rib) of three or more adjacent ribs
anteriorly or laterally often result in an unstable chest wall physiology known as flail chest.
This injury is characterized by a paradoxical inward movement of the involved portion of the
chest wall during spontaneous inspiration and outward movement during expiration.
Although this paradoxical motion can greatly increase the work of breathing, the primary
cause of the hypoxemia is contusion to the underlying lung.

Although possibly subtle at first, the flail segment may become more apparent as contusion
develops and lung compliance falls. Patients may fatigue rapidly because of the decreased
ventilatory efficiency and increased work of breathing. A vicious cycle of decreasing
ventilation, increasing fatigue, and hypoxemia may develop, resulting ultimately in sudden
respiratory arrest.

Patients with mild to moderate flail chest and little or no underlying pulmonary contusion or
associated injuries can often be managed without a ventilator. Attention must be paid to relief
of pain by analgesics or intercostal nerve block and maintaining good ventilation and
pulmonary toilet. If SPO2 remains < 90% despite supplemental oxygen, ventilatory support
should be provided.

Chest Tube (Tube Thoracostomy) insertion Technique

Tube thoracostomy for treatment of traumatic pneumothorax or hemothorax is usually
inserted in the anterior axillary line at the level of the nipple in men or inframammary crease
in women (corresponding to the fifth intercostal space) just behind the lateral edge of the
pectoralis major muscle. For a pneumothorax, the tube should be directed toward the apex, as
high and anteriorly as possible. The tip of the tube should be directed away from the hilum
and mediastinum. For a hemothorax, the tube is usually inserted and directed posteriorly and
laterally.

An oblique skin incision should be made at least 1 to 2 cm below the interspace through
which the tube will be placed. A large clamp is then inserted through the skin incision and
into the intercostal muscles in the next higher intercostal space, just above the rib, with care
taken to prevent the tip of the clamp from penetrating the lung (Figure 1). The resulting
oblique tunnel through the subcutaneous tissue and intercostal muscles usually closes
promptly after the chest tube is removed, thereby reducing the chances of recurrent
pneumothorax
Figure 3. Chest tube insertion, clamp is inserted through the incision and is tunneled up to
the next intercostal space.

Once the clamp is pushed through the internal intercostal fascia, it is opened to enlarge the
hole to approximately 1.5 to 2.0 cm. A finger is inserted along the top of the clamp through
the hole to verify the position within the thorax and to make sure that the lung is not adhered
to the chest wall.

For a simple pneumothorax, a 24F or 28F chest tube can be inserted. For a suspected hemo-
or hemopneumothorax, a 32F to 40F chest tube is preferred. When in doubt, the larger
tube should be chosen for most trauma situations, as smaller tubes may not drain blood
adequately. The tube is advanced at least until the last side hole is 2.5 to 5.0 cm inside the
chest wall.

The open end of the tube is attached to a combination fluid-collection water-seal suction
device. The intrathoracic position of the chest tube and its last hole and the amount of air or
fluid remaining in the pleural cavity should be checked with a chest radiograph as soon as
possible after the tube is inserted.

Chest tubes should be left in place on suction at least 24 hours after all air leaks have stopped
(if placed for a simple pneumothorax) or until drainage is serous and <200 mL/24 h (if placed
for hemothorax).However, in intubated patients, chest tubes should be maintained while
mechanical ventilation continues to prevent sudden development of a new pneumothorax.

Need for Operative Thoracotomy

Most patients with intrathoracic bleeding can be treated adequately by IV administration of

fluids and evacuation of the hemothorax with a chest tube. Fewer than 5% will require
operative management. Surgical exploration should strongly be considered in the following
circumstances: >1500 mL of blood is evacuated immediately after tube thoracostomy; chest
tube drainage of blood occurs at 150 to 200 mL/h for 2 to 4 hours; or persistent blood
transfusion is required to maintain hemodynamicstability.

What are the potentially life-threatening chest injuries?

 Other than the immediate life-threatening injuries discussed above we need to consider the
following injuries as potentially life-threatening in chest trauma patient the so called the
“hidden six”.

• Thoracic aorta disruption

• Tracheobronchial disruption

• Oesophageal disruption

• Myocardial contusion

• Pulmonary contusion

• Diaphragmatic tear.

11.3 Abdominal and pelvic trauma

Time: 1 hour

Learning Objectives
• Describe Abdominal and pelvic injuries.

• Learn how to diagnose Abdominal and pelvic trauma

• List management options for Abdominal and pelvic trauma

Introduction

Abdominal trauma accounts for 15% to 20% of all trauma deaths. These deaths primarily
occur soon after injury as a result of hemorrhage, although some occur later due to
complications from sepsis. Injuries to the abdomen can be from blunt or penetrating
mechanisms or occasionally, both.

Mechanism of Abdominal Injuries

Blunt Abdominal Trauma

The most common mechanism of blunt abdominal trauma is a motor vehicle crash.This
diffuse injury pattern puts all abdominal organs at risk for injury. The biomechanics of blunt
trauma to the abdomen involve compressive, shearing, or stretching forces. The outcome
may be injury to solid organs (e.g., liver or spleen) or hollow viscera (e.g., the GI tract).

Injury can also result from the movement of organs within the body. Some organs are rigidly
fixed, whereas others are more mobile. Injury is particularly common in areas of transition
between fixed and mobile organs. Examples at areas of transition include mesenteric or small
bowel injuries, primarily at the ligament of Treitz or at the junction of the distal small bowel
and right colon.

Penetrating Abdominal Trauma

Stab wounds directly injure tissue as the blade passes through the body. External examination
of the wound may underestimate internal damage and cannot define the trajectory. Assume
that any stab wound in the lower chest, pelvis, flank, or back causes abdominal injury
until proven otherwise.

Fig 4; Penetrating Abdominal Trauma

Gunshot wounds injure in several ways. Bullets may injure organs directly, by secondary
missiles such as bone or bullet fragments, or from energy transmitted from the bullet (blast
effect).Entrance and exit wounds can approximate the trajectory. Thus, all structures in any
proximity to the presumed trajectory must be considered injured.
Clinical Features

Abdominal injury often presents insidiously. Young patients may lose 50% to 60% of their
blood volume and remain asymptomatic.In addition, trauma to the abdomen may be
accompanied by neurologic alterations from concomitant brain injury or alcohol/drug
intoxication. Abdominal tenderness, distention, or tympany may not be present until patients
have suffered significant intra-abdominal blood loss. Therefore, a thorough, methodical, and
comprehensive approach to the diagnosis and management of abdominal trauma is essential.

Physical Examination

Clinical signs may be obvious (such as evisceration) or occult.Inspect the abdomen for
external signs of trauma (e.g., abrasions, lacerations, contusions, seatbelt marks). A normal-
appearing abdomen does not exclude serious intra-abdominal injury. Cullen’s sign and
GreyTurner’s sign (periumbilical and flank ecchymosis) generally represent delayed
findings of intraperitoneal bleeding. Following inspection, palpate the abdomen in all
quadrants, making note of tenderness, tympany, or rigidity. For patients who are observed in
the ED, serial assessments by the same provider are ideal.

Abdominal tenderness, rigidity, distention, or tympany may not be present during the initial
examination and may take hours or days to develop. Reliance on physical exam alone,
particularly with a worrisome mechanism of injury, may result in an unacceptably high
misdiagnosis rate. As many as 45% of blunt trauma patients thought to have a benign
abdomen on initial physical exam are later found to have a significant intra-abdominal injury.

Diagnosis

Although multiple diagnostic modalities exist to detect intra-abdominal injuries, no study is

fail proof. Therefore, a combination of careful physical exam, attention to the mechanisms
and circumstances of injury, and judicious selection of diagnostic studies is used for
diagnosis.

Ultrasonography

The focused assessment with sonography for trauma (FAST) examination is a widely
accepted primary diagnostic study. The underlying premise of the FAST exam is that many
clinically significant injuries will be associated with free intraperitoneal fluid. The
greatestbenefit of FAST is the rapid identification of free intraperitonealfluid in the
hypotensive patient with blunt abdominal trauma.

Advantages of the FAST examination are that it is accurate, rapid, noninvasive, repeatable,
and portable. The average time to perform a complete FAST examination of the thoracic and
abdominal cavities is 4 minutes or less.The main disadvantage of US compared to CT is the
inability to identify the exact source of free intraperitoneal fluid.

Figure 5. Red arrow showing a thin stripe of fluid in Morison's pouch.

Diagnostic Peritoneal Lavage

With the improved technology and availability of multislice CT scanners and the increasing
availability of US machines in the ED, DPL is no longer a first-line screening tool for the
diagnosis of hemoperitoneum.

CT- Scan
CT scanning has become the gold standard for the diagnosis of abdominal injury. Only
CT scanning can make the diagnosis of organ-specific abdominal injury. CT images both the
abdomen and the retroperitoneum. It is the diagnostic test of choice to investigate the
duodenum and pancreas. It can diagnose urinary extravasation and images the ureters. CT
can also quantitate the amount of blood in the abdomen.

Treatment

Laparotomy remains the gold standard therapy for significant intra abdominal injuries. It is
definitive, rarely misses an injury, and allows for complete evaluation of the abdomen and
retroperitoneum.All patients with hypotension, abdominal wall disruption, or peritonitis
need surgical exploration. In addition, the presence of extraluminal, intra-abdominal, or
retroperitoneal air on plain radiograph or CT should prompt surgical exploration.

Table 1. Indications for Laparotomy

Blunt Penetrating
Absolute Anterior abdominal injury with hypotension Injury to abdomen, back, and flank
with hypotension
Abdominal wall disruption Abdominal tenderness
Peritonitis GI evisceration
Free air under diaphragm on chest High suspicion for trans abdominal
radiograph trajectory after gunshot wound
Positive FAST or DPL in hemodynamically
unstable patient
CT-diagnosed injury requiring surgery
CT-diagnosed injury requiring surgery (i.e.,
(i.e., ureter or pancreas)
pancreatic transection, duodenal rupture,
diaphragm injury)
Relative Positive FAST or DPL in hemodynamically Positive local wound exploration after
stable patient stab wound
Solid visceral injury in stable patient
Hemoperitoneum on CT without clear source
Nonoperative Management of Blunt Trauma

The evolution of nonoperative therapy has been greatly advanced by the evolution of CT. CT
can not only make the diagnosis of solid visceral injury, but it can often rule out other
injuries requiring surgery. Solid visceral injuries can be graded as to severity.

11.4 Pelvic Injuries

Introduction

Pelvic fractures and associated injuries are a cause of significant morbidity and mortality.
Most pelvic fractures are secondary to automobile passenger or pedestrian accidents but are
also the result of minor falls in older persons and from major falls or crush injuries. The
mortality rate from all pelvic fractures is approximately 5%. However, with complex pelvic
fractures, the mortality rate is 22%.

Clinical Features

History

The possibility of pelvic fracture should be considered in every patient with serious blunt
trauma. Determine the mechanism of injury and the prehospital evaluation and treatment.
Ask the patient about areas of pain, last urination or defecation, present bladder sensation,
and the last solid and fluid intake. In addition, the time of the last menses or the presence of
pregnancy, brief past medical history, current medications, and allergies should be
ascertained.

Physical Examination

In trauma patients who are awake and alert, the physical examination is very sensitive for the
diagnosis of a pelvic fracture.Symptoms and signs of pelvic injuries vary from local pain and
tenderness to pelvic instability and severe shock. On inspection, examine for perineal and
pelvic edema, ecchymoses, lacerations, and deformities. Inspect for hematomas above the
inguinal ligament or over the scrotum (Destot sign). Examine the patient by palpating for
tenderness or movement at the iliac crests, pubic rami, ischial rami, sacrum, and coccyx.
Compress the pelvis lateral to medial through the iliac crests, anterior to posterior through the
symphysis pubis, and anterior to posterior through the iliac crests. Compress the greater
trochanters and determine the range of motion of the hips.Pelvicstability should be
tested by GENTLE manipulation and should only be performed ONCE, During the
physical examination, avoid excessive movement of unstable fractures as this could
produce further injury and additional blood loss.

Rectal examination may detect superior or posterior displacement of the prostate, rectal
injury, or an abnormal bony prominence or large hematoma or tenderness along the fracture
line (Earle sign). Proctoscopic examination may be required to fully assess for the presence
of rectal tears. Decrease in anal sphincter tone may suggest neurologic injury, and blood at
the urethral meatus may suggest urologic injury. Pelvic examination should be carefully
performed in women to detect the presence of blood or lacerations that suggest the possibility
of open fracture. Carefully evaluate neurovascular function. If a pelvic fracture is found,
assume intra-abdominal, retroperitoneal, gynecologic, and urologic injuries until
proven otherwise.

Radiologic Evaluation

The initial stabilization of the patient takes priority over obtaining radiographs. In patients
with suspected pelvic fracture, a standard anteroposterior (AP) pelvis radiograph is often
used to evaluate for bony injury. Indications for a pelvis radiograph include a
hemodynamically unstable blunt trauma patient, pelvic tenderness, or other finding on
physical examination concerning for pelvic fracture.With an unstable blunt trauma patient, a
pelvic radiograph can be used to identify a pelvic fracture quickly, allowing early
stabilization maneuvers and mobilizing resources for emergent angiography.

Treatment of Pelvic Injuries

Due to pelvic bleeding and associated injuries, patients with pelvic fractures may need
resuscitation with crystalloid, blood, and blood products. Retroperitoneal bleeding is an
inevitable complication of pelvic fractures, and up to 4 L of blood can be
accommodated in this space until vascular pressure is overcome and tamponade occurs.
Most bleeding in pelvic fractures is due to low-pressure venous bleeding and bleeding from
the bone edges. Only about 10% to 15% of patients with pelvic fractures have arterial
bleeding.

The pelvis can be stabilized with a bed sheet or other pelvic binding device to reduce
pelvic volume and stabilize fracture ends.

The simplest technique is the application of a folded bed sheet tightly wrapped around the
pelvis and upper legs and secured by towel clips.

Figure 6. Pelvic stabilization with bed sheet

If a patient with a pelvic fracture is hemodynamically unstable and other sources of bleeding
have been excluded, that is an indication for other treatment options such as angiography
with embolization and external fixation of the pelvic fracture.

In stable patient CT is a modality choice to guide for definitive treatment of pelvic fractures
once the patient has been stabilized and after other associated injuries have been addressed.
 11.5 Head Trauma

Time: 1 hours

Objectives:
At the end of this course participants will be able to:

 Describe classification of Traumatic brain injury

 Describe pathophysiology of Traumatic brain injury
 List General management principles of moderate to severe TBI

Introduction

Traumatic brain injury (TBI) is defined as impairment in brain function as a result of

mechanical force. The dysfunction can be temporary or permanent, and may or may not
result in underlying structural changes in the brain.

TBI is classified based on the clinical assessment of a patient's level of consciousness

with little or no regard to the actual underlying injury.The current classification system,
based on the Glasgow Coma Scale (GCS), divides TBI into:-

• Severe(GCS score of 3 to 8)
• Moderate (GCS score of 9 to 13)
• Mild (GCS score of 14 or 15) TBI.

Moderate TBI accounts for approximately 10% of head injuries. Mortality rates for patients
with isolated moderate TBI is <20%, but long-term disability is as high as 50%. In severe
TBI mortality approaches 40%, with most deaths occurring within the first 48 hours.

Pathophysiology

The brain consumes 20% of the body's total oxygen requirement and 15% of total cardiac
output. The brain is exquisitely sensitive to ischemia and low-oxygen states. Cerebral blood
flow changes and adapts to the regional needs of the tissue. Because it is difficult to measure
the cerebral blood flow accurately, especially regional differences and requirements, the
cerebral perfusion pressure (CPP) is used as a surrogate indicator for monitoring. The CPP is
the pressure gradient required to perfuse the cerebral tissue. CPP is calculated as the
difference between the mean arterial pressure (MAP) and the intracranial pressure
(ICP):

MAP – ICP = CPP

Where MAP can be approximated as: diastolic blood pressure + [(systolic blood pressure –
diastolic blood pressure)/3]. The local adjustment of cerebral blood flow within the brain
microcirculation is termed autoregulation. Local cellular oxygen demands can be met and
regional cerebral blood flow maintained over a wide range of CPPs (between 50 and 150 mm
Hg in a normally functioning system). Autoregulation is impaired in many TBI patients,
however, which results in cellular hypoxia in the setting of even modest drops in blood
pressure. An elevation in ICP further reduces the CPP and cerebral blood flow.

The cranium is an enclosed space with a fixed volume. Any changes to the volume of the
intracranial contents affect the ICP. Normal ICP is <15 mm Hg and is determined by the
volume of the three intracranial compartments:-

 Brain parenchyma (<1300 mL in the adult),

 CSF (100 to 150 mL), and
 Intravascular blood (100 to 150 mL).

When one compartment expands, there is a compensatory reduction in the volume of another
and/or the baseline ICP will increase (Monro-Kellie hypothesis). Normal values for ICP vary
with age.

Cerebral blood flow is generally maintained when the CPP is >60 mm Hg. This level is
considered the lower limit of autoregulation, below which local control of cerebral blood
flow cannot be adjusted to maintain flow adequate for function.6

Rapid rises in ICP may lead to a phenomenon known as the Cushing reflex (hypertension,
bradycardia, and respiratory irregularity). This triad is classic for an acute rise in ICP, but it
is seen in only one third of cases and is more common in children than in adults.
Management of Moderate and Severe Traumatic Brain Injury

The three primary goals of the management of patients with severe or moderate TBI are:-

 To prevent secondary brain injury

 To identify treatable mass lesions and
 To identify other life-threatening injuries.

Airway control, with cervical spine stabilization and assessment and support of breathing,
and circulation are the first priorities for all trauma patients.

ED Resuscitation

The goal of ED resuscitation is to prevent secondary insult (Treat hypotension,

hypoxemia, hyperthermia, and hyperglycemia) and potentially slow the expansion of
the underlying injury. A single occurrence of hypotension and hypoxia is associated with a
150% increase in mortality.Moreover, because TBI is a progressive injury, appropriate
management early in the course can have a greater impact on patient outcome than treatments
initiated later in the process.

Airway and Breathing

Hypoxia increases mortality, so aggressive airway management is needed. Patients with

severe TBI (GCS score of <8) require prompt airway control.Maintain oxygenation and
avoid hyperventilation.Prolonged (>6 hours) hypocapnia causes cerebral vasoconstriction
and worsens cerebral ischemia. Keep oxygen saturation >90%.

Circulation

Arguably the most important secondary insult is hypotension. Hypotension and subsequent
ischemia of vulnerable and injured neuronal tissue can dramatically exacerbate the
underlying secondary cascade and lead to an expansion of the injury and worse
outcomes. In severe TBI, a single episode of hypotension doubles mortality.Therefore,
aggressive fluid resuscitation may be required to prevent hypotension and secondary
brain injury. Adequate fluid resuscitation does not increase ICP, and guidelines recommend
that the systolic blood pressure be maintained at >90 mm Hg. There are no specific
recommendations for MAP; however, most studies in the guidelines report keeping a MAP
>80.

If fluid resuscitation is not effective, vasopressors should be used to maintain MAP at 80 mm

Hg to preserve CPP. Control external and internal bleeding quickly and maintain the
hematocrit at >30%.

Disability and the Neurologic Examination

The neurologic vital sign is the GCS . The GCS was developed as a standardized scoring
system to allow reliable interobserver neurologic assessment of patients with TBI. The GCS
has remained the principal clinical method for grading TBI severity.

An accurate and complete GCS can be obtained only after resuscitation and prior to sedation
or intubation.The motor score is reliable and correlates with outcome almost as well as the
full GCS.

The other important aspect of the neurologic examination is pupil assessment (size,
reactivity, and anisocoria). In an unresponsive patient, a single fixed and dilated pupil may
indicate an intracranial hematoma with uncal herniation that requires rapid operative
decompression. Also consider direct ocular trauma as a cause of unilateral pupil dilation.
Bilateral fixed and dilated pupils suggest increased ICP with poor brain perfusion. Bilateral
pinpoint pupils suggest either opiate use or a pontine lesion.

Glucose Control

Hyperglycemia in the setting of neurologic injury (both stroke and TBI) is associated with
worse outcome. Tight hyperglycemic control is recommended in patients with moderate to
severe TBI.

Temperature Control

Elevated temperature is associated with an increased metabolic demand. Elevated

temperature elevates ICP and worsens outcome in many neurologic critical care conditions
including TBI. Treat fever with the goal of normothermia. The evidence for hypothermia in
TBI is not sufficient to recommend its use.
Seizure Treatment and Prophylaxis

Seizures after head injury can change the neurologic examination, alter oxygen delivery and
cerebral blood flow, and increase ICP. Prolonged seizures can worsen secondary injury.
Treat acute seizures with IV lorazepam, and if seizures continue, treat as for status
epilepticus. Give prophylactic phenytoin if the GCS is ≤10, if the patient has an abnormal
head CT scan, penetrating head injury or if the patient has an acute seizure after the injury.

Increased Intracranial Pressure

Patients history and physical examination findings must be used to identify signs and
symptoms of increased ICP. Indicators of increased ICP include headache, nausea, vomiting,
seizure, lethargy, hypertension, bradycardia, and agonal respirations. Signs of impending
transtentorial herniation include unilateral or bilateral pupillary dilation, hemiparesis, motor
posturing, and/or progressive neurologic deterioration.

Management of Elevated ICP

 Elevate head of bed to 30 degrees

 Ensure adequate sedation & analgesia
 Ensure MAP > 80 with adequate IV fluids
 IV Mannitol 1 g/kg if not hypotensive
 Treat seizures aggressively
 Mild hyperventilation to PCO2 30-35 mmHg

Clinical Decision Rules for CT Imaging

Intubate and sedate as needed to facilitate CT scanning in mod-severe TBI.All patients with
mod-severe TBI ideally need a CT scan, if possible. Immobilize cervical spine until able to
clinically and/or radiographically clear it. Accompany patient to CT if intubated or clinically
deteriorating.

The two most commonly used evidence-based clinical decision rules for head CT in adults
are the New Orleans Criteria and the Canadian CT head rule.
11.6 Management of Burns

Time: 30 minutes

Learning objectives
List common causes of burn
Describe classification of burn
Manage burn based on ABC approach

Introduction
The commonest types of burns in our community are:
• Flame burns with associated burns caused by melted synthetics
• Liquids (i.e. scalds)
Although copious amounts of fluids and electrolytes can be lost, the commonest cause of
death in the first hour is smoke inhalation. Hence early attention to Airway, Breathing then
Circulation is vital.

Pathophysiology
Severity of Burns
• Dependent on temperature & duration of contact
• Scalds rarely cause more than partial thickness burns because the temperature of
water is usually below boiling point and contact is brief.
• Exceptions include
• Very hot liquids (e.g. fat) – Prolonged contact seen in young infants
who are unable to move away.
• Flame burns involve high temperatures and often prolonged contact, which lead to
severe burns.

Classification of Depth
1. Superficial burns:

Superficial epidermal burns

• To epidermis only
• Skin pink or red, painful, no blisters
• Not included in evaluation of burn area

Superficial dermal burns or Partial Thickness

• Injury to epidermis and dermis
• Painful, blisters, oedema, hairs intact
• Non- blanching indicates a more severe burn
• Healing usually occurs without scarring
2. Deep burns:

Deep dermal burn

• May have some blistering
• Base of the blister demonstrates an appearance of a blotchy red coloration = the loss of the
capillary blush phenomenon. This demonstrates that the burn has destroyed the dermal
vascular plexus.
• The dermal nerve endings are also situated at this level and so in these burns sensation to
pinprick will be lost.
Full Thickness
• Injury to epidermis, dermis and extending into subcutaneous tissue
• Painless, white or charred, no hairs
• Leathery to touch
• Healing only occurs by epithelial migration or contracture

Primary Survey and Resuscitation

Airway compromise is due to:
 Inhalation
 Severe burns to face
 Signs of inhalation injury include:
- Carbonaceous sputum
- Singed nostril hairs, oral erythema, blistering
- Upper airway oedema
- Mechanism of Injury e.g. Burn / Explosion in confined space
- Burns above inter nipple line
- Singed nasal hairs
- Burnt red oral mucosa, Burns to Mouth, Nose and Pharynx
- Dysphagia
- Change in voice / dysphonia/hoarse voice
- Stridor /Brassy cough/Bronchospasm/Respiratory Difficulty
An unconscious patient has carbon monoxide intoxication until proven otherwise.
Management:
Airway
Assess patency and support airway as needed Oedema can rapidly develop therefore early
intubation must be considered. Rapid sequence using Suxemethonium can be performed if
burns are less than 5 days old.

Consider performing intubation before signs of respiratory obstruction become evident

particularly before transfer to upgraded medical care if inhalation injury suspected.
Beware concurrent cervical spine injuries – immobilize as necessary

Breathing
• Once airway is secured, breathing is assessed.
• All patients should initially receive high flow oxygen (humidified if possible and high
concentration will wash out the excess carbon monoxide).
• If breathing inadequate, assist with bag-valve-mask ventilation with high flow oxygen.
• Intermittent positive pressure ventilation with bag-valve-mask or with ventilator if
saturation not adequate
• Attend to serious (life-threatening) respiratory conditions if present.

Circulation
• Insert IV line x 2 into non-burnt area if possible
• Consider intraosseous route if above not possible
• Take blood concurrently for CBC, biochemistry, Group and Match, glucose.
• Treat shock if present (see below).

Secondary Survey and Assessment of Burns Surface Area

Rule of 9‘s
Applicable >14 years old, 9% each upper limb ,9% head,18% each lower limb,18% back and
front of torso,1% perineum.

Depth
(1) Superficial
• Epidermal burns
• Superficial dermal/partial thickness burns
(2) Deep
• Deep dermal burns
• Full thickness
Special Areas
• Face and mouth- airway compromise
• Hands and feet functional loss if scarring
• Perineum - prone to infection
Investigations
Determined by severity and extent of burns.
Consider: • Electrolytes, RFT, CO level if available
• CBC with Cross match, Urinalysis for haemoglobinuria/myoglobinuria

Secondary Survey and Management of Burns

Analgesia
• Use IV opioids: e.g. Morphine titrated to effect
Running tap water or a Cool Saline pack and apply on the area
• Good symptomatic relief
• At least 20 minutes
• Beware of hypothermia
Fluid therapy
• Treat shock with fluid boluses (in pediatrics = 20ml/kg)
(1) Maintenance fluid requirements plus
% burn X weight (kg) X 4 (in ml)
• 50% given in first 8 hours following time of burn, remainder in next 16 hours. (Estimate
time since burn and not since arrival of patient)
• This is a guide only and should be monitored.
Aim for a urine output of:
a) Adult > 50ml/hour
b) Pediatrics 1-2ml/kg/hour
• Treat as per trauma patient with monitoring of vital signs rather than with blind
formula but is a good starting point.

REFERENCES
• Tintinallis Emergency Medicine 8th edition
• ATLS 9th Editio
 CHAPTER TWELVE: COMMON PEDIATRICS
EMERGENCIES

12.1 Pediatric Triage

Duration :45 minutes

Objective
At the end of the attachment, the trainee will be able to:
 Outline the principle of triaging
 Identify the three steps of triaging
 Recognize the importance of re-triaging

Definition
Triage is the sorting of patients into priority groups according to their need and the resources
available. The aim of triage is to identify very sick children quickly so they may be treated
without delay

Those with EMERGENCY SIGNS who require immediate emergency treatment.

If you find any emergency signs, do the following immediately:
- Place the patient immediately to resuscitation bed the assigned person has to start to
give appropriate emergency treatment
-Call a senior health worker and other health workers to help.
Carry out emergency laboratory investigations.
 Those with PRIORITY SIGNS, indicating that they should be given priority in the
queue, so that they can rapidly be assessed and treated without delay.
 Those who have no emergency or priority signs and therefore are NON- URGENT
cases.
These children can wait their turn in the queue for assessment and treatment. The majority of
sick children will be non-urgent and will not require emergency treatment. After these steps
are completed, proceed with general assessment and further treatment according to the
child’s priority.

HOW TO TRIAGE?
Keep in mind the ABCDO steps: Airway, Breathing, Circulation, Coma, Convulsion,
Dehydration and Others

The ABCDO concept

Triage of patients involves looking for signs of serious illness or injury. These emergency
signs relate to the Airway-Breathing-Circulation/Consciousness- Dehydration and Other are
easily remembered as “ABCDO”.
Each letter refers to an emergency sign that, when positive, should alert you to a patient who
is seriously ill and needs immediate assessment.

To assess if the child has airway or breathing problems you need to know:
 Is the child breathing?
 Is the airway obstructed?
 Is the child blue (centrally cyanosed)?
 Look, listen and feel for air movement. Obstructed breathing can be due to blockage
by the tongue, a foreign body, a swelling around the upper airway (retropharyngeal
abscess) or severe croup which may present with abnormal sounds such as stridor.
 Does the child have severe respiratory distress?
 Is the child having trouble getting breath so that it is difficult to talk, eat or
breastfeed? Is he breathing very fast and getting tired, does he have severe chest
indrawing or is he using auxiliary respiratory muscles?

Circulation:
Assess the pulse. Is it fast or feeble?
Assess the extremity .Is it cold or warm?
Asses the capillary refill .Does it take more than 3 seconds?
Coma:
Assess using AVPU
A - Alert
V- Voice response
P - Pain response
U - Un response
If a patient is on the V level has to be taken us emergency

Convulsion:
If patients have convulsing now has to be taken as an Emergency

Dehydration:
Assess if patient has two signs of dehydration has to be taken as emergency:
- Sunken eye ball
- Skin pinch goes back slowly
- Lethargic or unconscious

Others:
- Poisoning if they are presenting in the first hours
- Bleeding child, trauma with open fracture
- Exposing the child after poly trauma also is an emergency assessment)

Priority signs
Besides the group of emergency signs described above, there are priority signs, which should
alert you to a child who needs prompt, but not emergency assessment. These signs can be
remembered with the symbols
3 TPR MOB
Tiny baby
Temperature 3T
Trauma
Pallor
Poisoning 3P
Pain
Restless
 Respiratory distress 3R
Referral
Malnutrition/ marasmus M
Oedema O
Burns B

The frequency with which children showing some of these priority signs appear in the
outpatient department depends on the local epidemiology.

The triaging processes

Triaging should not take much time. For a child who does not have emergency signs, it takes
on average 20 seconds. The health worker should learn to assess severalsigns at the same
time. A child who is smiling or crying does not have severe respiratory distress, shock or
coma. The health worker looks at the child, observes the chest for breathing and priority
signs such as severe malnutrition and listens to abnormal sounds such as stridor or grunting.

12.2 Pediatrics Airway

Objective
At the end of this chapter, the trainee should be able to:
 Identify the knowledge and skills on how to open the airway
 Describe the Unique feature of pediatrics airway
 Outline the Management of foreign body in the airway

Introduction
 The letters A in “ABCD” represent “airway”.
 It is evident that an open (patent) airway is needed forbreathing.
 An airway problem is life threatening and must receive your attention before you
move on to other systems.

It is therefore convenient that the first letter of the alphabet represent the most important
areas to look for emergency or priority signs

Unique features of the pediatric airways:

1. Tongue relatively large in proportion to oral cavity

2. Infants <2 months of age are obligate nose breathers
3. Trachea is smaller and shorter than that of adults
4. Smallest diameter of trachea is at the cricoid ring, below the cords,
5. Chest wall of infants relatively weak and unstable
6. Larynx is relatively anterior and high: C2 in neonate, C3-4 in child, C5-6 in adult
cords may be difficult to visualize during laryngoscopy.
7. Immunologic immaturity leads to increased susceptibility to respiratory infections
8. Developmental immaturity leads to increased susceptibility to foreign body
aspiration.

Air way emergency:

1.The patients tongue in a patient who is unconscious

2. Foreign body obstruction

Management
 Open air way head tilt chin lift in a patient who has no trauma if there is trauma jaw
thrust
 Suction the airway
 Insertion of oro-pharyngeal air in unconscious
 In conscious nasopharyngeal air
 Remove the foreign body if suspected

Figure 1 Head tilt chin lift

 Figure 2 open air way (Jo thrust)

Foreign-Body Airway Obstruction (Choking)

- Signs of Foreign-Body Airway Obstruction include a sudden onset of respiratory

distress with coughing, gagging, stridor, wheezing

- If there is foreign body obstruction:

- For an infant, deliver 5 back blows (slaps) followed by 5 chest thrusts repeatedly until
the object is expelled or the victim becomes unresponsive
-For a child, perform sub-diaphragmatic abdominal thrusts (Heimlich maneuver) until the

object is expelled or the victim becomes unresponsive

-If the victim becomes unresponsive, lay should perform CPR but should look in to the
mouth before giving breaths
Figure 3 chest thrusts and back slap

Figure 4 abdominal thrusts

12.3 Pediatrics Respiratory Emergency

Objective
At the end of this chapter, the trainee should be able to:
 List steps in assessment of breathing?
 Manage upper air way, lower air way and lung parenchyma
 Demonstrate Ways of administering of oxygen

Introduction

 If there is no problem with the airway, you should look for signsB

 To assess if the child has breathing problem you need to know: - Is the child
breathing?
 Is the airway obstructed?

Is the child blue (lips and fingers)?

Does the child have difficulty of breathing?

If the child is not breathing or if the airway appears obstructed, you

must first open the airway.

9.2 Pediatrics respiratory emergencies

 Acute Severe Asthma

 Bronchiolitis
 Croup
 Epiglottis

1. Severe Asthma

Asthma is a chronic inflammatory disease of the airways characterized by reversible

airways obstruction and bronchospasm. It is worsening of asthma symptoms of
shortness of breath, cough, wheezing or chest tightness and progressive decrease in
lung function. Asthma exacerbation is usually preceded by viral infections. Patients at
increased risk of asthma related death should be identified
- Three components of obstruction:
. Bronchoconstriction,
. Mucosal edema,
. Increased secretions.

Management:

- Position as comfortable
- Check the airway
- Administer oxygen high flow o2 to maintain saturation >95%
- Hydration has to be maintained
- Check for possible complication
- Salbutamol puff 0.5-1.5 mg 3-4 puff has to be repeated every 20minute three times
if no improvement
- Hydrocortisone 4-5 mg/per dose every 6 hour Iv orpo
- Adrenaline 0.01ml/kg 1:1000 sc in severe case

2.Bronchiolitis
A Viral infection causing obstruction of lower airways and symptom complex similar
to asthma.
-Most common in children <2 years old.

- Epidemics occur in winter months.

- Characterized by diffuse crackles, wheezing, and increased work of
Breathing

Management Bronchiolitis
- High-flow oxygen and expedite transport.
- Goal is to improve air exchange and maintain adequate oxygenation
(>90%).

Inhalation Therapy:
- 1ml of adrenalin in 5 ml of Normal saline vianebulizer.
- If no improvement with patient in moderate to severedistress:
- 1ml of adrenalin in 5 ml of Normal saline via nebulizer May repeat x1.
- Maintain hydration status

3.Croup

- Viral infection causing edema of vocal cords and adjacent trachea (upper air way
obstruction)
- Accounts for approximately 90% of infectious upper airway problems in children.
- Occurs more commonly in cold season
- Children 6 months -3 years most commonly affected
- Clinical syndrome consists of cold symptoms and fever for several days, followed
by respiratory distress, stridor, and barking cough.
- Symptoms often worse at night

Croup Management:
- Positioning
- High flowo2
- Nebulizer 1ml of adrenaline 3ml of N/S
- Dexamethasone 0.6 mg/kg IV
- Nebulization can be repeated every 30 to 1 hour
- If no improvement intubation has to be considered

4. Epiglottitis
Life-threatening bacterial infection causing inflammation and edema of the epiglottis
and/or adjacent structures above the larynx
- Has associated with fever.

- Respiratory distress occurs

- Fever and drooling within 12 hours of appearance of fever

- Muffled voice or refusal to talk

- Difficulty swallowing suggests upper airway obstruction.

- High pitched noise heard on inspiration

- Children are usually older than 12months.

Epiglottises Management
- Minimize interventions if child is conscious and maintaining own airway.

- Do not try to visualize the oral cavity

- Administer 100% O2 only as tolerated.

- You can try to nebulize until you are sending to the hospital but there should not

have delay in referring

 - Immediately refer the patient for intubation

- If no improvement considers needle cricothryoidotomy

- Antibiotic Ceftriaxone 75mg/kg in two divided dose

Oxygen administration

1.Nasal prongs Nasal prongs - are short tubes inserted into the nostrils. Place them
just inside the nostrils and secure with a piece of tape on the cheeks near the nose.
Set a flow rate of 0.5-1 liters/min in infants and 1-2 liters/min if older in order to
deliver 30-35% oxygen concentration in the inspired air.

2.Nasal catheter -is made from tubing of 6 or 8 FG size such as a nasogastric tube
or suction catheter.
Set a flow rate of 0.5-1 liters for infants and 1-2 liters/min for older children,
which delivers an oxygen concentration of 45 % in the inspired air.

1. Face Mask- rate of 5 liters for infants and 5 liters/min for older children, which
delivers an oxygen concentration of 45-60 % in the inspired air.

12.4 Pediatrics Circulation

Objective
At the end of attachment, the trainee is expected to:

 Identify early sign of circulatory problem

 Timely manage shock in children

If A and B has no problem, you can assess C

Assess the circulation

First in this section we will look at the assessment of circulation and signs of shock. To
 assess if a child has a circulation problem or (compensated shock) you need to know:
1- Does the child have warm hands?
2- Is the capillary refill time longer than 3seconds?
3- Is the pulse weak or fast?

1. ARE THE CHILD’S HANDSWARM?

 If the child’s hands are warm, there is no problem with the circulation and you
can move to the next assessment.
 If they are cold, you need to assess the circulation further.
 If it feels cold, the child has circulation problem and you need to assess
capillary refill and pulse.
 If the child’s hands feel cold and the environment also cold you cannot take as a
sign of circulatory problem.
1. IS THE CAPILLARY REFILL TIME LONGER THAN 3 SECONDS?
7.

 Capillary refill is a simple test that assesses how quickly blood returns to the
skin after pressure is applied.
 It should be refilled in less than 3 seconds. If it is more than 3 seconds the child
has circulatory problem
 Capillary refill is prolonged in shock because the body tries to maintain blood
flow to vital organs and reduces the blood supply to less important parts of the
body like the skin by peripheral vasoconstriction.
 You need to check the pulse only if the room is cold.
 The pressure is applied for 3 seconds and then released. Time of capillary refill
from the moment of release until total return to the pink color. If the refill time
is longer than 3 seconds, the child may have a circulation problem with shock.
 To confirm, it is necessary to check the pulses.

1. IS THE PULSE WEAK ANDFAST?

The radial pulse should be felt. If this is strong and not obviously fast, the pulse is
adequate; no further assessment is needed.
  If the radial pulse is difficult to find, you need to look for a more central pulse
(a pulse nearer to the heart).
 In an infant (less than one year of age) the best place to look is at the middle of
the upper arm, the brachial pulse
 If the child is lying down you could look for the femoral pulse in the groin.
 In an older child you should feel for the carotid pulse in the neck.
 The pulse should be strong.
 If the more central pulse feels weak, decide if it also seems fast.
 If the central pulse is weak and fast, the child needs treatment for shock.

Note: The blood pressure to assess for shock in early phase not recommended because
of two reasons:

1. Low blood pressure is a late sign in children and may not help identify compensated
phase of shock
2. The unavailability of BP cuff may delay in diagnosing uncompensated shock which
can be diagnosed without BP cuff.

Shock
The most common cause of shock in children is due to loss of fluid from circulation,
either through loss from the body as in severe diarrhea or when the child is bleeding, or
through capillary leak in a disease such as severe infection.
 In all cases except obstructive, it is important to replace this fluid quickly.
 An intravenous line must be inserted and fluids given rapidly in shocked
children without severe malnutrition carcinogenic shock.
 The recommended volumes of fluids to treat shock depending on the
age/weight of child 20ml/kg every 20 min three times
 If the child has severe malnutrition, you must use a different fluid and a
different rate of administration and monitor the child very closely.
 Therefore, a different regime is used for these children.
 Treatment of shock
Treatment of shock require steam work.
 The following actions need to be started simultaneously:
 If the child has any bleeding, apply pressure to stop the bleeding give oxygen
 Make sure the child is warm feeling the brachial pulse in an infant
 Weigh the child.
 Insert an intravenous line (and draw blood for emergency laboratory
investigations).
 Fix the cannula and immobilize the extremity with a splint.

If the child has severe malnutrition

 15 ml/kg 1/2 N/S and ½ 5% DW give over 1hour
 Stay with the child and check the pulse and breathing rate every 5-10minutes.
 Discontinue the intravenous infusion if either of these increase (pulse greater
than 15,
 respiratory rate greater than 5/min).

If there is improvement: Pulse and breathing rate fall. Repeat 15ml/kg over 1 hour

If the child has NO severe malnutrition

 Insert an intravenous line (and draw blood for emergency laboratory
investigations).
 Fix the annual and immobilize the extremity with a splint.
 Attach Ringer’s lactate or normal saline -make sure the infusion is running
well.
 Infuse 20 ml/kg as fast as possible. The circulation should be reassessed as
described before

If there is NO improvement:
 Reassess the circulation again, and if there is still no improvement
 Give another 20 ml/kg of Ringer’s lactate or Normal saline, as quickly as
possible.
 The circulation should be assessed again.
 If there is still NO improvement:

 Give 20 ml/kg as fast as possible

 If there is ongoing loss while you are treating the patient has to get
replacement treatment 10ml/kg for every ongoing loss.
 The circulation should be assessed again.
 After three boluses of 20ml/kg of fluid give blood and refer

12.5 Basic life support

Objectives
At the end of this chapter the students expected to
 Identify When and how to initiate CPR
 Describe the difference between infant and child CPR
 Choosing appropriate size of face mask
 How to do proper ventilation
 How to do effective cardiac compression
 Has to know proper way of coordination ventilation and cardiac compression
-
-

Basic life support sequence

Initiate CPR –The actions that constitute cardiopulmonary resuscitation (CPR) are
opening the airway providing ventilations and performing chest compression.

The sequence in which the actions of CPR for infants and children should be
performed as follow:
C-A-B-D
 Assess the circulation and breathing at the same time.
 If the pulse is less than 60/min or no pulse.
 If there is no pulse or pulse is < 60 bpm, begin ventilation and chest
Compressions
  Coordination of compression and ventilation may be facilitated by counting
com. If the child is having gasping type of breath, we have to start CPR.

chest compressions—Essential elements for effective chest compressions:

 Hard
 fast chest compression
 with full chest recoil
 Minimal interruptions

Chest compressions should be performed over the lower half of the sternum
Compression below the sternum can cause trauma to the liver, spleen, or stomach, and
must be avoided.

The effectiveness of compressions can be maximized by attention to the following:

The chest should be depressed by one-third to one-half of its anterior posterior

diameter with each compression

- The optimum rate of compressions is approximately 100 per minute

- Each compression and decompression phase should be of equal duration.
- The sternum should return briefly to its normal position at the end of each
smooth compression-decompression rhythm with minimum interruption

Infants — Chest compressions for infants ( under one year) may be performed with
either two fingers or with the two thumb-encircling hands technique. Two Techniques
is recommended when there is a single rescuer
 Figure 5 two fingers chest compression

Two thumb encircling hands — the two thumb-encircling hands technique

provides optimum chest compressions when there are two rescuers
 Figure 6 Encircling chest compression

Children — for children (from one year until the start of puberty), compressions
should be performed over the lower half of the sternum with either the heel of one
hand or with two hands, as for adult victims

COMPRESSION TO VENTILATION RATIO — Chest compressions in infants

and children should always be accompanied by ventilation. For one rescuer, two
ventilations should be delivered during a short pause at the end of every 30
thcompression.

For two rescuers, two ventilations should be delivered at the end of every 15th
compression.

 Open airway and check breathing

 If there is no breathing, give two rescue breaths
 If there is no response, check pulse
 If pulse 60 beats per minute (bpm), continue ventilationpression

Ventilation — Breathing support can be provided with mouth-via-devise to mouth,

mouth-to-nose via devise, or with a bag and mask. Each rescue breath should be
delivered over one second. The volume of each breath should be sufficient to see the
chest wall rise.
 Figure 7 choosing appropriate size of mask

Figure 8 bag mask ventilation

A child with a pulse 60 bpm who is not breathing should receive one breath every 3 to 5
seconds (12 to 20 breaths per minute). Infants and children who require chest
compressions should receive 2 breaths per 30 chest compressions for a lone rescuer 2
breaths per 15 chest compressions
 12.6 Management of Pediatrics Burn

Objectiv
eeeeeveiv At the end of the attachment the trainees are expected
e
to:
 Describe Initial assessment of a major burn
 Classify burn
 Describe burn fluidmanagement

Burn
A major burn is defined as a burn covering 25% or more of total body surface area, but
any injury over more than 10% should be treated similarly. Rapid assessment is vital. The
general approach to a major burn can be extrapolated to managing any burn. The most
important points are to take an accurate history and make a detailed examination of the
patient and the burn, to ensure that key information is not missed.

Classification of burn depths

Burns are classified into two groups by the amount of skin loss. Partial thickness burns do
not extend through all skin layers, whereas full thickness burns extend through all skin
layers into the subcutaneous tissues. Partial thickness burns can be further divided into
superficial, superficial dermal, and deep dermal:

Superficial—The burn affects the epidermis but not the dermis (such as sunburn). It is
often called an epidermal burn

Superficial dermal—The burn extends through the epidermis into the upper layers of the
dermis and is associated with blistering

Deep dermal—The burn extends through the epidermis in to the deeper layers of the
dermis but not through the entire dermis.
Initial assessment of a major burn

Perform an ABCDEF primary survey

A—Airway with cervical spine control, B—Breathing, C—Circulation, D—
Neurological disability, E—Exposure with environmental control, F—Fluid
resuscitation

 Assess burn size and depth (see later article for detail
 Establish good intravenous access and give fluids
 Give analgesia
 Catheterize patient or establish fluid balance monitoring
 Take baseline blood samples for investigation
 Dress wound
 Perform secondary survey, reassess, and exclude or treat associated injuries
 Arrange safe transfer to specialist burns facility

Fluids
Calculate resuscitation formula based on surface area and time since burn

F—Fluid resuscitation

1) Total fluid requirement for first 24hours ;4 ml × ( total burn surface area)×(wt in
kg)/24hours

2) Half to be given in first 8 hours, half over the next 16hours

3) Subtract any fluid already received from amount required for first8hours
4) Calculate hourly infusion rate for first 8hours
5) Calculate hourly infusion rate for next 16 hours

Maintenance fluid required for a child

A 24 kg child with a resuscitation burn will need the following maintenance fluid:
Children receive maintenance fluid in addition, at hourly rate of:

 4 ml/kg for first 10 kg of body weight plus

 2 ml/kg for second 10 kg of body weight plus
  ml/kg for > 20 kg of body weight

End point
Urine output of 1.0-1.5 ml/kg/hour in children

Analgesia
Superficial burns can be extremely painful. All patients with large burns should receive
intravenous morphine at a dose appropriate to body weight. This can be easily
titrated against pain and respiratory depression. The need for further doses should be
assessed within 30 minutes.

Investigations
The amount of investigations will vary with the type of burn Hematocrit /Hct/, Total
Serum Protein/TSP/

Secondary survey
At the end of the primary survey and the start of emergency management, a secondary
survey should be performed. This is a head to toe examination to look for any
concomitant injuries.

Dressing the wound

Once the surface area and depth of a burn have been estimated, the burn wound should be
washed and any loose skin removed. Blisters should be deroofed for ease of dressing,
except for palmar blisters (painful), unless these are large enough to restrict movement.
The burn should then be dressed. For an acute burn which will be referred to a burn
center, cling film is an ideal dressing as it protects the wound, reduces heat and
evaporative losses, and does not alter the wound appearance. This will permit accurate
evaluation by the burn team later.

12.7 Pediatrics Snake bite and poisoning

Objectiv
ee At the end of the attachment the trainees are
expected to:
 Identify snake bite
 Assess and initiate immediate management
Snakes Bites: Several different types of snakes must be differentiated due to the varying
effects of their venoms.
Many snake bites are provoked and thus involve the upper extremities some the snake’s
venom is voluntarily injected by venom gland contraction.
Snakes type has a neurotoxin which may lead to paralysis and respiratory arrest. There
may be varying hemotoxins which profoundly decrease platelet and clotting factors.

Treatment

First Aid Management

 Initiate BLS as necessary (ABCs) - Move the patient to a health care facility as
rapidly as possible
 Minimize movement of an affected extremity and keep the extremity below the
level of the heart
 Avoid ice, aspirin (coagulopathies possible), alcohol or sedatives
 Tourniquets not universally recommended; although constriction band in
experienced hands may be useful when incision and suction are indicated or a
long transport anticipated. Incision and Suction these should be considered only
if:
 Patient is more than one hour from a medical facility
 Theonlyincisionstobemadeareextensionsofnotmorethan1cmlongand
0.5 cm deep.
DO NOT MAKE AN X SHAPED CROSS INCISION, and always keep in mind
underlying structures.

Tourniquets
A varying portion of venom may be absorbed via the lymphatic system. Given this, if a
medical facility is not nearby wide constricting band may be placed around an extremity.

Use of a tourniquet is a controversial topic. A BP cuff at 15-20 mmHg is adequate.

Otherwise the band should be wide and two fingers able to pass freely under it.
The band should be tight enough to occlude lymphatic flow but loose enough to palpate
pulses distal to the bite. If swelling occurs, place a second tourniquet above the first one
before removal of the firstband.

Before this is done it is recommended that 2 IV’s are in place, fluid resuscitation is
underway, and the antitoxin is given.
TAT 1500IU IM STAT after skin test has be given
If there is antivenom give through IV route only. Dilute antivenom in any isotonic
solution (5-10ml/kg, bigger children dilute in 500mls of IV solution) and infuse the
whole amount in one hour.

12.8 pediatrics poisoning

Objective
At the end of the attachment the trainees are expected
to:
 Describe Initial assessment of poisoning
 Demonstrate immediate management of
poisoning
 Describe burn fluid management

A poison is any substance that causes harm if it gets into the body. Harm can be mild (for
example, headache or nausea) or severe (for example, fits or very high fever), and
severely poisoned people may die. Almost any chemical can be a poison if there is
enough in the body.

Acute exposure is a single contact that lasts for seconds, minutes or hours, or several
exposures over about a day or less. Chronic exposure is contact that lasts for many days,
months or years.
Routes of Exposure

 Through the mouth by swallowing (ingestion)

 Through the lungs by breathing into the mouth or nose (inhalation) Through the
skin by contact with liquids, sprays or mists
 By injection through the skin

Epidemiology
Poisoning is divided into accidental poisoning and non-accidental or self poisoning.

Most cases of accidental poisoning occur within the home. The poisoning agents are
usually household agents, medicaments and plant material.

Non-Accidental Poisoning (Self-poisoning)

Self-poisoning is usually seen in older children and adolescents suffering from

depression, serious illness, or alcohol dependence in an attempt to commit suicide or to
attract attention.

Consequences of Poisoning

The effects of poisoning maybe none, mild or severe depending on:

- The amount of poisoningested.
- The nature of thesubstance
- The age of thechild.
- The nutritional status of thechild.
- The state of the stomach-whether empty or full offood.

The effects of poison

The effects of poisons can be local or systemic. A local effect is limited to the part of the
body in contact with the chemical A systemic effect is a more general effect that occurs
when a poison is absorbed into the body.

Local effects
On the skin chemicals can cause itching, rash, pain, swelling, blisters or serious burns
Inside the air passages and lungs irritation from vapors and gases can cause coughing,
choking and lung edema

Systemic effects
There are many ways in which poisons can cause harm by damaging organs such as the
brain, nerves, heart, liver, lungs, kidneys, or skin. Poisons can also lead to muscle
paralysis.

Common Substances Causing Poisoning in Children

The commonest substances causing poisoning in East and Southern Africa are household
chemicals followed by drugs.

Management

The management of the poisoned child is at two levels; at home where first aid is
administered and, in the hospital, where specific treatment is given.

First aid at home

First aid treatment should be administered by the person who finds the child after the
poisoning episode. Care should be taken so that the first aid treatment does not cause
severe complications that may be worse than the original poisoning.
 Treatment in hospital
The clinician should take a brief history, examine the child thoroughly and rapidly and
then do the following:

1. Ensure a clear airway and support respiration.

2. Treat shock if present.
3. Remove poison from the body before it is absorbed, by inducing vomiting or doing a
gastric lavage if victims comes within one hour except when kerosene or a corrosive
has been ingested.
4. Reduce absorption by administering activated charcoal which absorbs many toxins and
prevents subsequent absorption. ( 0.5-1gm/kg of activated charcoal)
5. Anti-dotes should be used but these are available for very poisons.
6. General supportive measures are important to ensure adequate hydration, temperature
control, fluid and electrolyte balance, nutrition intake and control of convulsions

12.9 Newborn Resuscitation

Objective
At the end of this chapter the participants are expected to:
 Handle new born immediately after delivery

1. Recognize air way obstruction and theirmanagement

Resuscitation efforts should focus on improving respiratory status and maintaining
2. Identify the peculiarity of new bornresuscitation
bodytemperature.
1.
2.
A.3.Evaluation and Treatment Priorities
- 4.During delivery, suction mouth then noses before delivery of body.
5.
- This is especially important if there is meconium in the amniotic fluid.
- Dry infant and maintain warm environment.
- Wrap the baby in a thermal blanket.
 - Cover the infant’s head to preserve warmth.
B. Open and position the airway in the “sniffing” position.
- Suction airway again using bulb syringe, mouth first thennasopharynx.
- Avoid hyperextension of the neck.
If thick meconium is present in apneic and/or hypotonic infant:
- Initiate suctioning before the infant takes firstbreath.
- Suction the airway while withdrawing the suctiontube
- Repeat suction only if meconium is not cleared and infant remains apneic and/or
hypotonic, then ventilate infant withBVM
- If infant becomes bradycardic (<60), discontinue suctioning and provide ventilation
immediately.
- Assess Breathing and adequacy ofventilation.
- Stimulate the infant by rubbing the back or flicking the soles of thefeet.

If evidence of central cyanosis:

- Oxygen 100% via blow-by administration.

If infant is apneic:
- BVM at 40-60 breaths/minute with 100% oxygen.
- Assess Heart Rate – Auscultation or palpation of brachial artery or umbilical cord
stump.
- If heart rate is <60 and signs of poor perfusion are persistent after 30 seconds of
assisted ventilation with 100% oxygen initiate the following:

Continue ventilation
- Begin chest compressions and CPR: ratio of 1 to 3 rate of 100 compressions per minute
(hard and fast)
- Stop CPR when heart rate >60 with signs of improved perfusion
- If heart rate is 60 – 100/minute
 Continue ventilation
- Assess skin color – If cyanosis use blow-by oxygen
- If heart rate is >100/minute Continue assisted ventilation until patient is breathing
adequately on own and is vigorous.

Reassess the infant frequently

- Pulse, respiratory rate, tone, color, and response.

- Contact direct medical control for additional instructions
- Continued care of mother.
- Place two clamps 6 and 8 inches from baby, cut umbilical cord between clamps.
- Transport delivered placenta to hospital with the baby

Over all Activities

• Discussion on case scenario#26-31

• Simulation practice in small group
• General discussion on questions raised by participant

REFERENCES
1) Yang WC, Lee J, Chen CY, et al. Westley score and clinical factors in predicting
the outcome of croup in the pediatric emergency department. PediatrPulmonol
2017; 52:1329.
2) Gelbart B, Parsons S, Sarpal A, et al. Intensive care management of children
intubated for croup: a retrospective analysis. Anaesth Intensive Care 2016;
44:245.3.
3) Acworth J., Babl F., Borland M., et al. Patterns of presentations to the Australian
and New Zealand paediatricemergency research network. Emergency Medicine
ustralasia. 2009; 21 (1): 59-66.

4) Rimmer E, Houston BL, Kumar A, et al. The efficacy and safety of plasma
exchange in patients with sepsis and septic shock: a systematic review and meta-
analysis. Critical care. 2014;18:699.
5) Holst LB, Haase N, Wetterslev J, et al. Lower versus higher hemoglobin threshold
for transfusion in septic shock. The New England journal of medicine.
2014;371:1381–91
6) Stark MJ, Hodyl NA, Belegar V KK, Andersen CC: Intrauterine inflammation,
cerebral oxygen consumption and susceptibility to early brain injury in very
preterm newborns. Arch Dis Child Fetal Neonatal Ed 101: F137– F142, 2016.
7) Orman G, Wagner MW, Seeburg D, Zamora CA, Oshmyansky A, Tekes A,
Poretti A, Jallo GI, Huisman TA, Bosemani T: Pediatric skull fracture diagnosis:
should 3D CT reconstructions be added as routine imaging? J NeurosurgPediatr
16: 426– 431, 2015
8) Arrey EN, Kerr ML, Fletcher S, Cox CS, Sandberg DI: Linear nondisplaced skull
fractures in children: who should be observed or admitted? J NeurosurgPediatr
16: 703– 708, 2015.
9) Truitt CA, Brooks DE, Dommer P, et al. Outcomes of unintentional beta-blocker
or calcium channel blocker overdoses: A retrospective review of poison center
data. J Med Toxicol. 2012;8:135139.
10) Konca C, Yildizdas RD, Sari MY, et al. Evaluation of children poisoned with
calcium channel blocker or beta blocker drugs. Turk Arch Ped. 2013138144.
 CHAPTER 13: OBSTETRIC EMERGENCIES

13.1 HYPERTENSIVE DISORDER OF PREGNACY

Objectives
- By the end of this session, participants will be able to:

 define hypertension and proteinuria

 List major classes of hypertensive disorders of pregnancy

 Diagnose preeclampsia with or without severe disease

 Manage preeclampsia and eclampsia

 Definition: -
o hypertension which is induced by pregnancy and this disorders
resolves postpartum
 Hypertension (HTN): Systolic blood pressure (SBP) >140
mmHg or diastolic blood pressure (DBP) > 90 mmHg on
two occasions at least 4hr apart; Or a single record of BP >
160/110 mmHg
 Proteinuria: ≥ 0.3gm in 24 hr urine specimen Or dipstick
≥1+

1.1 Gestational hypertension

 Definition –New onset of hypertension at ≥20 week of gestation in the absence of
proteinuria and end organ dysfunction
 Prevalence:- 6 to 17% in nulliparous; 2 to4% in multiparous
 Highest prevalence occurs in woman with previous preeclampsia, twin pregnancy
and obesity

 Risk factor – same as preeclampsia

o Past history of preeclampsia or family history of preeclampsia
o Preexisting medical condition(DM,HTN,CKD)
o Twin pregnancy
o First pregnancy
o advanced maternal age
o ART (Artificial Reproductive Technology)
o Diagnostic evaluation
 The main goal of initial evaluation of newly developed hypertension is to
differentiate gestational hypertension from preeclampsia
o Measure protein excretion(to r/o proteinuria)
 Urine dipstick
 Protein to creatinine ratio
o Evaluate for feature of severe disease(to r/o end organ dysfunction)
o Asses fetal well being
 Non stress test biophysical profile

Management for gestational hypertension

 Management is different based on the rise of blood pressure

 BP <160/110 mmHg
o Outpatient management with weekly /2x ANC visit (for BP, urine protein check up)
o Antihypertensive therapy is not recommended
o Timing of delivery: at term
o No need of intrapartal MgSo4

 BP ≥ 160/110 mmHg
 o These patients have rates of pregnancy complication comparable with those with severe
preeclampsia
o Antihypertensive therapy to decrease risk of stroke with BP goal of 130-150 systolic and
80-100mmHg diastolic BP
o Timing of delivery –suggested for gestational age ≥34 week if BP is easily controlled and
if no preeclampsia and fetus healthy delivery is favored at 34 to 36 weeks
o MgSo4 is administer for seizure prophylaxis

1.2 Preeclampsia

 Definition: multisystem progressive disorder characterized by new onset of

hypertension and proteinuria or hypertension and significant end organ dysfunction
with and without proteinuria after 20 weeks of gestation in previously normotensive
patients
 Preeclampsia with severe features
o SBP>=160mmHgor DBP>=110mmHg and proteinuria (with or with out
significant end organ dysfunction)
o SBP>=140mmHg or DBP>=90(with or without proteinuria) one or more
of the following
 New onset of cerebral or visual disturbance(photopsia , scotomata,
severe headache that persist despite analgesics altered mental
status)
 Severe persistent RUQ pain and serum transaminase>=2xUNL
 Thrombocytopenia (,100000platelate)
 Progressive renal insufficiency(serum creatinine >1.1mg/dl or
doubling of creatinine
 Currently as massive proteinuria (5g/24hr) IUGR and oliguria was
removed as feature of severe disease
 Prevalence- 4.6 %of pregnancy worldwide were complicated by preeclampsia
 Risk factor- mentioned in gestational hypertension
 Clinical presentation
 o On history –persistent and severe head ache, visual disturbance, epigastric
and RUQ pain, altered mentation dyspnea
o On physical exam-Elevated blood pressure
o Laboratory –CBC, RFT, LFT, urine protein, coagulation profile(not
routinely done unless complication occur Abruptio placentae, severe
bleeding, severe liver dysfunction)
o Asses fetal status(for IUGR, oligohydraminos)

Help syndrome
 Definition: an acronym that refers to a syndrome characterized by
hemolysis elevated liver enzyme and low platelet
 Incidence: it occurs in 10 to 20 % of women with severe preeclampsia or
eclampsia
 Patient presentation- the commonest is abdominal pain and
tenderness(right upper quadrant) nausea vomiting less common jaundice
headache and asites
 Laboratory findings
o Microangiopathic hemolytic anemia on blood smear
o PLT<100000
o Total bilirubin ≥1.2mg/dl
o Serum AST ≥2xUNL

Management of preeclampsia
 Definitive treatment for preeclampsia is delivery this is to prevent development of
maternal or fetal complication of diseases progression
 Timing of delivery is based on combination factor including
o Disease severity
o Maternal and fetal condition
o Gestational hypertension
 Preeclampsia with feature of severe disease (formerly called severe
preeclampsia)
o Severe preeclampsia is an indication for delivery
 o Route of delivery is based on standard obstetrical indication
o Conservative management for-
 Gestational age less than 34 week but viable
 mother and fetus should be stable
 should be admitted in hospital with appropriate level of new born
care
 Preeclampsia without feature of severe disease
o Previously called mild preeclampsia
o Delivery is recommended for Term pregnancy (>=37 week)
o For preterm pregnancy
 <36 week-conservative management
 Delivery is indicated at 37 week or as soon as they develop severe
features or eclampsia whether cervix is favorable or not
 Fluid management in preeclampsia
o Fluid balance should be monitored
o Excessive fluid administration should be avoided preeclamptic mother are
at risk of pulmonary edema and third spacing
o For maintenance: use ringer or NS at rate os 80ml/hr(unless patient has no
ongoing loss)
Management of hypertension

 First line agents: Labetalol and Hydralazine

o Labetalol
 its effective, has rapid onset of action and good safety
profile
 Dose=Labetalol 20 mg IV push over 2 minutes. Repeat as
needed every 10 minutes, doubling the dose up to 80 mg for
desired effect. Maximum total cumulative daily dose is
300mg
 BP will fall within 5 to 10 min
 Continuous cardiac monitoring is not routinely done
o Hydralazine
 begin with 5mg iv if bp goal is not achieved within 20 min
give 5 to 10mg iv max dose 20mg if total dose of 30 mg
doesn’t achieve BP control add another agent
 Fall in BP begin within 10 to 30 min and lasts from 2 to 4
hours
o Nifedipine: alternative agent
 Experience with this drug are more limited than the iv drugs
 Dose-10 to 20 mg PO at 20 minute interval until BP goal
achieved
o Nitroglycerin
 Rarely used for hypertension associated with pulmonary
edema if resistant to iv diuretics
 Dose 5mcg/min increase every 3 to 5 min to max dose
100mcg/min
 Second line therapy
o Esmolol or nicardipine by infusion pump
o Nitroprusside as last resort
 MgSO4 should not be substituted for antihypertensive therapy
 Target blood pressure
o 130 to 150 mmHg systolic: 80 to 100mmHg diastolic
 o Aggressive blood pressure lowering result in cerebral and
myocardial ischemia therefore blood pressure lowering should be
MAP by no more than 25 %over 2 hr

Seizure prophylaxis

 Candidate for seizure prophylaxis

o Severe preeclampsia during evaluation, labor and continued for 24-48 hrs
after delivery
o Eclampsia immediately continue until 24 -48hr after delivery or last seizure
 Magnesium sulphate
o is drug of choice for prevention of eclampsia
o Timing-initiated at the onset of labor induction or cesarean delivery
o Dosing Before administration: ensure RR > 16/minute, DTRs are present.
 Loading dose: MgS04 (20% solution) 4 g IV over 5 minutes. Then 10
g 50% MgS04 IM, 5 g in each buttock. If convulsions recur after 15
minutes, give 2 g MgS04 (50% solution) IV over 5 minutes.
 Maintenance: 5 g MgS04 (50% solution) + 1 mL lignocaine 2% IM
every 4 hours into alternate buttocks.
 If respiratory arrest: assist ventilation, give calcium gluconate 1 g (10
mL of 10% solution) IV slowly until respiration begins.

1.3 Chronic HTN

 HTN that exists before pregnancy HTN that is present on at least two occasions
before the 20 week of gestation or that persist longer than 12 week post partum

1.4 Pre-eclampsia superimposed on chronic HTN

 Chronic HTN + New onset proteinuria or significant end organ damage or both after
20 weeks of gestation; or worsening of preexisting proteinuria
o A rise of BP to the severe range or severe symptoms or resistant
HTN
 1.5 Eclampsia
 Definition-Occurrence of new onset generalized tonic clonic seizure or
coma in a woman with preeclampsia
 Incidence eclampsia occur in 2 to 3%of women severe features of
preeclampsia not receiving antiseizure prophylaxis up to 0.6%fo mild
preeclampsia

Management of eclampsia
 Initial stabilization
o Maintaining airway patency
o Adequate oxygenation
 Put the patient on supplemental oxygen 8-10 l/min via
non rebreather mask to treat hypoxia from
hypoventilation during the seizure
o Protection from trauma
 Position the patient on lateral side
o Prevent aspiration
 Treatment of severe hypertension if present
 Prevention of recurrent seizure
o magnesium sulphate –drug of choice
o Persistent seizure despite MgSo4 use alternative drug
diazepam or lorazepam
o Diazepam-5 to 10 mg iv every 5 to 10 min at rate <=5mg/min
max dose 30 mg
 Evaluation for prompt delivery
o Definitive management -delivery
o Eclampsia is an absolute contra indication for expectant
management
 Summary
o Definitive management for preeclampsia/ecclampsia is
DELIVERY
o Anti hypertensives are recommended for severe and persistent
hypertension
o Magnesium sulphate is the drug of choice for prevention of
seizure
 13.2 Vaginal bleeding during pregnancy

Objectives

At the end of this session, participants are expected to

 Classify vaginal bleeding during pregnancy based on trimester
 Identify causes for vaginal bleeding during pregnancy
 Describe management principles for vaginal bleeding during
pregnancy

Introduction
 Vaginal bleeding is common event at all stage of pregnancy
 This include:-

o 1st trimester vaginal bleeding

o 2nd trimester vaginal bleeding
o 3rd trimester vaginal bleeding
o Postpartum hemorrhage

2.1 First trimester bleeding

 Vaginal bleeding which occur up to 14 week

 It occur 20 to 40 % of pregnant women
 The most common cause is abortion unlike ectopic which is less common but the
most life threatening therefore this diagnosis must be exclude in every pregnant
woman with bleeding
  Differential diagnosis

2.1.1Ectopic pregnancy:
o Definition- It is exrauterine pregnancy (Gestational sac outside of uterus). It
should be ruled out in all pregnant women with vaginal bleeding the majority of
ectopic pregnancy occur in fallopian tube (84%)
o clinical presentation
 he most common are 1st trimester vaginal bleeding- which is preceded
by amenorrhea and Abdominal pain
 it can be ruptured or unruptured
 Ruptured ectopic is a life threatening hemorrhage ,suggestive
symptoms are severe &persistent pain Peritonitis, abnormal vitals loss
of consciousness
o Diagnostic evaluation
 Do hCG and confirm pregnancy
 Evaluate for hemodynamic stability
 If unstable, patient should be transferred to resuscitation area
o Bilateral iv line should be secured and resuscitate with1-2 liter of NS
,sample should be sent for blood group RH &cross mach Blood
product should be prepared
o Stabilize with fluid and blood if needed
o Simultaneously urgent Consultation and transfer to obstetrician for
further surgical mgt(laparatomy)
 If patient stable-transfer to obstetrics for further diagnostic evaluation and
medical therapy can be tried
 Asses for pregnancy location
 Do transvaginal ultrasound
o Unlikely if Intra uterine pregnancy on ultrasound

2.1.2 Abortion
 the most common cause it can be induced or spontaneous
 Spontaneous abortion: a pregnancy loss which occur before 28 week of gestation
according to Ethiopia (WHO ,20 weeks of gestation,<500gm of weight)
o Inevitable -bleeding with dilated cervix& open internal os but there is no
passage of POC
o Incomplete -open os, there is passage of only parts of POC but it not fully
expelled
o complete -closed os, fetus and placental materials fully expelled)
o Threatened - bleeding + closed internal os Cx + US with IUP. Risk of
abortion 35-50%.
o Septic abortion: fever, abdominal pain; can complicate any abortion.
o Missed abortion: Spontaneous abortion in a patient with or without
symptoms and with closed cervical os
Management of abortion

 Assess hemodynamic stability

 If unstable –give priority for resuscitation
 Based on the type of abortion
o Threatened – patient can be safely discharged with close follow up
o Inevitable /incomplete-
 Evacuation can be medically with Misoprostol PO 600microgram or
surgically with dilation and curettage
o Complete- do USG: if no RPC, discharge with close follow up

2.1.3 Molar pregnancy

 Definition- is part of a group of disease classified as gestational trophoblastic disease

(GTD)
 Originates in the placenta and has a potential to locally invade the uterus and
metastasize
 Clinical presentation
o vaginal bleeding
o Hyperemesis
o Pregnancy induced hypertension before 24 week
o On physical exam uterus larger than the gestational age
 Diagnostic evaluation
 Lab- abnormally high HCG level
 Sonographic feature
o Snowstorm or Swiss chess pattern
o Large central fluid collection
 Management
o Consult OB if no marked bleeding, Suction curettage if bleeding, ensure OB
follow up to trend hCG
 2.2 Second trimester vaginal bleeding
 Bleeding prior to 28 weeks should be treated like 1st trimester bleeding
 Bleeding after 28 weeks should be treated like 3rd trimester bleeding

2.3 Third trimester vaginal bleeding (APH)

 Definition: APH (antepartum hemorrhage is vaginal bleeding from the 28th week
of gestation until fetus is delivered.
 Evaluation of APH
o Assess amount of visible bleeding.
o Do not perform digital vaginal or speculum exam until placenta previa
ruled out.
 Investigation Hgb, Blood group and Rh, Ultrasound exam

 Causes of APH
 Placental causes: Abruptio placentae, Placenta previa, Vasa previa(rarely).
 Uterine rupture
 Local causes of the cervix, vagina and vulva
 Preterm labour /bloody show
 Indeterminate: no cause identified even after delivery and examining the placenta

2.3.1 Abruption Placentae

 Definition: is a premature separation of the whole or part of a normally

implanted placenta from uterine bleeding after 28 week

Diagnosis
 Clinical presentation –depend on the degree of abruption
o Severe abruption
 Heavy vaginal bleeding
 severe frequent uterine contraction
 fetal distress
 coagulopathy
 vital sign derangement (hypotension, shock)
 o Mild /moderate abruption
 mild/moderate of vaginal bleeding
 Mild /moderate abdominal pain
 Normal maternal vital sign
 No fetal distress
o Lab-CBC, blood group and Rh, fibrinogen level
o Imaging USG is specific but not sensitive it can’t rule out abruption
 Maternal Complications
o hemorrhagic shock
o DIC
o utero-placental insufficiency
 Fetal complication
o IUGR
o fetal distress
o IUFD

Management option for APH

 Initial stabilization(ABC’s)
o Open double iv line, sent sample for BLG/RH and cross match resusitate with
fluid and blood based on patient response
 Delivery is the definitive management.
o expectant management (admission, steroid administration)
 Indicated-for milder abruption or remote from term
 Aim of management- to prevent prematurity.
o Immediate delivery
 For Moderate and severe abruption (irrespective of gestational age)
 abruption at term (irrespective of degree)
 Mode of delivery is vaginal
 Cesarean section

 Is indicated for severe bleeding endangering maternal life and

fetal distress, when vaginal delivery seems unlikely within a
 reasonable time and for other obstetrics indication.

Coagulation defect must be corrected early.

2.3.2 Placenta Previa

 Definition: is the presence of placental tissue lying adjacent to or overlying the

internal cervical.
 Placenta previa is classified based on nearness of the placental edge to internal-os of
the cervix:
o Low lying placenta
o Marginal placenta previa
o Major placenta previa (may be partial or total)

Diagnosis
 Clinical presentation
o Painless vaginal bleeding
o Brisk, bright red bleeding
o Do not perform digital vaginal exam
 Lab-CBC, blood group and Rh, fibrinogen level
 Imaging USG- helps for confirmation
Treatment
 Initial stabilization(ABC’s)
o Open double iv line, sent sample for BLG/RH and cross match resuscitate
with fluid and blood based on patient response
 Delivery is the definitive management of placenta previa. In cases of mild and non-
recurrent bleeding, do conservative management to prevent prematurity.
o Mode of delivery: Cesarean section.
o Vaginal delivery may be considered if low lying placenta.
o
2.3.3 Local Causes
 All local causes of APH have minimal spotting or bleeding. An exception to such
a presentation is the occasional profuse bleeding of ruptured vaginal varicose
 vein. Once placenta previa is excluded, digital and speculum examination may
confirm the specific local cause.

 Summary
o Vaginal bleeding during pregnancy is categorized depending on
gestational age
o Ectopic pregnancy should be excluded in patients with abdominal pain and
vaginal bleeding
o Do not perform digital vaginal or speculum exam until placenta
previa ruled out
 13.3 Post Partum Hemorrhage (PPH)

Objectives
At the end of this session, participants are expected to
 Diagnose PPH
 Identify causes for PPH
 Know management principles for PPH

 Definition:-Vaginal bleeding > 500ml after singleton vaginal delivery of >28 weeks. (If
cesarean delivery or multiple vaginal birth, bleeding >1000ml)

 Evaluation of PPH
o Vital signs, estimate the blood loss, uterine size and extent of contraction,
completeness of the placenta.

 Causes of PPH

 Atonic Uterus (Uterus not contracted)

o The most common cause of primary PPH.
o Hypotonic uterus leads retention of the placenta and excessive bleeding.
o Diagnose if: soft, not contracted uterus with fundus above the umbilicus.
 Retained placenta
o The common cause of placental retention is poor uterine contraction.
o In retention of the placenta without bleeding, pathological adherence
(accreta, increta and percreta) should be considered.
o Manual removal of the placenta has to be done in the operating room with
all the preparation for laparotomy and possible hysterectomy.
 Traumatic causes
 o Risk factors for tears of the birth canal (including uterine rupture) and
PPH: Fetopelvic disproportion (leading to obstructed labor), instrumental
deliveries and scarred uterus.
o Diagnosis: bright red (arterial) bleeding with a contracted uterus.
 Coagulation defects
o Risk factors: abruption placenta, intrauterine fetal death, infection etc.
o Physical examination: gross haemostatic failure is revealed.
o Bed side clotting tests and deranged laboratory coagulation profiles
support the diagnosis.
 Acute inversion of the uterus
o The uterus may rarely turn inside-out during delivery. Causes shock by
bleeding or neurogenic shock due to increased vagal tone from stretching
of the pelvic parasympathetic nerves.
o With the placenta detached, is described as cherry red mass.
Management of PPH

 Once PPH is diagnosed, shout for help and gather the team
 Immediately initiate resuscitation, and perform diagnostic and treatment activities
promptly.
 ABCs first and while stabilizing initiate specific treatment. If the cause is not known,
do the following:
o Retained placenta: PPH with undelivered placenta:
 Apply controlled cord traction (CCT)
 If CCT fails, manual removal of the placenta in operating room
 Consider laparatomy for possible pathological adherence if both fails.
o Atonic uterus: if PPH with delivered placenta and atonic uterus:
 Stimulate contraction by massaging the uterus.
 Start oxytocine infusion (20IU/1000ml, 30drops/minute).
 If there is no response, perform bimanual compression of the uterus;
consider compression of the abdominal aorta.
 Administer other uterotonics such as misoprostol (800mcg sublingual)
or ergometrine 0.2mg IM. If persistent bleeding, consider uterine
tamponade with intrauterine balloon or condom tamponade (condom
tied to end of Foley catheter, inserted into uterus, and filled with
350ccs NS).
 If there is no response subsequent management involves laparotomy
uterine or utero-ovarian artery ligation, or hysterectomy.
o Genital trauma: if PPH with delivered placenta and well contracted uterus:
 Explore the genital tract manually and using speculum and repair
vaginal/cervical tear; if uterine rupture detected laparatomy is
indicated.
o Clotting abnormality: Correct with fresh frozen plasma or whole blood.
o PPH after acute inversion of the uterus: under appropriate analgesia, apply:
 Immediate gentle upward transvaginal pressure.
  The Johnson technique calls for lifting the uterus and the cervix into
the abdominal cavity with the fingers in the fornix and the inverted
uterine fundus on the palm.
 Gently push the fundus back through the cervix. The operator’s hand
should be kept in the uterus until the fundus begins to climb up. If the
placenta is still attached, it should not be removed until after the uterus
is replaced through the cervix. Tocolysis may be used.
 Oxytocin only after successful replacement. If this fails unsuccessful
(in delayed recognition) laparotomy for abdominal replacement is
indicated.

Summary

 PPH is a life threatening obstetric emergency

 PPH should be prevented by active management of third stage
of labor
 Rapid diagnosis and intervention is mandatory
 Resuscitation is the cornerstone of management

13.4 Trauma during Pregnancy

Objectives
At the end of this session, participant are expected to
o Understand approach to pregnant patients with trauma
o Describe management principles of trauma in pregnancy
o Describe disposition plan of patients with mild trauma
 Approach to trauma in pregnacy

 Approach patient according to ATLS

 Air way-
o Maintain airway patency and immobilize cervical spine if necessary
 Breathing-
o If breathing inadequate, assist with bag-valve-mask ventilation with
high flow oxygen via mask with reservoir
 Circulation:
o put the patient on monitoring (both maternal and fetal) pulse, BP,
capillary refill. Secure double I/V line
o Sent sample for cross match resuscitate with two bags of NS
o Lie patient flat in left lateral position or at least have right hip elevated
if possible (can tilt the trauma board as a whole if on a trauma board
and manipulate the uterus to the left side) this will avoid supine
hypotension syndrome Prepare and give blood product if
needed(FAST)
o Do bed side USG
 Test neurological disability

Minor Trauma

 Up to 22 weeks - Routine trauma care with confirmation of FHTs

 After 22 weeks (including falls, whether abdomen was hit or not)
o Routine trauma care. Continuous fetal monitoring/tocograph for 4 hours after
trauma.
o Patient may be discharged after this time if above is reassuring.
o Patient should return if “tightening” or back pain.
o Patient should also return for repeat monitoring at 24 hours (bleeding caused
by mild/small marginal separations that are the result of trauma can dissect
 into myometrium or under placenta and cause PTL and/or fetal distress after
initial trauma, usually 24- 48 hours after)
Summary
o Approach to pregnant with trauma should follow ATLS and team approach
o Fluid resuscitation should be twice that of the non pregnant patients
o Resuscitating the mother is resuscitating the baby
o Left lateral position should be done to avoid caval compression
o Strict fetal monitoring is recommended .