MINISTRY OF HEALTH- ETHIOPIA

NATIONAL INTEGRATED EMERGENCY MEDICINE

TRAINING

Participants manual

September, 2021

ADDIS ABABA, ETHIOPIA

I
TABLE OF CONTENT
Contents Page

FORWARD ........................................................................................................................................... VI

ACKNOWLEDGEMENT .......................................................................... Error! Bookmark not defined.

TABLE OF CONTENT ........................................................................................................................... II

ABBREVIATIONS AND ACRONYMS ................................................................................................ VI

LIST OF TABLES ................................................................................................................................ XII

LIST OF FIGURES .............................................................................................................................. XIII

CHAPTER ONE ................................................................................................................................... 16

1. EMERGENCY MEDICAL SERVICES SYSTEM (EMSS) .............................................................. 1

1.1 Historical back ground ................................................................................................................... 2

1.2 Rationale of facility emergency development in Ethiopia ............................................................... 3

1.3 EMSS Structure ........................................................................................................................... 5

1.4 Facility emergency service ..................................................................................................... 10

1.5 ED/ER Work Flow ................................................................................................................. 11

1.6 Communication in ED ............................................................................................................ 13

1.7 Summary ..................................................................................................................................... 14

CHATER TWO..................................................................................................................................... 15

2. ADULT TRIAGE ........................................................................................................................... 15

2.1 Triage .................................................................................................................................... 15

2.2 Benefits of triage .................................................................................................................... 16

2.3 Organization and prioritization of emergency patients ............................................................ 17

2.4 Clinical Activities of Triage ................................................................................................... 17

2.5 Triage Acuity Level/ Category ............................................................................................... 18

2.6 Summary ............................................................................................................................... 20

CHAPTER THREE ............................................................................................................................... 21

II
3. RESUCITATION ........................................................................................................................... 21

3.1 Basic Life Support (BLS) ....................................................................................................... 22

3.2 Approach to critically ill Patient ............................................................................................... 3

3.3 Airway and Breathing Assessment and Management .............................................................. 13

3.4 Oxygen therapy and none invasive positive pressure ventilation ............................................. 28

3.5 Introduction to basic ECG ...................................................................................................... 37

3.6 Arrhythmia / Dysrhythmia...................................................................................................... 51

3.7 Cardiac arrest resuscitation ..................................................................................................... 61

3.9 Approach to shock ................................................................................................................. 71

3.10 Approach to altered mental status ........................................................................................... 81

3.11 Summary ................................................................................................................................... 86

CHAPTER FOUR ................................................................................................................................. 87

4. COMMON MEDICAL EMERGENCIES ....................................................................................... 87

4.1 Asthma .................................................................................................................................. 88

4.2 Heart failure ........................................................................................................................... 93

4.3 Acute coronary syndrome ....................................................................................................... 99

4.4 Diabetic Ketoacidosis (DKA) ............................................................................................... 106

4.5 Emergency management of hypoglycemia ............................................................................ 110

4.6 Seizure ................................................................................................................................. 112

4.7 Status Epilepticus ................................................................................................................. 116

4.8 Approach to poisoning ......................................................................................................... 118

4.9 Summary ................................................................................................................................... 123

CHAPTER FIVE ................................................................................................................................. 124

5. ASSESSMENT AND MANAGEMENT OF TRAUMA ............................................................... 124

5.1 Approach to traumatic Patient .............................................................................................. 125

III
 5.2 Chest trauma ........................................................................................................................ 135

5.4 Head trauma ......................................................................................................................... 149

5.5 Management of burn ............................................................................................................ 155

CHAPTER SIX ................................................................................................................................... 160

6. COMMON GYN/OBS EMERGENCIES...................................................................................... 160

5.6 Summary ................................................................................................................................... 159

6.1. Hypertensive Disorder of Pregnancy .................................................................................... 161

6.2. Vaginal bleeding during pregnancy ...................................................................................... 167

6.3 Post-Partum Hemorrhage (PPH) ........................................................................................... 173

6.4 Trauma during Pregnancy .................................................................................................... 175

CHAPTER SEVEN ............................................................................................................................. 178

7. COMMON PEDIATRICS EMERGENCY ................................................................................... 178

6.5 Summary ................................................................................................................................... 177

7.1 Pediatric triage ..................................................................................................................... 179

7.2 Pediatrics Airway ................................................................................................................. 182

7.3 Pediatrics Respiratory Emergency ........................................................................................ 185

7.4 Pediatrics Circulation ........................................................................................................... 188

7.5 Basic life support ................................................................................................................. 191

7.6 Management of Pediatrics Burn............................................................................................ 195

7.7 Pediatrics Snake bite and poisoning ...................................................................................... 197

7.8 Child hood poisoning ........................................................................................................... 198

7.9 Newborn Resuscitation......................................................................................................... 200

7.10 Childhood seizure management ............................................................................................ 201

7.11 Summary ................................................................................................................................. 204

IV
CHAPTER EIGHT .............................................................................................................................. 205

8. DISASTER PREPAREDNESS AND RESPONSE ....................................................................... 205

8.1 Introduction to Disaster ........................................................................................................ 206

8.2 Disaster preparedness and response ...................................................................................... 208

8.3 Types of Disaster Preparedness and Response ...................................................................... 210

8.4 Health facility disaster preparedness and response ................................................................ 216

8.5 Summary ................................................................................................................................... 223

9. REFERENCES............................................................................................................................. 224

V
FORWARD

The Ethiopia Ministry of Health (MOH) has been leading a sector wide reform effort aimed at
significantly improving the quality and accessibility of health service at all levels of the country’.
As the part of this reform, health facilities throughout the country have been streamlining there
operational process and building their capacities with a view to making their services more
effective and efficient.

Recognizing the importance of strengthening emergency services at all level; pre facility and
facility level is one of the priority areas. Obtaining and equipping ambulances and ongoing
initiatives towards increasing number of Emergency medical technician/paramedics to promote
pre facility health care and improving accessibility of health facilities for mothers and acutely
ill or injured patients are some off the activities on progress.

At health facility level recognizing services into emergency and nonemergency staffing by case
teams with a well-rounded skill mix, equipping emergency units in hospitals with triage and
resuscitation equipment’s, supporting hospitals with on job emergency medicine trainings are
areas getting focus on the improvement process of intra facility emergency services.

The national integrated emergency medicine training focuses on common emergency health
problems of all age and sex, and aims on the primary emergency care approach, resuscitation and
stabilization in emergency department or emergency rooms until patients will stream to their
respective departments. This manual contains facilitator guide, participant manual, practical
sessions, case scenario and pretest. While primarily intended for training of hospital personnel,
it is hoped that health professionals across all level of national health facilities will also find
these guideline to be useful. Mid-level and high level health professionals working in health
facilities can use this manual as a reference.

Revision of the first document was required because of the update of different scientific
managements and algorithms in the emergency care which should be included in the previous
document .This document will help emergency professionals to be up-to-date and will help them
to guide their clinical management by improving their knowledge and skill.

VI
At this venture, I would like to take this opportunity to express my profound appreciation to all
partners that have participated in the revision and update of this important reference and training
document. Special thanks go to our colleagues’ from St.Paul Hospital Millennium Medical
College ,Black lion Hospital, AaBET Hospital ,St Peter Hospital and Yekatit 12 hospitals for
mobilizing specialists for the development of this reference guideline.

Dr. Alegnta G/yesus

Emergency and Critical care Directorate Director

VII
 APPROVAL STATEMENT OF THE MINISTRY

The Federal Ministry of health of Ethiopia has been working towards standardization and
institutionalization of In-Service Trainings (IST) at a national level. As part of this initiative, the
ministry developed a national in-service training directive and implementation guide for the
health sector. The directive requires all in-service training materials fulfill the standards set in the
implementation guide to ensure the quality of in-service training materials. Accordingly, the
ministry reviews and approves existing training materials based on the IST standardization
checklist annexed on the IST implementation guide.

As part of the national IST quality control process, this National Integrated Emergency
Medicine Training package has been reviewed and revised based on the standardization checklist
and approved by the ministry in September, 2021.

Assegid Samuel Cheru

Human Resource for Health Development Directorate
Director
Ministry of Health- Ethiopia

VIII
ACKNOWLEDGEMENT
Ministry of Health would like to acknowledge Emergency Medicine and critical Care physicians
as well as nurses for their immense technical and academic support. The MOH would like to
acknowledge the following authors for their participation on updating the second Integrated
Emergency Medicine participants training manual.

No Name Affiliation
1 Dr. Alegnta G/Eyesus FMOH
2 Dr. Anteneh Mitiku Yekatit 12 HMC

3 Dr. Ayalew Zewdie SPHMMC

4 Dr. Beza Girma FMOH

5 Mr. Haimanot Geremew FMOH

6 Mr. Kibatu Gebre SPHMMC

7 Dr. Muluwork Tefera AAU

8 Ms. Nejat Ibrahim MOH
9 Dr. Rediet Solomon SPHMMC
10 Dr. Sofia Kebede AAU
11 Dr. Tesfaye Getachew SPHMMC
12 Dr. Tigist Tesfaye SPSH
13 Dr Bethlhem workye MOH
14 Tewabech Geremew MOH
15 Gete Fiseha MOH

IX
ABBREVIATIONS AND 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
ESI Emergency Severity Index
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

X
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
TS Triage Scale
U/A URINE ANALYSIS
UFH Unfractionated Heparin
URT Upper Respiratory Tract
UTI Urinary Tract Infection
WBCs White Blood Cell
Y12 HMC Yekatit 12 Hospital Medical College

XI
LIST OF TABLES
Tables Pages

Table 1: Triage Early warning Score (TEWS) and ESI ........................................................................... 19

Table 2: TEWS (Triage Early Warning Score) ....................................................................................... 20
Table 3: Axis determination ................................................................................................................... 45
Table 4: List of vasopressors, their dose and effects on the cardiovascular ............................................. 79
Table 5: Glasgow Coma Scale ............................................................................................................... 85
Table 6: Classification of severity of an asthma attack ........................................................................... 89
Table 7: A sample flow sheet is presented as follows: follow up sheet for a patient with shock.............. 99
Table 8: DKA follow up sheet ............................................................................................................. 109
Table 9: The commonly used antidotes ................................................................................................ 123
Table 10: GCS components and scoring............................................................................................... 132
Table 11: Indications for Laparotomy .................................................................................................. 145
Table 12: Clinical decision rule for head CT ........................................................................................ 155
Table 13: Types of disaster .................................................................................................................. 208

XII
LIST OF FIGURES
Figures Pages

Figure 1: Pre-Hospital Emergency Medical Service at big cities ............................................................... 6

Figure 2: A Standard ambulance with internal compartment. ................................................................... 7
Figure 3: Dispatch center ......................................................................................................................... 8
Figure 4: Hospital EMS structure............................................................................................................. 9
Figure 5: CPR Technique A. Two Hand Technique B. One Hand Technique ............................... 24
Figure 6: Two Finger CPR Technique.................................................................................................... 26
Figure 7: The ABCDE approach to critically ill patient ............................................................................ 4
Figure 8: Head tilt and Chin lift maneuver ............................................................................................. 16
Figure 9: Jaw thrust Maneuver ............................................................................................................... 16
Figure 10: Recovery Position ................................................................................................................. 17
Figure 11: (A) Oropharyngeal airway and figure (B) Nasopharyngeal airway ......................................... 18
Figure 12: Laryngeal mask airway ......................................................................................................... 19
Figure 13: anatomic location of Cricothyroid membrane ........................................................................ 23
Figure 14: Procedures shows needle cricothyroidotomy ......................................................................... 24
Figure 15: One-person bag-valve mask ventilation ................................................................................. 27
Figure 16: Two-handed mask seal BVM ................................................................................................ 27
Figure 17: Nasal prong .......................................................................................................................... 30
Figure 18: Simple face mask .................................................................................................................. 32
Figure 19: Non-rebreather mask (NRB) ................................................................................................. 32
Figure 20: Bag Valve Mask ................................................................................................................... 33
Figure 21: One hand C&E technic and two hands technique using jaw thrust ......................................... 34
Figure 22: Oxygen sources .................................................................................................................... 34
Figure 23: Non-Invasive positive pressure ventilation ............................................................................ 36
Figure 24: Electrical conduction pathway starting from SA node to AV node then ................................. 37
Figure 25: Electrical conduction starting from AV node ......................................................................... 38
Figure 26: Normal electrical conduction system ..................................................................................... 39
Figure 27: Cardiac electrical activity depicted on ECG .......................................................................... 39
Figure 28: ECG lead placement sites with ECG Display ........................................................................ 40
Figure 29: ECG paper (X-axis shows Time, Y–axis shows Voltage) ...................................................... 41
Figure 30: ECG paper in detail (Small box, larger box, paper speed) ...................................................... 41
Figure 31: Normal ECG......................................................................................................................... 42
Figure 32: P wave (Blue-right atrial, Red –left atrial) ............................................................................. 42
Figure 33: ST segment (red), J point (Green) ......................................................................................... 43
Figure 34: ECG rate calculation regular rhythm (5 large box ,regular ; Rate =300/5=60 beats/min) ........ 45
Figure 35: ECG rate calculation irregular rhythm (5 Intervals:5x6=30bpm) ........................................... 45
Figure 36: Normal P wave versus large P wave in Right atrial enlargement ............................................ 47
Figure 37: Pmitrale (wide P wave showing left atrial enlargement) ........................................................ 47
Figure 38: ECG showing LVH(Based on voltage criteria) ...................................................................... 48
Figure 39: ECG showing RVH (Prominent R wave in V1, ST depression with T wave .......................... 48

XIII
Figure 40: Normal vs. Prolonged QT interval ........................................................................................ 50
Figure 41: Classification of tachyarrhythmia .......................................................................................... 53
Figure 42: Paroxysmal SVT(No visible P wave, narrow QRS, Rate of 150) ........................................... 54
Figure 43: Atrial flutter (Saw toothed P wave, narrow QRS) .................................................................. 54
Figure 44: Atrial fibrillation (No well-defined P wave, Narrow QRS, Irregular) ..................................... 54
Figure 45: Ventricular tachycardia (No P wave, regular, wide QRS) ...................................................... 55
Figure 46: Ventricular fibrillation (No P wave, irregular, wide QRS) ..................................................... 55
Figure 47: Tachyarrhythmia instability signs and management............................................................... 56
Figure 48: Brady-arrhythmia ................................................................................................................. 58
Figure 49: Sinus bradycardia ................................................................................................................. 58
Figure 50: First degree AV Block .......................................................................................................... 58
Figure 51: Second-degree mobitz type 1 ................................................................................................ 59
Figure 52: Second degree mobitz type 2 ................................................................................................ 59
Figure 53: 3rd degree AV Block ............................................................................................................ 60
Figure 54: Approach to bradyarrhyhmia ................................................................................................ 60
Figure 55: Chain of survival for out of hospital cardiac arrest (OHCA) .................................................. 61
Figure 56: Chain of survival for in hospital cardiac arrest (IHCA) .......................................................... 62
Figure 57: A systole .............................................................................................................................. 63
Figure 58: Adult cardiac arrest algorithm ............................................................................................... 63
Figure 59: Sequential approach of BLS .................................................................................................. 64
Figure 60: Hemodynamic response to ‘ideal’ chest compressions. .......................................................... 66
Figure 61: Full cardiac arrest algorithm ................................................................................................. 68
Figure 62: Reversible causes of cardiac arrest and therapies ................................................................... 70
Figure 63: Post cardiac arrest algorithm ................................................................................................. 70
Figure 64: Flow chart of assessment of patient with sepsis ..................................................................... 78
Figure 65: How to use inhaler ................................................................................................................ 91
Figure 66: Anterior MI Pattern – Tombstoning .................................................................................... 102
Figure 67: Septal involvement (lead V2) and a bit laterally, as well (lead V5 and V6) .......................... 102
Figure 68: Anterior MI Pattern – Typical ST Segment Elevation .......................................................... 103
Figure 69: Timing distribution of trauma deaths compared with the historical trimodal distribution ...... 126
Figure 70: Jaw thrust ........................................................................................................................... 128
Figure 71: Cervical spine motion restriction technique ......................................................................... 129
Figure 72: Three-way valve dressing for sucking chest wound ............................................................. 130
Figure 73: Massive Hemothorax .......................................................................................................... 136
Figure 74: Flail chest ........................................................................................................................... 139
Figure 75: Chest tube insertion, the clamp is inserted through the incision and is tunneled up to the next
intercostal space. ................................................................................................................................. 140
Figure 76: Penetrating Abdominal Trauma .......................................................................................... 142
Figure 77: Red arrow showing a thin stripe of fluid in Morison's pouch. .............................................. 144
Figure 78: Pelvic stabilization with bed sheet ....................................................................................... 149
Figure 79: Head tilt chin lift ................................................................................................................. 183
Figure 80: Open air way (Jaw thrust) ................................................................................................... 183

XIV
Figure 3 Figure 81: Chest thrusts and back slap ................................................................................... 184
Figure 82: Abdominal thrusts .............................................................................................................. 185
Figure 83: Two fingers chest compression ........................................................................................... 192
Figure 84: Encircling chest compressions ............................................................................................ 193
Figure 85: Choosing appropriate size of mask ...................................................................................... 194
Figure 86: Bag mask ventilation .......................................................................................................... 194
Figure 87: Basic Command Structure Single Command ....................................................................... 212
Figure 88: shows disaster organization site at scene ............................................................................. 213
Figure 89: Activities by AMP .............................................................................................................. 214
Figure 90: Triage ................................................................................................................................. 215
Figure 91: Victims flow from entry to AMP to evacuation to hospital .................................................. 216
Figure 92: Organizational structure of the incident command system ................................................... 218
Figure 93: Simple Triage and Rapid Treatment (START). ................................................................... 220
Figure 94: Jump START for pediatrics MCI triage .............................................................................. 221
Figure 95: Triage tag ........................................................................................................................... 221

XV
INTRODUCTION TO THE MANUAL

This manual is prepared by the Emergency and Critical Care Service Directorate of the Federal
Ministry of Health to align with the national HSTP related emergency care service equity and
quality Emergency care is a medical specialty which is a field of practice based on the
knowledge and skills required for the prevention, diagnosis and management of acute and urgent
aspects of illness and injury affecting patients of all age groups with a full spectrum of
undifferentiated physical and behavioral disorders. It further encompasses an understanding of
the development of pre-hospital and in-hospital emergency medical systems and the skills
necessary for this development.

According to WHO, 52% of the mortality is caused by non-communicable diseases including

injuries .Ethiopia is one of the countries with a high burden of road traffic accidents, which is
more than 56 deaths per 10,000 vehicles. This is causing increased morbidity and mortality in the
economically active groups leading to high socio-economic 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 systems by developing guidelines and protocols.
Therefore, it’s being considered as a priority to implement 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 the
national integrated emergency manual, they will be able to train other health professionals
who are working in Emergency rooms/ departments.
The core competency of this training course is:

 Evaluate and Triage patients

 Manage and Access critically ill/injured patients in all age groups and obstetric

 Promptly utilize emergency drugs and equipment’s effectively

 Establish and develop emergency medical service system

Course Syllabus

Course Description

This 6 days course is designed to equip participants on the basic emergency care, knowledge,
skill and attitude, they need to use to save lives and limbs in hospital settings with available
resources.

Course Goal

To improve competency of health professionals on emergency patients’ assessment and

management of critically sick/injured patients.

Participant learning Objectives

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

 Describe EMS structure and functions

 Demonstrate adult triage

 Manage airway and breathing problems

 Mange Medical emergency

 Assess patients with trauma

 Identify common gynecological and obstetric emergencies

 Practice common pediatric emergencies

 Manage Disaster preparedness and response

Training methods

 Interactive lectures

 Demonstration

 Case study

 Small group discussions

 Individual and group exercise

 Simulations

 Videotapes and discussions

Training Materials/Equipment

 National Integrated Emergency Medicine Training Participant Manual

 National integrated Emergency Medicine Training Facilitator Guide

 Ethiopian Hospital Reform Implementation Guideline

 Power Point slides

 Training videos.

 Mannequins (pediatric, neonatal, adult and obstetrics) and other trauma care equipment’s

 Laptop and LCD projectors for lecture presentations

 Flip chart, markers, pens, notebooks.

Participant’s selection criteria

 Health professional (physicians, nurses, Heath officers, and other health workers)
Trainer selection criteria

 TWG who developed this straining manual

 TOT training on National Integrated Emergency Medicine

 Basic training on National Integrated Emergency Medicine with facilitation skill training

Evaluation methods

Trainees evaluation

Formative

 Pretest

 Question and answer

 Group discussion with feedback

 Presentations with feedback

 Case studies with feedbacks

 Participant attendance

 Recap

 Practical skill

Summative

 Post-course test (75 %)

 End of course evaluation

Certification criteria

 Certificate will be provided to participants who have scored more than 80% on
summative assessments with 100% attendance.

Course evaluation

 Daily evaluation

 End-of-course evaluation

 Participant oral feedbacks

Suggested class size

 The number of trainees shall be 20 - 25 in each training session and at least 4 trainers.

Course Duration

 6 days training for basic and 7-days for TOT.

Training venue

 The training will be conducted at selected national and regional IST centers/CPD
providers having appropriate facilities, trainers, and attachment health facilities.

Certification criteria:

 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 results and 100% of attendance.

Continuing Educational Unit (CEUs)= 15 CEU

Course Schedule
Day Time Activity Facilitator Moderator
1
8:30 – 8:45 Registration
8:45 – 9:15 Welcome and introduction
9:15 – 9:45 Pre-Test
9:45 – Introduction to EMS
10:45
10:45 – Tea Break
11:00
11:00 – Adult Triage
12:00
12:00 – Lunch
1:00
1:00 – 2:00 Approach to critically ill
patient
2:00 – 2:15 Approach to critically ill
patient Discussions
2:15 – 3:30 Airway and Breathing
Assessment with practice
3:30 – 3:45 Tea break
3:45 – 5:00 Airway and Breathing
Assessment with practice
Day 8:30 – 8:45 Recap
2
8:45- Practical Session Airway
10:15 and Breathing
10:15- Tea break
10:30
10:30– Approach to Basic ECG
12:30
12:30 – Lunch
1:30
1:30 – 3:00 Common Arrhythmia
3:00 – 3:30 Common Arrhythmia
discussion
3:30 – 3:45 Tea break
3:45 – 4:45 Cardiac Arrest
4:45 – 5:00 Wrap up and daily
evaluation
Day 8:30 – 8:45 Recap
3
8:45 – Video show and practice
10:45 on CPR
 10:45 – Tea break
11:00
11:00 – Approach to shock
12:30
12:30 – Lunch
1:30
1:30 – 2:15 Altered mental status
2:15- ACS
3:3:15
3:15-3:30 Tea Break
3:30 – 4:30 Heart failure and
Pulmonary edema
4:30– 5:15 Acute Asthma
5:15 – 5:20 Daily evaluation and rap
up
Day 8:30 – 9:00 Recap
4
9:00– 9:40 Seizures and status
epileptics
9:40-10:40 DKA and Hypoglycemia
10: 40 – Tea Break
11:00
11:00 – Approach to poisoning
12:30
12:30 – Lunch
1:30
1:30 – 3:00 Gyn/Obs
3:00 – 3:15 Tea Break
3:15– 4:45 Gyn/Obs
4:45 – 5:00 Wrap up and daily
evaluation
Day 8:30 – 8:45 Recap
5
8:45– Approach to trauma with
11:15 practice
11:15 – Tea Break
11:30
11:30– Chest trauma and practices
12:30
12:30 – Lunch
1:30
1:30 – 2:45 Abdomen and pelvic
trauma
2:45 – 3:00 Tea break
 3:00 – 4:00 Head trauma
4:00- Burn
4:30
4:30 – 5:00 Wrap up and daily
evaluation
Day 8:30 – 9:00 Recap
6
9:00-10:30 Pediatrics Emergency
10:30- Tea break
10:45
10:45 - Pediatric Emergency
12:30
12:30 – Lunch
1:30
1:30 – 3:15 Pediatric emergency
3:15 – 3:30 Tea Break
3:00 – 4:20 Pediatric emergency
4:20-4:45 Post test
4:45-5:00 Certificate and closure
CHAPTER ONE: EMERGENCY MEDICAL SERVICES SYSTEM
(EMSS)
Duration: 1hr

Chapter Description: Emergency Medical Service System /EMSS/ is network of services

and resources coordinated to provide aid and medical assistance from primary response to
definitive care. This chapter describes on; Historical background and rationale of Emergency
care development in Ethiopia, EMSS Structure, Pre-hospital EMS, In Hospital Components of
EMSS, ER work flow and Communication in ED.

Chapter objectives:
By the end of this chapter the participants will be able to:
 Describe historical developments, list activities and components, pre
hospital and facility structural activities of EMSS.
Enabling objectives:
By the end of this training session, the participants will be able to:
 Explain EMSS

 Describe historical background of EMSS.

 List major activities and components of EMS

 Portray pre hospital structures of EMS and its activities

 Depict structural organization facility emergency service

 Describe ED communications

Outline

1.1 Historical back ground.

1.2 Rationale of Emergency care development in Ethiopia.
1.3 EMSS Structure
1.4 Communication in ER
1.5 Summary

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 Group Exercise:

Be in group of 4

Discuss on EMS system in Ethiopia

Time: 10 Minutes

Introduction
Emergency Medical Service System (EMSS) is 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 back ground

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 pre hospital emergency care from trained professionals.

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 became
obvious that injured soldiers benefited from emergency care in the field before 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 1960s. During that decade, the
National Academy of Sciences Research council advocated professional training for pre-hospital

2|P a g e
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 pre hospital 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 and quality emergency care; triaging, resuscitation, trauma care, trauma
Activation, documentation…etc. for facility emergency. 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 facility emergency development in Ethiopia

In Ethiopia except for recent efforts to establish and organize pre-hospital services there was no
formal EM system .In addition when emergency condition arises family or friends would take
patients to nearby health facility or to traditional healers. Although means of transport varies in
different regions and districts, by and large in the rural areas patients are carried by community
members on traditionally prepared stretchers or back of animals.

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. 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 a double burden of diseases. Ethiopian population is relatively
young with a high growth rate and there are large maternal 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 into
facility-based and pre-hospital Care. In hospital care, the Emergency directorate is one of the

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three directorates in addition to inpatient and outpatient ones Pre-hospital care in Ethiopia is a
new approach, which has come into attention in the past few years. Until a few years ago, the
Red Cross and hospital/health center ambulances have been transferring patients from place to
place but with no medical care in the ambulance.

FMOH directive for rearrangement of emergency service in health facilities , established a reform
program in September 2010, Categorizing hospital services according to three types: emergency
services, ambulatory care, and inpatient services. This created new impetus to advance
emergency medicine initiatives under its own independent management and resource structure.
Many hospitals in the country have adopted this principle and are allocating revenues for
emergency medical services development. Through this initiative, the Saint Paul Hospital
established a new Emergency Department, which began operating in 2011.

1.3.1 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),
 The 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.
1.3.2 Components of EMS, current standards include
 Regulation and policy, each state/country must have laws, regulations, policies, and
procedures that govern its EMS system.
 Resource management, each state/country must have central control of EMS resource so
that each locality and all patients have equal access to acceptable emergency care.

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  Human resources and training, all personnel who staff ambulance and transport patients
must be trained to at least the EMT-Basic level. In Emergency facility professionals
should be trained, in Emergency patient care, trauma patient handling and care, triage,
critical patient resuscitation, communication…etc.
 Transportation, Patients must be provided with safe reliable transportation by ground or
air ambulance.
 Facilities (different levels of health facilities), each seriously ill or injured patient must be
delivered in a timely manner to an appropriate medical facility. Quality and timely
appropriate care for patients
 Communications, a system of communications must be in place to provide public access
to the system and communication among dispatchers, EMS personnel, and hospital enter
departmental and inter facility.
 Public information and education, EMS Personnel should participate in a 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 that oversees patient care and delegates appropriate medical practice to EMT
basics and other EMS personnel.
 Trauma systems (an organized network of resources and procedures for providing care to
critically injured patients), each state/country 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 patients 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

EMSS structure is classified in to pre hospital and facility Emergency. Major activities of EMSS
are Prevention of injury and acute illness; recognition of the event by bystanders; activation of
the EMS system, bystander care; arrival of First responders, emergency care at the scene and
transport to the receiving facility and Components of EMS current standards are;

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 1. Regulation and policy.
2. Resource management.
3. Human resources and training.
4. Transportation
5. Facilities
6. Communications

7. Public information and education

8. Medical oversight
9. Trauma systems
10. Evaluation
1.3.1 Pre-hospital EMS in big city

Fire Department

Fire Fighters Rescue Ambulance Service

Figure 1: Pre-Hospital Emergency Medical Service at big cities

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 danger to themselves and the
others, and take appropriate measures to ensure their safety on the scene (environmental,
electricity, chemicals, radiation…etc.)

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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.

Figure 2: A Standard ambulance with internal compartment.

Dispatch center and Ambulance stations: The public must be able to notify the EMS system
promptly for the EMS system to be of value. The most efficient way to do so is through a 3-digit
system in which trained dispatchers collect information from the caller and activate the
appropriate level of response.

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Figure 3: Dispatch center

Pre-hospital Levels of EMSS Training

There are Four Internationally accepted levels of pre-hospital 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 arrives.
EMT Basics: The basic course prepares an EMT Basics to function in three areas
 Control life treating situations,
 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,
 Using non-medical skills such as 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
Is EMT who has completed training beyond the EMT-Basics level.
The training includes the human system, Emergency pharmacology, venous access and
medication administration, patient assessment, medical conditions, traumatic injuries, obstetrics,

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neonatal resuscitation, pediatrics and geriatrics. Additional skill includes; manual defibrillation,
medication administration, endotracheal intubation and use of alternative advanced airway
devices, and ECG interpretation

Paramedics

 Are EMTs who has advanced training in patient assessment, medical emergencies,
pharmacology, trauma, obstetrics, rescue behavioral emergencies, and other advanced
EMS activities.
 They have a wider scope of knowledge of disease processes and provide advanced life
support for patients with a variety of problems.
 The other responsibilities of an EMT-Paramedic are providing patient education and
community injury and illness prevention activities.
1.3.2 Facility Emergency 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.

Figure 4: Hospital EMS structure

In our context, coordinated Emergency medical support is provided at the health facility level
with a 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

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patients with a broad spectrum of illnesses and injuries, which could be life-threatening and
requiring immediate attention.

1.4 Facility emergency service

A typical emergency department has several different areas; each specialized for patients with
particular severities or types of illness. Facility emergency service should be:
 ER clearly labeled and easily visible.
 Should have an ambulance parking near Emergency area
 Emergency service lay out:
 Emergency room should be leveled and clearly seen
 Emergency Department should have waiting area visible to triage.
 ED should have short stay beds
 The ER should have 24 hrs. Accesses to services; ER triage, laboratory, pharmacy,
radiology, Operation theater, Blood product service, etc.
 Disaster preparedness plan and trauma care service.
 Ambulance parking near Emergency service area and should waiting area,
1.4.1 Main rooms of Facility Emergency Department
1. In the triage area, Is situated at the at the entrance of ED. 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 to be seen directly by
a physician. The triage nurse has to go to the resuscitation area and complete the triage
form, and patients relatively stable can be sent to the waiting area while re triaging and
reassurance is maintained. The triage room should have, one examination and
resuscitation beds, emergency drugs, registration book, monitor and examination
equipment and protocols.
Triage sheets should be properly filled and attached with patient,

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, cardiac monitor, advanced airway equipment, oxygen, intravenous sets and

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 fluids, crash cart with full emergency drugs. Resuscitation areas also have ECG
machines, and portable X-ray facilities to perform chest and pelvic fractures. Other
equipment may include non-invasive ventilation (NIV), fast intubation equipment, and
portable ultrasound.
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 areas: Such as stores, laboratory, dispensary for emergency drugs, isolation rooms
and decontamination rooms have to be considered.

1.5 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 Emergency trained general practitioner, Health officers
or professional nurses. 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 the 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 lead this process in all health facilities.

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1.5.1 Emergency Department, Human resource

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

1.5.1.1 Physicians

Different categories of physicians depending on the hospital level. It includes emergency

Medicine physicians, general practitioners trained in 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
Emergency Care would take responsibility.

1.5.1.2 ED/ER Nurses

Emergency Nurse Initiates care according to the urgency in ED, consult doctors in difficulty and
so they are an integral part of the management process.

1.5.1.3 Runners/Porters

They transport only stable patients from an 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 have BLS training to handle patients professionally and even assist nurses in
delivering care.

1.5.1.4 Environment keeping/Cleaners

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

1.5.1.5 Guards

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

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1.5.1.6 Registration Rooms and officers

Registration and recording room must be adjacent and easily accessible. The system must be
designed in a modern way so that information can easily be retrieved and analyzed..

1.5.2 ED Service
 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 these are set standards, thus, mandatory not a recommendation.
 Emergency drugs and supplies should always be available and accessible, emergency
drug box/crash carts should always be filled with resuscitation and essential drugs.
 Checklist of such items must be available with periodic revision and refilling.
 There must be a standard of ED equipment and drugs to each level and specialties, this
must also be worked out and annexed.

1.6 Communication in ED

ED of hospitals needs to communicate with Dispatch center, pre-hospital care, and other health
facilities, RHB

 There should be vertical communication -with dispatch centers 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, 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).

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1.7 Summary
 Pre-hospital care activities are, detecting, reporting, response, on scene care and care on
exit. Emergency components at a facility are: triage, resuscitation, observation and
treatment area, procedure, store, pharmacy, lab, isolation and decontamination area.

 During emergency period, after being evaluated and treated, patients are transferred
according to the severity of illness/trauma or to their nearby health facility as soon as
possible.

Good communication system with team sprite within hospitals and pre-hospital level improve s
the outcome of critically ill patients EMS quality patient care and practical activities should be
monitored and evaluated by health professionals

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CHATER TWO: ADULT TRIAGE
Duration: 1hr
Chapter Description
This chapter is designed to provide participants with the knowledge, skills and attitude required
to properly and competently do adult triage documentation for patients presented to emergency
room. It focuses on having participants expand their knowledge of adult triage and attitudes
through reflection in and on action in clinical settings

Chapter objective
At the end of this chapter, participants will be able to:
 Will know and demonstrate on how to do adult triage and proper
documentation
Enabling objectives
 Describe triage during different situations
 List organization and prioritization of emergency patients
 Demonstrate triage documentation

Outline
2.1.Triage
2.2.Benefits of triage
2.3.Organization and prioritization of emergency patients
2.4.Clinical Activities of Triage
2.5.Triage Acuity Level/ Category
2.6.Summary

2.1 Triage

Group Exercise:

Be in group of 4

Discuss on Triage and its activities

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Time: 10 Minutes
Introduction

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 to
ensure that medical and nursing staff facilities are used most efficiently.
In triage, patients with the greatest need are helped first.
2.1.1 Types of triage

A. Patient to triage

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

B. 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 less often

2.1.2 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

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  Facilitate streaming of less urgent patients

2.3 Organization and prioritization of emergency patients

 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
 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

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

 All arriving patients receive a “quick look” to determine ABCD stability and “Sick”. Sick
in this sense is to mean those patients with abnormalities in airway, breathing, circulation
and neurological function
 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)

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 - Follow verbal command (CAN DO)
* All of these indicate the patients may have adequate initial oxygenation and perfusion
B. Conduct the appropriate focused history and physical examination
 Triage physical assessment
 General appearance
 ABC stability
 Focused P/E
 Pain assessment
Triage history should include
 Chief complaint
 Pain assessment
 Medications
 Allergies
 Past medical history
Investigations at triage
 Finger prick RBS
Treatment
 Follow the triage protocol
 Secure iv line, start fluid, oxygen administration as indicated
 Medication administration as indicated
C. 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

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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
Table 1: Triage Early warning Score (TEWS) and ESI

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

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Table 2: TEWS (Triage Early Warning Score)

2.6 Summary
 Triage is a process of sorting injured or sick people according to the severity of their
sickness or injury
 Triaging speed up emergency care delivery and helps to save life and limb,
improves patient satisfaction and flow, decrease overall length of stay etc
 All arriving patients receive a “quick look” to determine ABCD stability and “Sick”
 After the evaluation, score the patient's condition using the TEWS and categorize
according to ESI

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CHAPTER THREE: RESUCITATION
Duration: 13 hours

Chapter description
This course is designed to provide participants with the knowledge, skills and attitude required to
care competently and safely for critically ill patient who require resuscitation. It focuses on
improving participant’s knowledge and skill towards approach to critically ill and or in cardiac
arrest systematically and organized manner. This chapter includes approach to critically ill,
common arrhythmias and advanced cardiac resuscitation, approach to shock and patients with
altered mental status.

Chapter objectives: By the end of this chapter the participants will be able to:
 Manage critically ill patient with arrhythmias, cardiac arrest and shock
systematically with ABCD.
Enabling objectives:
By the end of this training session, the participants will be able to:
 Describe ABCDE approach to a critically ill patient
 Perform proper airway assessment and management
 Interpret normal ECG and arrhythmia systematically
 Perform high quality CPR
 Identify types of shock and manage it
 List causes and management of altered mental status

Outline

3.1. Basic Life Support

3.2. Approach to critically ill patient
3.3. Airway and breathing assessment and management
3.4. Oxygen Therapy
3.5. Introduction to ECG
3.6. Arrhythmia
3.7. Advanced cardiac resuscitation
3.8. Approach to shock
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3.9. Approach to altered mental status
3.10. Summary
 3.1 Basic Life Support (BLS)

Introduction: This session describes measures taken in patient with cardiac arrest at any level of
setup and outside hospital, also discusses the steps of providing BLS to arrest patient.

Group Activity

Case study

Instruction: be in a group of three to four and reflect on the following case scenario

60 years old man arrived to the ED, supported by his family. On arrival he was conscious and
communicating. During triage his main complaint was fatigue and palpitation. While you are
doing the triage documentation he collapsed and you checked the pulse and no pulse

 What will be the main cause of his collapse?

 Describe your approach

Time: 30 minutes

Cardiac arrest is a common problem in emergency &intensive care setup and it needs prompt
recognition and immediate resuscitation. Cardiac arrest is cessation of circulation of blood
because of absent or ineffective cardiac mechanical activity. Cessation of circulation and
resulting organ ischemia can cause cell, organ and patient death if not rapidly reversed. In adults
the main cause of cardiac arrest is underlying cardiac problem, where as in 70% pediatric age
respiratory failure cause cardiac arrest. In contrast to adults, sudden cardiac arrest is uncommon
in pediatrics. Anticipation is a key to the prevention of cardiopulmonary arrests. If it occurs
immediate detection and cardiopulmonary resuscitation (CPR) is needed, and this chapter will
enable the trainee to do the procedure with a good confidence.

3.1.1 Introduction to BLS

BLS- It is a skill, which includes chest compression and artificial ventilation to provide blood
flow and oxygen to preserve the brain function until measures are taken to restore spontaneous
blood circulation. Its Components are: It is chest compression and artificial ventilation or CPR. It

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is initiated anywhere by a person who is trained to do so, and most of the time it doesn’t need
special equipment. It has to be followed by ACLS for restoration of cardiac activity.

Advanced cardiac Life Support (ACLS) and Pediatric Advanced Life Support (PALS)–it is
a continuation of BLS with better setup and expertise, and hence in hospital setup like ICU this
procedure is immediately started. In addition to the basic CPR, defibrillation, pharmacologic
treatment and advanced airway management is included. Survival from cardiac arrest is highly
dependent on high quality CPR, ACLS or PALS &Post cardiac arrest care. These steps and care
is also described as chain of survival.

Chain of survival: For effective result of resuscitation there should be:early access to the
patient or victim, early CPR initiation, early defibrillation, and early & effective post
resuscitation care.

3.1.2 Approach to pulseless patient

Check patient responsiveness: Assess to make sure the scene is safe for you to respond to the
down patient. When patient is unresponsive or suspected to have cardiac arrest call for help,
Position the victim and start CPR. During resuscitation function as a team and have a team leader
that guides the quality of the CPR.

 The recommendation in single rescuer resuscitation is to initiate chest compressions

before giving rescue breaths (C-A-B rather than A-B-C) to reduce delay to first
compression and also all rescuers can start chest compression immediately because
airway management requires manipulation and positioning of the patient.
 If alone and collapse is un witnessed: perform 2 minutes of CPR and call the emergency
response team and bring an AED to the patient but if alone collapse is witnessed: call the
emergency response team and bring an AED first, then start CPR

IF pulse present

 No breathing, provide rescue breathing - every 3 seconds for infants, and every 5 - 6
seconds older children and adults.

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If no pulse

 No carotid pulse in adult, or no femoral or brachial pulse in pediatrics (carotid are not
choice for pediatrics because of short neck) - start chest compression and artificial
ventilation on hard flat surface, if possible.
 Adults - compressions should be performed over the lower half of the sternum with the
heel of two hands as depicted below in Figure X
 Older Children- In addition to the above method, the heel of one hand can be applied
over the lower half of the sternum during CPR in older children.

Figure 5: CPR Technique A. Two Hand Technique B. One Hand Technique

Infant: One Hand technique- This technique is recommended when there is a single rescuer.
Compressions are performed with index and middle fingers, placed on the sternum just below the
nipple see figure X .

 The two thumb-encircling hands technique- is suggested when there are two
rescuers. The thorax is encircled with both hands and cardiac compressions are
performed with the thumbs. The thumbs compress over the lower half of the
 Sternum, avoiding the xiphoid process, while the fingers are spread around the
thorax

 Figure 6: Two Finger CPR Technique



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Figure 6: Two Finger CPR Technique

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Circulation

 There is continued emphasis on the characteristics of high-quality CPR:

 Press the heels of the hands straight dawn on the center of the chest.
 PUSH FAST: give compressions at a rate of 100 -120 per min. (Count compressions out
loud).
 Give 30 compressions to 2 breaths with one or two rescuer CPR in adult. But 30:2 ratios
in single rescuer and 15:2 ratios in two or more rescuers in pediatrics.
 PUSH HARD Depress the chest at least 5cm(2 inches) but not greater than
6cm(2.4inches) depth in adults or 1/3rd -1/5th of chest antero-posterior diameter in infants
and older children
 ALLOW COMPLETE CHEST RECOIL- release completely, allowing the chest
completely recoil in each compression. This allows the heart to refill with blood.
 MINIMIZE INTERUPTIONS -try to limit interruptions in chest compressions to 10
seconds or as needed for interventions (e.g. defibrillation) ideally compressions are
interrupted only for ventilation (until advanced airway is secured) and rhythm check and
actual shock delivery.
 Once an advanced airway is in place, provide continuous compression and without pause
for ventilation.
 AVOID EXESSIVE VENTILATION –each rescue breath should be given over 1
second and each rescue breath should result in visible chest raise.
 After every 5 cycle/2min. or sooner when tired check for spontaneous breathing and
circulation for 5 sec
 Rapid identification and intervention of shock is an essential component of pediatric
resuscitation.

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1. Air way

 To open the air way, use head tilt and chin lift maneuver
 In suspected trauma stabilize the neck before airway opening maneuver.
 Use jaw thrust in patients with suspicion of cervical spine injury

2. Breathing

 In cardiac arrest give 30 chest compressions immediately before any rescue breaths are
attempted and give two rescue breaths mouth to mouth if the incidence is outside health
facility or with bag valve mask (BVM) when available. For adult for both single and two
rescuers 30:2 for single rescue in pediatrics 15:2 for two rescuer in pediatrics. Do not over
inflate the chest; connect the BVM with O2 source.
3. Continue BLS until ACLS team arrives or you are tired
4. Asses patient after every five 30:2 sickles
5. Your assessment shouldn’t take more than 6sec
6. When the ACLS team arrives give brief information on the patient’s condition and your
activities
7. Assist the team as required

3.3.3 Practical session on BLS

3.2 Approach to critically ill Patient

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

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  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.

Figure 7: The ABCDE approach to critically ill patient

3.2.1 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 more critical patients 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.

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Potential critically ill patients may present with:

 Altered mental status (unresponsive or confused/agitated)

 Noisy respiration (gurgling, stridor, and 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)

3.2.2 The ABCDE Sequence

 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

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 through the sequence.
A – Airway with C-spine Control

3.2.3 Focused clinical assessment for impending/actual airway compromise:

 Noisy respirations (gurgling, stridor, and 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
3.2.4 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 cricothyroidotomy
 The airway is always associated with the phrase, “with c-spine control”.

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  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 slid 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.
3.2.5 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

3.2.6 Focused clinical assessment for evidence respiratory failure

 Cyanosis, inability to speak full sentences without needing a breath, confused/agitated

or unresponsive with:
 Rate: too slow, shallow, agonal, gasping (age-dependent, generally rates <10 in an
adult are abnormal)
 Rate: too fast and/or deep (again age-dependent but >20 in a resting adult is

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 abnormal, and > 30 is significantly abnormal)
 Abnormal lung sounds:
 Unilateral decreased breath sounds (either dull or hyper-resonant)
 Wheezing or poor air movement
 Rales (fine crepitation) or rhonchi
 Chest wall abnormalities affecting breathing dynamics – flail chest/open punctures
 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.

 If still not clear as to a management strategy, add point-of-care testing, i.e., lung
sonography or upright portable CXR.
3.2.7 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

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 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
3.2.8 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

 Tachycardia: > 100 abnormal in adults, > 150 frequently clinically symptomatic.
 Bradycardia: < 60 abnormal, < 30 frequently clinically symptomatic.
 Hypotension: systolic < 90
 Perfusion and cardiovascular assessment may include
 Skin – i.e., cool, diaphoresis, pale, poor capillary refill, hives, erythema
 Mental status changes – i.e., confusion, slow responses, agitation
 Rhythm/quality of pulses in all four extremities
 Assessment for hidden blood loss, i.e., rectal for melena, pelvic instability, pulsatile
abdominal mass

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  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:

 Signs of end-organ damage/involvement, i.e., encephalopathy and/or papilledema,

pulmonary edema, cardiac ischemia, renal impairment, and/or neurological
abnormalities.
 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.
3.2.9 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 crossmatch 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
flank 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).
 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) –

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 cardiovert per ACLS
 Unstable bradydysrhythmia – administer meds (i.e., Atropine, etc.)/place external
pacemaker per ACLS
3.2.10 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)
3.2.11 Management Algorithm for Disability problems

 Fix the airway, breathing and circulation conditions first

 Check fingerstick 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

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 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 log rolling.
 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.,

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 hydrocarbon pesticides), caustics, radiation or objects causing continued burns, etc.
3.2.12 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.

3.3 Airway and Breathing Assessment and Management

3.3.1 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:

 There is an open pathway between a patient’s lungs and the atmosphere.

 The lungs are safe from aspiration

3.3.2 Airway Emergencies, which need immediate intervention

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Causes of upper airway obstruction include:

 The patient's tongue, in patients with impaired consciousness

 Secretions in patients who are unconscious with suppressed airway reflexes
 Foreign body
 Swelling (Anaphylaxis)
 Infection ( e.g. Epiglottitis)
 Facial trauma or burn etc

3.3.3 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;

 Look for dyspnea;

 Hoarseness or weakness of the patient’s voice,
Stridor: an abnormal, high pitched sound produced by turbulent airflow through a partially
obstructed upper air way during inspiratory phase.

3.3.4 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.

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3.3.5 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.

 Presence of any foreign body or secretions –suction or remove manually if the foreign
body is reachable
 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
 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
3.3.6 Airway Opening Manuevers (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

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Figure 8: Head tilt and Chin lift maneuver
B. 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 9: Jaw thrust Maneuver

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 C. 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 has to be in left lateral position if no
contraindications.

Figure 10: Recovery Position

3.3.7 Airway adjutants

A. 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).

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Figure 11: (A) Oropharyngeal airway and figure (B) Nasopharyngeal airway

B. Nasopharyngeal airway

 It 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

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 C. 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 12: Laryngeal mask airway

3.3.8 Advanced Airway Management

3.3.8.1 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.

A. Types of Intubation

 Rapid sequence intubation is the preferred method of intubation in emergency situation,

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 because patients NPO time is not known and due to their acute illness they have
increased sympathetic flow that makes slow GI motility.
 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
 Elective or ordinary intubation: for patients with stable condition and at least fasting
for >4hrs or empty stomack
Intubation in ED is more complicated than done in Operation Theater and found associated with
severe hypoxia and even cardiac arrest due to:

 Patients in the ED are physiologically unstable,

 The airway is not well assessed,
 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.

B. Indication for intubation:

 Respiratory arrest or failure

 Inability to protect airway
 Inability to oxygenate/ventilate
 Anticipated deterioration

C. Preparation for intubation

Prepare equipment, personal Airway experts, and more assistants present) equipment and drugs.

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Equipment can be remembered by the acronym SOAP ME

S: Suction,

O: Oxygen,

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. Maclntosh 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, bugi, 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.

P: prepare pharmacy

 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)
 Muscle relaxant (suxamethonium 100-150mg, or 0.5-1mg/kg).
Succinylcholine is contraindicated

 If there is hyperkalemia,

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  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.

ME: Monitoring equipment: ECG monitors, and pulseoxymeter

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

D. 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.
3.3.8.2 Cricothyroidotomy

The cricothyroid membrane joins the thyroid with the adjacent cricoid 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.

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This technique is used in emergency condition when intubation and ventilation are
impossible with the usual methods.

Figure 13: anatomic location of Cricothyroid membrane

A. 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.
B. Contraindications

 Children < 8 years old - Needle cricothyroidotomy with jet insufflations is preferred.

C. Complications

 Immediate: Haemorrhage, Creation of a false passage into the tissues, Hematoma

formation, Laceration of the esophagus, Laceration of the trachea,
 Longer term: Sub glottis stenosis, Laryngeal stenosis, Vocal cord paralysis hoarseness

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Figure 14: Procedures shows needle cricothyroidotomy

D. 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
3.3.9 Assessment of Breathing and Management

3.3.9.1 Assessment of Breathing

 Respiratory Rate and breathing pattern
 Increase due to lower respiratory or airway problem, pyrexia and metabolic
acidosis

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  Decrease due to fatigue: over dose of sedation drugs, or opiods , exhaustion,
poisoning
 Use of accessory muscles
 Sternocleidomastoid, Intercostal, subcostal, and 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
 Pulseoximetry
3.3.9.2 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 adjuvants if the breathing is inadequate or no breathing start assist/rescue breath
mouth to mouth or with bag valve mask.
A. 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 almost
always 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

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  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
 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

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Figure 15: One-person bag-valve mask ventilation

Figure 16: Two-handed mask seal BVM

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

3.4 Oxygen therapy and none invasive positive pressure ventilation

Case Scenario: oxygen therapy

A 49 year old male patient is sleepy and suffering from carbon monoxide poisoning after being
rescued from a burning building. His saturation is 78%. How do you approach this victim?

3.4.1 Introduction

Hypoxemia is a major cause of morbidity and mortality in both adults and children. Oxygen
therapy is used not only for primary lung diseases, but also for many other conditions that result
in hypoxemia, such as sepsis, different types of shock, severe malaria, status epilepticus, trauma;
and obstetric and neonatal conditions.

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3.4.2 Causes of hypoxia

1. Central: CNS depression due to trauma, space occupying lesion (SOL), infections, status
epilepticus,
2. Neuromuscular diseases:
3. Chest and lung injuries or infections
4. CVS: shock, anemia

3.4.3 Indications for Instituting Oxygen Therapy in Adults

1. Cardio respiratory arrest

2. Respiratory distress (respiratory rate >24/min) in adult; in pediatrics according the age
3. Hypoxia with pulse oximeter measurement (saturation of oxygen <90%) except for
COPD patients and infants
4. Hypotension (systolic blood pressure <90 mm Hg)
5. Low cardiac output and metabolic acidosis (bicarbonate<18 mmol/l)

3.4.4 Methods to Improve Oxygenation

1. Increase FiO2- initiate supplemental administration of oxygen with nasal prong, different
type of face mask and start to treat the causes
2. Increase minute ventilation (MV)- assist breathing with bag valve mask(BVM), non-
invasive CPAP, invasive mechanical ventilation
3. Increase Cardiac Output- treat causes of hypotension and shock
4. Increase oxygen carrying capacity – blood transfusion when there is symptomatic anemia
5. Optimize V/Q relationship – treat pulmonary edema, with drugs and when necessary with
PEEP/CPAP
6. Decrease oxygen consumption from- pain, shivering or fever – optimal use of analgesics

3.4.5 Oxygen Administration Devices and Techniques

Oxygen is a drug and has to be prescribed and the prescription has to indicate:

1. Flow rate,

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 2. Delivery system,
3. Monitoring
4. When to report
5. When to change the device
6. When and how to stop oxygen administration

3.4.5.1 Methods of Oxygen Administration

1. Nasal cannula, nasal prongs

2. Face mask – simple, partial rebreathing, non-rebreathing;
3. Ambubag or Bag Valve Mask (BVM) – assist breathing;

1. Nasal prongs or catheter

 Used for correction of mild hypoxia and when there is no marked tachypnea;
 Oxygen administration via nasal prongs range 1-5 liter/minute.
 Can deliver FIO2 of 0.25-0.4
 Position the patient on semi seating position where applicable
 Use humidifier
 Oxygen administration has to be started from 5L/minute, monitor the patient’s response,
 If the saturation is above 93% and other vital signs are stabilized titrate down ward
gradually.
 If the saturation is not improving change to the next step which is facemask with high-
flow rate

Figure 17: Nasal prong

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  Care should be taken to keep the nostrils clear of mucus, which could block the flow of
oxygen.
 Clean the nasal prong at least twice to avoid blockade
 Children: 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 using nasal prongs.

2. Face Mask

 They could be with reservoir or without, none rebreathing or simple.

 A flow rate of 6-15 liters/minute provides a rise in inspired oxygen concentration(FIO2) up
to 60-70 percent, when the mask is simple or above 80% when face mask is with reservoir
and non- rebreathing.
 The flow rate shouldn’t be less than 6 liters/minute to avoid rebreathing, i.e. breathing of
their own exhaled gas which is rich on CO2.
 Start from the higher flow, which is 10-15L/m, and titrate down ward according the
patients response.
 Non-rebreather mask (NRB) allows for the delivery of higher concentrations of oxygen.
Before attaching to the patient the reservoir bag has to be full of O2, at least 2/3 of the bag
 Exhaled air is directed through a one-way valve around the connection of the mask, which
prevents the inhalation of room air and the re-inhalation of exhaled air. The valve, along
with a sufficient seal of the mask around the patient's nose and mouth, allows for the
administration of high concentrations of oxygen, approximately 60% - 80% oxygen.
 Before a NRB is placed to the patient,
 Children: Face Mask- rate of 0.5-1 liters for infants and 1-2 liters/min for older children,
 The reservoir bag is inflated with oxygen to greater than two-thirds of its volume, at a rate
of 15 liters per minute.
 It has to be connected continuously to the oxygen source with high-flow.
 Make sure the reservoir bag is always inflated with oxygen.

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Figure 18: Simple face mask

Figure 19: Non-rebreather mask (NRB)

 If patients oxygenation and general conditions is not improving and signs of hypoxia or
hypercarbia are persisting consider the next technique of oxygen administration, which is
non-invasive respiratory support (CPAP) if the patient has adequate breathing effort and
conscious and cooperative or invasive (intubation and ventilation with mechanical
ventilator) respiratory support.
 Children:

3. Bag Valve Mask (BVM)/Ambubag

 BVM is used for temporary assist breathing and oxygenation during respiratory arrest, bradypnea
or low breathing rate<10b/m, pre oxygenation
 This device is lifesaving and the techniques on how to use them has to be practiced by all
professionals.

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Bag Valve Mask (BVM) has three parts:

 Bag with oxygen connector

 Unidirectional valve between the face mask and the bag
 Face mask

Figure 20: Bag Valve Mask

BVM implementation technique

 Check the functionality of the BVM;

 Position the patient supine;
 Make head tilt and chine lift if patient is medical or non-trauma or jaw thrust for all
trauma patients;
 Choose appropriate size of face mask that covers the patients nose and mouth only;
 Connect the BVM with the oxygen source with high-flow, 10-15L/M;
 Fix the facemask covering the nose and the mouth using C&E method( see picture
below)
 Squeeze the bag just to raise or inflate the lungs. But remember do not over inflate, this
creates injury to the lungs and decrease the venous return;
 Give a rate of 10-12breaths/minute, and according the age of the child in pediatrics
 If the chest is not moving when you squeeze the bag reposition the head and neck and
insert oro-pharyngeal airway.

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Figure 21: One hand C&E technic and two hands technique using jaw thrust

Figure 22: Oxygen sources

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4. 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, and tracheostomy). Its use has become
more common as its benefits are increasingly recognized.
A. 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 [PaCO 2] >45 mmHg or pH <7.30)
 Cardiogenic pulmonary edema
 Acute hypoxemic respiratory failure
 NIPPV may also be helpful for preventing post-extubation respiratory failure
B. Pre-requisite to use NIPPV
 Patients must be conscious
 Cooperative
 Able to breathe spontaneously
 Able to protect their airway
 Have good air way reflexes
C. 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

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Figure 23: Non-Invasive positive pressure ventilation

D. Types of Positive pressure Ventilation

 Continuos Positive Airways Pressure Ventilation (NIV- CPAP)

Constant pressure on inspiration and expiration
 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
E. Application of NIPPV
 Oxygen flow - A gas flow of 6-10 L/min
 For CPAP-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
F. 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

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 G. 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
H. 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

3.5 Introduction to basic ECG

ECG records an electrical activity of the heart.

Cardiac Physiology: The Pacemakers

Figure 24: Electrical conduction pathway starting from SA node to AV node then

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 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 25: Electrical conduction starting from AV node

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Figure 26: Normal electrical conduction system

Cardiac electrical activity

Figure 27: Cardiac electrical activity depicted on ECG

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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 – the 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

Figure 28: 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. The e 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 the
Vertical axis represents voltage.

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 Voltage

Time

Figure 29: ECG paper (X-axis shows Time, Y–axis shows Voltage)
The ECG is recorded on to standard paper traveling 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.

Figure 30: ECG paper in detail (Small box, larger box, paper speed)

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3.5.1 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

Figure 31: 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

Figure 32: P wave (Blue-right atrial, Red –left atrial)

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  QRS complex: represents ventricular depolarization. Duration is <0.12 sec.
 Q is the initial downward deflection
 R is the first positive deflection
 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 – the origin of it is uncertain
 PR interval: represents conduction delay in the AV node. Duration is 0.12-0.2
sec
 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.

Figure 33: ST segment (red), J point (Green)

Anatomical relations of leads in a standard 12 lead ECG
 II, III, and aVF: the inferior surface of the heart
 V1 to V4: anterior surface
 I, aVL, V5, and V6: lateral surface

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3.5.2 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
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Figure 34: 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.

Figure 35: 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
Table 3: Axis determination

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Lead I Lead aVF
Positive Positive

Positive Negative

Negative Positive

Negative Negative

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)

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Figure 36: Normal P wave versus large P wave in Right atrial enlargement

Figure 37: Pmitrale (wide P wave showing left atrial enlargement)

Step 4.2 QRS

Assess the duration and Voltage of the QRS complex.
QRS is wide when the duration is >0.12 sec. Some of the causes of 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
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  LAE

Figure 38: 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)

Figure 39: ECG showing RVH (Prominent R wave in V1, ST depression with T wave

Low voltage criteria

 R+S<5 limb leads

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  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?
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

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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, hypocalcaemia, hypothermia
- Prolonged QT has the risk of degeneration to Torsade de Pointes

Figure 40: Normal vs. 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)
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3.6 Arrhythmia / Dysrhythmia
3.6.1 Arrhythmia /Dysrhythmia: is any rhythm that is not the normal sinus rhythm with
normal atrioventricular (AV) conduction.
Classification of arrhythmia
• Tachyarrhythmia: arrhythmia with rate >100
• Brady-arrhythmia: arrhythmia with rate <60
3.6.2 Tachyarrhythmia
A. Mechanisms of Tachy-arythmias
 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
B. Approach to Tachyarrhythmia:
The following 4 KEY QUESTIONS should be asked.
1.Is my patient stable or unstable?

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 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 hypo perfusion/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

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Wide Complex
 Regular
 Ventricular tachycardia
 Irregular
Ventricular fibrillation
 Torsades de Pointe

Figure 41: Classification of tachyarrhythmia

PSVT-Paroxysmal supraventricular tachycardia

 Characteristics
 No P wave
 Regular
 Narrow QRS
 Rate >150

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Figure 42: Paroxysmal SVT(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 43: Atrial flutter (Saw toothed P wave, narrow QRS)

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

Figure 44: Atrial fibrillation (No well-defined P wave, Narrow QRS, Irregular)

Ventricular tachycardia
 Characteristics
 No P wave
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  Wide QRS
 Regular

Figure 45: 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 46: Ventricular fibrillation (No P wave, irregular, wide QRS)

Treatment of tachyarrhythmia
Treatment depends on whether patient Stable or unstable
 What are the instability signs
 What is the therapy for unstable tachyarrhythmia

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Figure 47: Tachyarrhythmia instability signs and management
Pulse less Ventricular tachycardia and ventricular fibrillation require early CPR and
defibrillation.
Stable narrow complex Tachyarrhythmia
 Iv access, put on monitor, give oxygen
 Vagal maneuvers- valsalva, carotid massage, eyeball massage, water immersion
 Adenosine -6mg then 12 mg then12 mg iv push, follow with flush
 beta-blockers
 Calcium blockers
Stable wide complex tachyarrhythmia
 IV access, put on monitor, give oxygen

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  Amiodarone -150 mg over 10 min, then 1mg/min
 Procainamide -25-50 mg /min
 Lidocaine
Group Exercise
 Case study: A 25 years old female lady presented with palipitation 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
Time: 10 minutes

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 –vagalmanuever, 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

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Figure 48: Brady-arrhythmia
Definition: Rate<60, symptomatic usually when below 50bpm
 Causes ‘DIE’
 Drugs
 Electrolyte abnormality
 Ischemia
 Hypoxemia is the commonest cause
 Look for signs of respiratory distress, pulse oximetry reading
Classification
 Sinus bradycardia: Sinus rhythm with Rate <60

Figure 49: Sinus bradycardia

 AV Blocks
 First degree AV Block: PR Prolonged >0.2 ,Defect in AV node

Figure 50: First degree AV Block

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

Figure 51: Second-degree mobitz type 1

 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-purkinje system

Figure 52: Second degree mobitz type 2

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

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Figure 53: 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 a normal physiologic change like athletes

Figure 54: Approach to bradyarrhyhmia

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Treatment of 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

3.7 Cardiac arrest resuscitation

Cardiac arrest is defined as an 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

Figure 55: 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
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  Early high-quality CPR
 Early defibrillation
 Post cardiac arrest care

Figure 56: Chain of survival for in hospital 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 the 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 is 2 main types of cardiac arrest algorithms.
These are shock able rhythm and the non-shockable rhythms.
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  Ventricular fibrillation and pulseless ventricular tachycardia are shockable rhythms
whereas asystole and pulseless electrical activity /PEA/ are non-shockable rhythms.
Pulseless electrical activity /PEA/ is an organized rhythm without a central pulse. It
requires a high quality CPR and Adrenaline.
 A systole is a 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)

Figure 57: A systole

 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 58: Adult cardiac arrest algorithm

A Systematic approach for cardiac arrest

The three main components during advanced cardiac arrest resuscitation are the following
1. Basic life support /BLS/ Assessment
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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 59: Sequential approach of BLS

3.8 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.
The Proper position for chest compression is at the center of the chest, mid sternum.

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Characteristics of High quality CPR

 Press the heels of the hands straight dawn on the center of the chest.
 PUSH FAST: give compressions at a rate of 100 -120 per min. (Count compressions out
loud).
 Give 30 compressions to 2 breaths with one or two rescuer CPR in adult. But 30:2 ratios
in single rescuer and 15:2 ratios in two or more rescuers in pediatrics.
 PUSH HARD Depress the chest at least 5cm(2 inches) but not greater than
6cm(2.4inches) depth in adults or 1/3rd -1/5th of chest antero-posterior diameter in infants
and older children
 ALLOW COMPLETE CHEST RECOIL- release completely, allowing the chest
completely recoil in each compression. This allows the heart to refill with blood.
 MINIMIZE INTERUPTIONS -try to limit interruptions in chest compressions to 10
seconds or as needed for interventions (e.g. defibrillation) ideally compressions are
interrupted only for ventilation (until advanced airway is secured) and rhythm check and
actual shock delivery.
 Once an advanced airway is in place, provide continuous compression and without pause
for ventilation.
 AVOID EXESSIVE VENTILATION –each rescue breath should be given over 1
second and each rescue breath should result in visible chest raise.
 After every 5 cycle/2min. or sooner when tired check for spontaneous breathing and
circulation for 5 sec
 Rapid identification and intervention of shock is an essential component of pediatric
resuscitation.

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Figure 60: Hemodynamic response to ‘ideal’ chest compressions.

1. Primary assessment during cardiac arrest

A-airway assessment and Management
Ask the following questions
 Is the airway patent?
 Is an advanced airway 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 rhythm?

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  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
2. 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

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Figure 61: Full cardiac arrest algorithm

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Figure 62: 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 63: Post cardiac arrest algorithm

Team Dynamics
 Team with team leader
 Clear roles and responsibilities
 Mutual respect
 Knowledge sharing

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  Closed loop communication
 Clear message

Terminating resuscitation
 Consider factors:
 Time from collapse to CPR
 Time from collapse to the 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

3.9 Approach to shock

Shock: 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 it also defined as a clinical state of
cardiovascular collapse characterized by acute reduction of blood volume which is

 Systolic BP < 90 mmHg, or

 MAP < /= 60 mmHg
 Reduction of systolic BP > 30 mm Hg from the patient’s baseline

Generally, shock has the following three stages:

1. Pre-shock or compensated shock - this stage is characterized by compensatory

mechanisms to counter the decrease in tissue perfusion, including tachycardia, peripheral
vasoconstriction, and changes in systemic blood pressure

2. Shock - this stage, most of the classic signs and symptoms of shock appear due to early
organ dysfunction, resulting from the progression of the pre-shock stage as the
compensatory mechanisms become insufficient.

3. End-organ dysfunction - This is the final stage, leading to irreversible organ dysfunction,
multiorgan failure, and death.

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3.9.1 Types of Shock

1) Hypovolemic Shock

 Hypovolemic shock is characterized by decreased intravascular volume and increased

systemic venous assistance (compensatory the mechanism to maintain perfusion in the early
stages of shock).

 In the later stages of shock due to progressive volume depletion, cardiac output also
decreases and manifest as hypotension.

 Hypovolemic shock divides into two broad subtypes:

A) Hemorrhagic

B) Non-hemorrhagic.

A. Common causes of hemorrhagic hypovolemic shock include

 Gastrointestinal bleed (both upper and lower gastrointestinal bleed (e.g., variceal
bleed, portal hypertensive gastropathy bleed, peptic ulcer, diverticulosis) trauma

 Vascular etiologies (e.g., aortoenteric fistula, ruptured abdominal aortic aneurysm,

tumor eroding into a major blood vessel)

 Spontaneous bleeding in the setting of anticoagulant use (in the setting of

supratherapeutic INR from drug interactions)

B. Common causes of non-hemorrhagic hypovolemic shock include

 GI losses - the setting of vomiting, diarrhea, NG suction, or drain.

 Renal losses - medication-induced diuresis, endocrine disorders such as

hypoaldosteronism

 Skin losses/insensible losses - burns, Stevens-Johnson syndrome, Toxic epidermal

necrosis, heatstroke, and pyrexia

 Third-space loss - in the setting of pancreatitis, cirrhosis, intestinal obstruction,

trauma

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3.9.2 Clinical features

 Hypotension ororthostatic hypotension, tachycardia, tachypnea,

 Flattened jugular venous pulsations, decreased skin turgor, dry skin, dry axillae, tongue/
buccal mucosa, postural hypotension, decreased JVP

 Obtundation, or abnormal mental status, cold, clammy extremities, mottled skin

 oliguria, metabolic acidosis, and hyperlactatemia

 Features pertaining to the underlying cause of the shock: Pallor if its secondary to
hemorrhage or have squeal of chronic liver disease (in case of variceal bleeding).

2) Cardiogenic Shock

Due to intracardiac causes leading to decreased cardiac output and systemic hypo-perfusion.

Different subtypes of etiologies contributing to cardiogenic shock include:

 Cardiomyopathies - include acute myocardial infarction affecting more than 40% of the
left ventricle, acute myocardial infarction in the setting of multi-vessel coronary artery
disease, right ventricular myocardial infarction, fulminant dilated cardiomyopathy,
cardiac arrest (due to myocardial stunning), myocarditis.

 Arrhythmias - both tachy- and Brady arrhythmia

 Mechanical - severe aortic insufficiency, severe mitral insufficiency, rupture of papillary

muscles, or chordae tendinea trauma rupture of ventricular free wall aneurysm.

 Clinical findings include: chest pain suggestive of cardiac origin, narrow pulse pressure,
elevated jugular venous pulsations or lung crackles, and significant arrhythmias on EKG
and diffuse crackles on lung.

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 3) Obstructive Shock

Mostly due to extra cardiac causes leading to a decrease in the left ventricular cardiac output

 Pulmonary vascular - due to impaired blood flow from the right heart to the left heart.
Examples include hemodynamic ally significant pulmonary embolism, severe
pulmonary hypertension.

 Mechanical - impaired filling of right heart or due to decreased venous return to the
right heart due to extrinsic compression. Examples include tension pneumothorax,
pericardial tapenade, restrictive cardiomyopathy, constrictive pericarditis.

 Clinical findings depend on the cause of the obstruction. For e.g. if it is tension
pneumothorax signs includes tachypnea, unilateral pleuritic chest pain, absent or
diminished breath sounds, tracheal deviation to the normal side, distended neck veins
and also has pertinent risk factors for tension pneumothorax such as recent trauma,
mechanical ventilation, underlying cystic lung disease .

4) Distributive Shock

Is a type of shock that is characterized by peripheral vasodilatation. It has different subtypes,

namely:

 Septic shock

 Sepsis is defined as life-threatening organ dysfunction resulting from deregulated

host response to infection. Septic shock is a subset of sepsis with severe circulatory,
cellular, and metabolic abnormalities resulting in tissue hypo perfusion manifested as
hypotension which requires vasopressor therapy and elevated lactate levels (more
than 2 mmol/L)

 Clinical findings may be suggestive of the source of infection

 Systemic inflammatory response syndrome

 Systemic inflammatory response syndrome (SIRS) is a clinical syndrome of the

vigorous inflammatory response caused by either infectious or noninfectious causes.

 Infectious causes include pathogens such as gram-positive (most common) and gram-
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 negative bacteria, fungi, viral infections (e.g., respiratory viruses), parasitic (e.g.,
malaria), rickettsia infections.

 Noninfectious causes of SIRS but are not limited to pancreatitis,burns,fat embolism,

air embolism and amniotic fluid embolism

 Anaphylactic shock

 Anaphylactic shock is a clinical syndrome of severe hypersensitivity reaction

mediated by immunoglobulin E (Ig-E), resulting in cardiovascular collapse and
respiratory distress due to bronchospasm.

 The immediate hypersensitivity reactions can occur within seconds to minutes after
the presentation of the inciting antigen.

 Common allergens include drugs (e.g., antibiotics, NSAIDs), food, insect stings, and
latex.

 Clinical findings include: hypotension, flushing, urticaria, tachypnea, hoarseness of

voice, oral and facial edema, hives, wheeze, inspiratory stridor, and history of
exposure to common allergens such as medications or food items the patient is
allergic to or insect stings.

 Neurogenic shock

 Neurogenic shock can occur in the setting of trauma to the spinal cord or the brain.

 The underlying mechanism is the disruption of the autonomic pathway resulting in

decreased vascular resistance and changes in vagal tone.

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,

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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
3.9.3 Management of Shock

A. Hemorrhagic shock
 Ensure adequate ventilation/oxygenation
 Provide immediate control of hemorrhage, when possible (e.g., traction for long bone
fracture, direct pressure)
 Initiate judicious infusion of Normal Saline or lactated ringer’s solution (10-20ml/kg)
 With evidence of poor organ perfusion and 30-minutes anticipated delay to
hemorrhage control, begin PRBC infusion (5-10 ml/kg)
 Adjunctive therapy
Rewarming techniques (e.g. warm fluids, blankets, radiant lamps, head covers)- as
hypothermia is a common consequence of massive blood transfusion that can contribute to
cardiac dysfunction and coagulation abnormalities.
Antibiotics: when open dirty or contaminated wounds are present to prevent and treat bacterial
infections.
B. Cardiogenic shock
 Put the patient on cardiac and pulse oximetry monitoring
 Ameliorate increased work of breathing: provide oxygen; pain control, e.g. Morphine
for acute MI; PEEP for pulmonary edema
 Preload augmentation: give fluid: 250ml of NS
 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

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 be considered. The most important part is titration of the dose of inotropes and
vasopressors based on patient’s response.
 Diuresis after inotropic support if there are signs and symptoms of pulmonary edema
 Reverse the underlying pathology (e.g. treatment of arrhythmias, MI etc.)
C. Septic shock
 Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host
response to infection. The consensus document describes organ dysfunction as an
acute increase in total Sequential Organ Failure.
 Septic shock is a subset of sepsis in which underlying circulatory and
cellular/metabolic abnormalities are profound enough to substantially increase
mortality. Septic shock is defined as lactate levels rising above 2 mmol L−1 without
hypervolemia and initiation of vasopressor treatment to keep mean arterial pressure
above 65 mmHg.
 Organ dysfunction is defined as an increase of two or more in the Sequential Organ
Failure Assessment (SOFA) scoring system, and it was determined that this caused a
more than 10% increase in hospital mortality.
 Assessment (SOFA) scores two points consequently to the infection.
 qSOFA (quick Sequential Organ Failure Assessment) scoring system should create a
suspicion of sepsis and organ dysfunction.

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Figure 64: Flow chart of assessment of patient with sepsis

Management
 ABC of life: airway stabilization-secure airway if indicated for air way protection
optimization of oxygenation and ventilation
 Remove work of breathing - Ensure adequate oxygenation by giving oxygen via face
mask, if possible or through nasal catheter or nasal prongs.
 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
 Initiate broad spectrum antibiotic therapy early within one hour, usually based the
possible focus of infection/septic focus.
 Source control intervention or surgical drainage/debridement of an abscess or dead and
necrotized tissue.
 If volume restoration fails to improve organ perfusion, begin vasopressor support.
 Corticosteroid administration- for refractory vasopressor-dependent shock.
 Blood transfusion only when hemoglobin concentration decreases to less than 7g/dl or if
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 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
 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.

Vasopressors:

 Vasopressors are potent pharmacologic agents that are used to increase blood pressure
and mean arterial pressure by vasoconstriction, which intern increase the systemic
vascular resistance.
 They should be reserved for cases of persistent hypotension and tissue hypo perfusion
after volume resuscitation has failed.
 Most vasopressors have multiple actions on the heart and vasculature and have a
propensity to cause arrhythmias. Some vasopressors are also inotropes and are used to
improve cardiac output, particularly in patients with left ventricular pump failure or
cardiogenic shock.
 There are different vasopressors that we use for different purposes, below are the
common vasopressor doses, effects and uses, the figure below shows us their dose
range, which receptor they act on, cardiovascular effects.
Table 4: List of vasopressors, their dose and effects on the cardiovascular

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 D. Anaphylactic shock
 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
edema or if you fail to correct oxygenation with face mask. Consider early definitive
airway control for those evidence of significant airway edema or if you fail to
correct oxygenation with a face mask.
 Secure bilateral wide bore needle IV lines and administer 20ml/kg of crystalloids as fast
as possible.
 Administer Epinephrine for control of acute symptoms.
 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)

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  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.
 Administer 5-10 mg/kg of hydrocortisone or 1-2 mg/kg of methyl prednisolone for late
control of symptoms for refractory vasopressor-dependent shock.
 Blood transfusion only when hemoglobin concentration decreases 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
 Glucose control: maintain glucose <= 180mg/dl
Don’t have any role in the control of acute symptoms.
 H2 receptor blockers
Case Scenario: Shock

A 33-year-old man sustained RTA. Examination reveals a possible fracture of the right
humerus distended abdomen and an unstable pelvis. The patient’s vital signs are :

BP 68/40, PR124, RR 18. what is your initial management for this patient?

3.10 Approach to 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. It is arousal system dysfunction with the content of consciousness affected as
well.

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Coma: is a failure of both arousal and content functions. It 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 (infratentorial)
 An expanding lesion, such as cerebellar hemorrhage or infarction, may cause
abrupt coma, abnormal extensor posturing, loss of papillary reflexes, and loss
of extra ocular movements.

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Investigations
 CBC, RBS, serum electrolytes, renal and liver function tests, blood film etc.

 Brain CT, CXR, ECG, Brain MRI

 Lumbar puncture: 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
 Hypoxic encephalopathy

 Metabolic encephalopathy (hypoglycemia, hyperosmolar state, electrolyte

abnormalities e.g. hyper/hyponatremia)

 Hypertensive encephalophathy

 Organ system failure (hepatic encephalopathy, uremia/renal failure, endocrine

(Addison disease, hypothyroidism), hypoxia, carbon dioxide narcosis)

 Toxins

 Drug reactions ( e.g. neuroleptic malignant syndrome)

 Environmental causes (e.g. hypothermia / hyperthermia)

 Sepsis
2. Coma from primary CNS disease or trauma
 Direct CNS Trauma
 Diffuse axonal injury
 Subdural hematoma
 Epidural hematoma
 Non convulsive status epilepticus

 Postictal state

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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 Vascular disease

 CNS infections

 Neoplasm
 Seizures
Causes.
Evaluation for readily reversible causes of coma, such as hypoglycemia and opioid toxicity,
demands priority.
E. ABC of life
Secure airway, breathing and circulation, take vital signs including RBS, secure IV line
 Indication for intubation
 Deep coma - GCS<9
 Status epilepticus

 Anticipated clinical worsening or rapidly deteriorating GCS despite initial

management

 If suspected poisoning and gastric lavage is planned.

F. Immobilization of C-spine if there is any concern of trauma
G. Coma cocktail
 Thiamine 100mg IV prior to dextrose in alcoholic patients

 Dextrose 50gm IV push

 Naloxone 0.01

 mg/kg if opiates suspected

 Flumazenil 0.2mg IV if benzodiazepine suspected (routine use in coma of unknown
etiology is not recommended)

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 H. If concern for increased ICP and herniation
 Elevate head 30degrees

 Consider mannitol 0.5-1gm/kg bolus

 If mass lesion- consider dexamethasone
I. 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.
J. Send the patient for investigation after stabilization
Table 5: Glasgow Coma Scale

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 3.11 Summary

 Basic Life Support: It is chest compression and artificial ventilation or cardiopulmonary

resuscitation (CPR). It is initiated anywhere by a person who is trained to do so, and
most of the time it doesn’t need special equipment. It has to be followed by ACLS for
restoration of cardiac activity.
 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.
 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.

 ECG shows the electrical activity of the heart

 Management to the patient with arrhythmia depends on the presence or absence of
instability signs
 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.

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CHAPTER FOUR: COMMON MEDICAL EMERGENCIES
Duration: 6.5 Hours

Chapter description

This chapter describes the knowledge, skills and attitude that are crucial for the recognition,
diagnosis and management of patients with acute heart failure with pulmonary edema, ACS,
Acute asthma, DKA and hypoglycemia, Seizures and status epileptics. Approach to a poisoned
patient also included in this chapter.

Chapter Objective:

At the end of this chapter participates will be able to

 Manage common medical emergencies encountered in the Emergency Department

Enabling objective: -

At the end of the session, participants will be able to:

 Explain management of patients with acute asthmatic exacerbation

 Describe management of patients with heart failure and pulmonary edema
 Describe management of patients with ACS
 Manage patients with DKA and hypoglycemia
 Follow proper handling of patients with medical emergency
 Discuss management of patient with acute poisoning

Outline

4.1.Acute Asthma Exacerbation

4.2.Congestive heart failure and Pulmonary edema
4.3.Acute Coronary Syndrome
4.4.Diabetic Ketoacidosis (DKA )
4.5.Hypoglycemia
4.6.Seizure
4.7.Status Epilepticus
4.8.Poisoning
4.9.Summary
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 Group Exercise:

Be in group of 4

Discuss common medical emergencies

Time: 10 Minutes

4.1 Asthma
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.

A. Triggering factors

Several stimuli trigger airway narrowing, wheezing, and dyspnea in asthmatic patients
Factors increasing the risk of severe life-threatening asthma include
 Previous ventilation. 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
 Hospital admission for asthma in the last year.
 Heavy rescue medication use.
 >3 classes of asthma medication.
 Repeated attendances at an 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 patients may
deteriorate very rapidly and present as respiratory or cardio-respiratory arrest
B. Initial assessment

 Patients presenting with an asthma attack may be at imminent risk of death

 Rapid and accurate assessment of vital signs

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 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 an imminent arrest, proceed with assessment and treatment
Table 6: Classification of severity of an asthma attack

Imminent
Parameter Mild Moderate Severe
respiratory arrest
Walking Can Talking Prefers At rest Hunched
Breathless
lie down to sit up forward
Talks in Sentences Phrases Words Unable to speak

Alertness May be agitated Usually agitated Always agitated Drowsy or confused

Respiratory rate Increased Increased Often > 30/min

Accessory muscles Paradoxical thoracic
and suprasternal Usually not usually usually and abdominal
retractions movements
Moderate,
Wheeze often only end - Loud Usually loud Absence of wheeze
expiratory
Pulse rate 100 100-120 >120 Bradycardia
<60% or (<
PEF after inhalation of >80% Impossible to
60-79% 100l/min in
salbutamol 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

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Acute severe asthma: Immediate therapy

Priorities of treatment
 Treat hypoxia.
 Treat bronchospasm and inflammation.
 Assess the need for intensive care.
 Treat any underlying cause if present.
Severe or life-threatening attack Initial treatment
 Oxygen – the highest percentage available
 Maintain O2 saturation > 92%
 Bronchodilators.
 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
The Technique of salbutamol puff.
 Test the inhaler: shake well and release one puff into the air
 Breathe out gently & place the mouthpiece in the mouth and close lips around it.
 Tilt head slightly backward, breathe in slowly and press down the canister to release 1
dose
 Remove the inhaler and hold a breath for 10 seconds and breathe out slowly
 Nebulization: 2.5-5mg every 20 mins for 3 doses then 2.5-10 mg Q 1-4 hrs.as
needed
 MDI -4 puffs every 10 mins, 8 puffs every 20 mins

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Figure 65: How to use inhaler

 Add Ipratropium bromide 0.5 mg 4-6 hourly if an initial response to B agonist is poor :
 500 mcg via nebulizer every 20 minutes for three doses, then as needed.
 Obtain IV access.
 Start steroids
 Hydrocortisone 200 mg IV, continue with either hydrocortisone 100 mg QID IV or
prednisolone 30-50mg Po daily. (IV steroid treatment is not more effective than oral
treatment)
 If no improvement:
 Add magnesium sulfate 2 gm administered over 20 minutes or
 Aminophylline
 Loading dose- 5mg/kg or 250 mg over 20 minutes (dilute with IV fluid to a
concentration of 1mg/ml) followed by continuous infusion
 Do not give loading dose in patients taking oral theophylline
Figure 65: salbutamol puff, how to inhale.

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

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

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

 Oral prednisolone =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%)
 The 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.
 At discharge you should keep the patient on inhaled corticosteroids
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 (maybe more wheeze) Pulse oximeter- aim O2 saturation
of 94-98% Monitor heart rate and Oxygen saturation continuously and measure BP frequently.

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4.2 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.

A. 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 the
filling of the heart, but the contractility remains to be normal).
B. Causes
 Hypertrophic cardiomyopathy,
 Restrictive cardiomyopathy,
 chronic hypertension,
 Ischemic heart disease,
 Diabetes.
The 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 neurohumoral 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.
 Heart failure can complicate with 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

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 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.
C. Etiologies of heart failure
 Heart failure with depressed Ejection Fraction
 Coronary heart diseases.
 Chronic pressure overload
 Hypertension.
 Valvular obstruction.
 Chronic volume overload
 Valve Regurgitation
 Dilated cardiomyopathy.
 Toxic/drug-induced
 Viral
 Heart failure with preserved Ejection Fraction
 Hypertrophic cardiomyopathy
 Hypertension
 Restrictive cardiomyopathy
 Pulmonary heart diseases
 Corpulmonal
 Chronic anemia
 Thyrotoxicosis
 Common presentation of patients with heart failure includes:
 Progressive dyspnea, and orthopnea (shortness of breath in lying position),
Palpitation, Paroxysmal nocturnal dyspnea (waking up from sleep due to severe
shortness of breath)

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  Swelling of the body starting from the feet progressing upwards, swollen
abdomen, cough productive of pink frothy sputum,
 Fatigue, weakness, angina, syncope.
 Other diseases could present in similar ways and should be considered in the
differential.
D. 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
E. 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,
 Narrow pulse pressure (<25mmHg),
 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 a possible underlying cause and precipitating factor for the heart failure. Quick history
and physical examination, we should look for evidence for the underlying cause: Imagine the
anatomy of the heart and which structures could be affected to lead to heart failure. Common
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underlying causes of heart failure include:
 Valvular heart disease – the commonest cause of heart disease in our setup ,with the
affection of the different valves of the heart, either alone or in Combination with
cardiomyopathies (hypertrophic, dilated, restrictive cardiomyopathies)
 Ischemic heart disease – due to the 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 and Ventricular septal defect, etc.
 Pericardial diseases – Effusive pericarditis, constrictive pericarditis, Viral pericarditis, and
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 the 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 a diagnosis.

Work up should be individualized.
 CBC, Urinalysis, Renal function test.
 CXR, ECG, Echocardiography.
 Serum electrolytes (potassium, sodium).
 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 an
emergency ultrasound.
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 F. 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 the requirement of the inotropic drug in systolic failure as
opposed to diastolic failure. The general principles of management of heart failure are mentioned
here below:

Initial stabilization

 Assessment of the airway, oxygenation, and prescription of oxygen Oxygen support

 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.

Addressing symptoms and signs related to congestion or low perfusion

 Diuretics
 A Potent diuretic, preferably parenteral loop diuretic should be initiated early to manage the
fluid overload state.
Dose: The dosage of the loop diuretics e.g. Furosemide is an ideal choice (vasodilator reducing
preload in addition to its diuretic effect)
 Furosemide can be started at <0.5mg/kg or 40 mg IV, with 40 mg increments every
hour.
 If no adequate response to the loop diuretic alone
 Continuous IV infusion 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

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  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, urgent diuresis
measures can be taken
 Addition of a thiazide diuretic e.g. Hydrochlorothiazide
 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 :Improve pulmonary congestion, ↑ coronary blood flow, and ↓
afterload
 Sublingual Nitroglycerin (0.4 mg x 3 every 5 min)– first line for cardiogenic
pulmonary edema
 If pulmonary edema persists and no evidence of shock 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.
 Unable to use after 24 hrs. due to tolerance.
 S/E: Headache, hypotension.
 Other vasodilators: Isosorbidedinitrate, Nitroprusside
 Some medications to treat chronic heart failure like Beta Blockers, and ACEI’s
have deleterious effects in the acute setting and should be discontinued or used
very cautiously.
 NSAIDs should be avoided - they reduce the efficacy of diuretics
G. Monitoring
Close patient monitoring is very important for an optimal outcome.
Important parameters to follow are:
 V/S monitoring (every 30 minutes) to adjust the diuretic dose
 Monitoring for optimal diuresis
 Assessment of urine volume.
 Daily weight measurement – better done with the same weight scale, at a fixed

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 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 on
individualized 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, and hypomagnesaemia.
A flow sheet should be prepared for use including the most important parameters to be followed.
Table 7: A sample flow sheet is presented as follows: follow up sheet for a patient with shock

Mental Insensible Diuretic BUN Daily

Date Vital signs Input Output
status loss dose Cr Weight

PR BP o RR Sao2
T

 Inotropic agents like: Dobutamine, Dopamine is used.

 Identification and management of precipitating factors:
 If atrial fibrillation with a fast ventricular response:- Digoxin or low dose beta
blockers could be used for rate control. Cardio-version can be attempted for
those with a new onset atrial fibrillation with hemodynamic
instability; Antibiotics for infection, etc.
4.3 Acute coronary syndrome

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.

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  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 a 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 and is 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 my necrosis, and persistent ST-segment
elevation.

Non-ST-segment elevation myocardial infarction: A with evidence of myocardial necrosis

(elevated cardiac biomarkers)

4.3.1 Clinical Assessment

A. Risk assessment

 Vital signs – frequently depending on the severity of the heart failure. E.g. A patient with
cardiogenic pulmonary edema might need frequent
B. History

 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 classic pain or discomfort location is sub-sternal 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 are associated with
more non-classic ACS presentations.
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 C. 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 wall myocardial 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 mitral regurgitation, or 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
D. 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 an abnormal elevation of cardiac biomarkers but may include ECG changes not
meeting the 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 a 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)

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 STEMI=New ST elevation in 2 contiguous leads >= 0.2 mV in men or 0.15 mV in
women 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)

Some examples of ECG findings for AMI

Figure 66: Anterior MI Pattern – Tombstoning

Figure 67: Septal involvement (lead V2) and a bit laterally, as well (lead V5 and V6)

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Figure 68: Anterior MI Pattern – Typical ST Segment Elevation
2. Cardiac biomarkers: serial testing at presentation & 6–12 h after symptom 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

4.3.2 Management of ACS

 Should focus on stabilizing the patient's condition, relieving ischemic pain, and
providing antithrombotic therapy to reduce myocardial damage and prevent further
ischemia. The goal is early revascularization.
A. 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 thrombo-embolism) prophylaxis
 NPO except for sips of water until stable; IV fluid – e.g. 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)
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  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)
B. 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 persistent chest pain *IV
NTG for persistent ischemia .C/I= low BP, sildenafil use
 Morphine sulphate sulfate: 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.

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Analyze and manage the following rhythms.

a.

b.

c.

d.

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4.4 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:
 Acute major illnesses such as MI, CVA, or pancreatitis.
 New onset type 1 diabetes

 Drugs (glucocorticoids, higher dose thiazide diuretics, sympathomimetic

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

 Cocaine use

 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.

 Poor compliance with the insulin regimen.

4.4.1 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.

A. Symptoms

 Nausea/vomiting ,poly symptoms(polydipsia, Polyphagia, Polyuria), Abdominal pain,

Shortness of breath
B. Physical Findings

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

 Serum Glucose:
 The serum glucose will be elevated(>200mg/dl)
 Serum bicarbonate
 is frequently <10 mmol/L
 Arterial PH
 Ranges between 6.8 and 7.3- depending on the severity of the acidosis.
 Serum electrolyte-
 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.
 Renal function test- Elevated blood urea nitrogen (BUN) and serum creatinine
levels reflect intravascular volume depletion.
4.4.3 Treatment
 Stabilize ABC of life
 Fluid management
 Insulin
 K+ repletion
 Treatment of precipitating factors
 Monitoring
 Long term management

A. General Measures
 Stabilize the ABC of life
 Obtain IV access
 Monitor RBS every hour, urine ketone every 2-4 hrs.
B. Identify and treat Precipitating cause of DKA

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 C. 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
D. 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
E. 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

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  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
 Overlap the last dose of regular insulin with the standing dose of long acting
insulin
 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
 In insulin-naive patients, insulin regimen should be started at a dose of 0.5 to 0.8
U/kg per day
 Measure RBS every 4-6hrs and give correctional dose of regular insulin(1-2IU for
every 50mg/dl rise above 200mg/dl
Table 8: DKA follow up sheet

F. 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.

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4.5 Emergency management of hypoglycemia
4.5.1 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.
4.5.2 Causes of Hypoglycemia

 Drugs (Insulin or insulin secret agogue, 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-insulin omapancreatogenous hypoglycemia, Post–gastric bypass hypoglycemia, Insulin
autoimmune hypoglycemia, Antibody to insulin, Antibody to insulin receptors
 Accidental, surreptitious or malicious hypoglycemia

4.5.3 Clinical manifestations

A. Symptoms:
 Hypoglycemia causes neurogenic (autonomic) and neuro glycopenic 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 parenthesis
(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.

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  Occasionally, transient focal neurologic deficits may be seen. Permanent neurologic
deficit may occur in patients with diabetes mellitus or prolonged hypoglycemia.
B. 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
C. 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 neuro glycopenia, 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.

D. 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)

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 E. 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.
4.6 Seizure
Seizures are episodes of abnormal neurologic functioning caused by pathologically excessive
activation of neurons, either in the cerebral cortex or in the deep limbic system.
Epilepsy is defined as recurrent unprovoked seizures caused by a genetically determined or
acquired brain disorder

4.6.1 Classification of seizures

A. Generalized seizures: involves brain diffusely
 Tonic-clonic (grand mal)

 Absence seizures (petit mal)

 Others (myoclonic, tonic, clonic, or atonic seizures)

B. Partial or focal seizures: electrical discharges begin in a localized region of the cortex.
The previous term partial is now being replaced with focal.
 Simple Focal: without impairment of Cognition

 Complex Focal: with impairment of Cognition.

The term cognition refers to involvement of at least two of five features—perception,
attention, emotion, memory, and executive function—and replaces the previously used
term consciousness.
C. Convulsive and non-convulsive seizures

 Convulsive seizures are characterized by uncontrolled, rhythmic motor movements and

can affect part or all of the body.

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  Non convulsive seizures do not result in abnormal motor activity; patients may display
confusion, altered mental status, abnormal behavior, or coma.

D. Clinical features
1. 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: Generalized seizures typically occur without an aura.
2. Brief duration: Seizures rarely last longer than 90 to 120 seconds, although bystanders
may overestimate the duration.
3. Loss of consciousness: Present by definition, except for focal seizures.
4. Purposeless activity: For example, automatisms and undirected tonic-clonic movements.
5. Unprovoked: Especially with regard to emotional stimuli; fever in children and substance
withdrawal in adults are notable exceptions.
6. Postictal state: An acute confusion state that typically occurs with all seizure types except
focal and absence.

2. 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.
E. Differential diagnosis
 Syncope
 Pseudo seizures
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  Hyperventilation syndrome
 Migraine headache
 Movement disorders
 Narcolepsy/cataplexy
F. 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 immuno compromised 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

G. Indications of CT in Seizure patients
 First seizure
 Acute intracranial process suspected
 History of acute head trauma
 History of malignancy
 Immuno-compromised status
 Fever
 Persistent headache
 History of anticoagulation
 New focal neurologic examination
 Age older than 40 years without epilepsy history
 Focal onset before generalization
 Persistently altered mental status
H. Treatment of uncomplicated seizure
1. Patients with active seizure
 Protect the patient from injury; do not try to restrain

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  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.

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 I. Selection of antiepileptic drugs
Generalized tonic clonic seizure
First line- Valproic acid, lamotrigine, topiramate

Alternatives- Phenytoin, carbamazepine, Phenobarbital

Focal seizure
First line- carbamazepine, phenytioin, lamotrigine

Alternative- valproic acid, Phenobarbital

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.

4.7 Status Epilepticus

Status epilepticus is continuous or intermittent seizures for more than 5 minutes without
recovery of consciousness. It has been classically defined as at least 30 minutes of persistent
seizures or a series of recurrent seizures without intervening return to full consciousness. The
time criterion has been shortened to 5 minutes with recognition that the duration of seizure
activity is related to outcome and that the likelihood of achieving seizure cessation with typical
treatments decreases with ictal duration.
 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.

4.7.1 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
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 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 are a focal tonic-clonic seizure activity with normal alertness
and responsiveness.

4.7.2 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.
A. 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, whereas 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.

B. Drug therapy of status epilepticus

 Diazepam 5-10mg Iv stat/ lorazepam 0.1- 0.15mg over 1-2min and repeat dose if no
response after 5 min

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

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  If seizure continues repeat phenytoin 7-10mg/kg at 50mg/kg or fosphenytoin 7-10mg/kg
at150mg/min

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

 If no response with the first dose repeat Phenobarbital 10mg/kg IV at 60mg/kg

 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.
NB : 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.

4.8 Approach to poisoning

4.8.1 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:

 An unintentional exposure to a clearly identified substance

 An estimate of the dose is known
 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

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 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.

A. 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.

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  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.

B. 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.

C. 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
D. 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.

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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.
E. Multi-dose 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.
F. Whole bowel irrigation
 Uses a laxative agent such as polyethylene glycol to fully flush the bowel of stool and
unabsorbed xenobiotic.
 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.
G. Urinary alkalization

 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

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  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.

H. 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.
I. 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)
J. Antidotes

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

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Table 9: The commonly used 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

Sulfonylureas Glucose/Octeoride
Benzodiazepines Flumazenil
Beta blockers Glucagon
Ethylene glycol, Methanol Fomepizole

Isoniazid Pyridoxine
Monomethylhydrazine mushrooms Pyridoxine

Organophosphates Atropine/Pralidoxime

4.9 Summary
 Asthma is a chronic inflammatory condition of the airways resulting in hyper-
responsiveness of the airways to various stimuli.
 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.
 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

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 CHAPTER FIVE: ASSESSMENT AND MANAGEMENT OF
TRAUMA
Duration: 6 hours

Chapter description: This chapter is designed to provide participants with the knowledge, skills
and attitude required to care competently and safely for trauma patients with different aspects of
injury. It focuses on having participants expand their knowledge base and master trauma care
psychomotor skills associated with assessment and provision of trauma care for patient with
acute life threatening injuries.

Chapter objectives:
By the end of this chapter participants will be able to manage trauma patients.
Enabling objectives:
By the end of this training session, the participants will be able to:
 Perform primary and secondary survey for the trauma patient
 Describe common life-threatening chest injuries
 List Management options for Abdominal and Pelvic injury
 List General management principles

Outline

5.1. Approach to trauma

5.2. Chest trauma
5.3. Abdominal and Pelvic Trauma
5.4. Head trauma
5.5. Management of Burn
5.6. Summary

Group Exercise:

Be in group of 4

Discuss what is a trauma and common type of trauma visit to hospitals

Time: 10 Minutes

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 Case Scenario: Trauma
Mr. Seifu was brought to the emergency department by his friends after he had involved in a
fight while he was having a drink. He was hit by a metal rod. He has deep lacerations on his
forehead and temporal area of the skull. He has also active bleeding and tenderness on his left
leg
On P/E= vitals revealed that B.P=80/50/60, PR=124bpm, RR=28bpm and Sao2= 86%.
He is moaning, and opens his eye when you pinch him. He has bleeding through the left ear and
flexes all extremities while you rub on his sternum. His mouth is full of foamy secretion.
How do you approach and manage this patient?
Time:15 minutes

5.1 Approach to traumatic Patient

Traumatic brain injury Describe management of burn according to World Health Organization
(WHO) and the Central for Disease Control (CDC), more than nine people die every minute
from injuries or violence, and 5.8 million people of all ages and economic groups die every year
from unintentional injuries and violence. Trauma is the leading cause of morbidity and mortality
in resource limited setting.
Death because of trauma occurs with trimodal distribution;
 The first peak occurs within seconds to minutes of injury,
 Caused by severe brain or high spinal cord injury or rupture of the heart, aorta,
or other large blood vessels
 The second peak occurs within minutes to several hours following injury also known as
the Golden hour
 Caused by subdural and epidural hematomas, hemopneumothorax, ruptured
spleen, lacerations of the liver, pelvic fractures, and/or multiple other injuries
associated with significant blood loss.
 The third peak occurs several days to weeks after the initial injury.
 Caused by sepsis and multiple organ system dysfunctions.

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Figure 69: Timing distribution of trauma deaths compared with the historical trimodal
distribution
Because timing is crucial, a systematic approach that can be rapidly and accurately applied is
essential. This approach, termed the “initial assessment,” includes the following elements:
 Preparation
 Triage
 Primary survey (ABCDEs) with immediate resuscitation of patients with life-threatening injuries
 Adjuncts to the primary survey and resuscitation
 Consideration of the need for patient transfer
 Secondary survey (head-to-toe evaluation and patient history)
 Adjuncts to the secondary survey
 Continued post resuscitation monitoring and reevaluation
 Definitive care

A. Preparation
Preparation For trauma patients occurs in the field /prehospital phase/,events are coordinated
with the clinicians at the receiving hospital and in the hospital phase, preparations are made to
facilitate rapid trauma patient resuscitation.

B. Triage
Involves the sorting of patients based on the resources required for treatment and the resources
that are actually available.

C. Primary survey
Encompasses the ABCDEs of trauma care and identifies life-threatening conditions by adhering
to this sequence:
 Airway maintenance with restriction of cervical spine motion
 Breathing and ventilation
 Circulation with hemorrhage control
 Disability (assessment of neurologic status)
 Exposure/Environmental control

D. Adjuncts used during the primary survey

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Include continuous electrocardiography, pulse oximetry, carbon dioxide (CO2) monitoring, and
assessment of ventilatory rate, and arterial blood gas (ABG) measurement.
E. The secondary survey
Is a head-to-toe evaluation of the trauma patient—that is, a complete history and physical
examination, including reassessment of all vital signs.

F. Adjuncts to the secondary survey

Include additional x-ray examinations of the spine and extremities; CT scans of the head, chest,
abdomen, and spine; contrast urography and angiography; trans esophageal ultrasound;
bronchoscopy; esophagoscopy; and other diagnostic procedures based on the assessment

G. Reevaluation
Reevaluation is required to ensure that new findings are not overlooked and to discover any
deterioration in previously noted findings.
Then definitive care will be done in the center which is equipped with materials and
professionals

Primary survey (ABCDEs) with immediate resuscitation

 Airway maintenance with restriction of cervical spine motion (A)
 During the initial assessment first assess the airway to ascertain patency.
 If the patient is able to communicate verbally, the airway is not likely to be in
immediate obstruction; however, repeated assessment of airway patency is prudent.
 Assessment for signs of airway obstruction includes inspecting for foreign bodies;
identifying facial, mandibular, and/or tracheal/laryngeal fractures and other injuries
that can result in airway obstruction; and suctioning to clear accumulated blood or
secretions that may lead to or be causing airway obstruction.
 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 a foreign body or abnormal swelling around the airway, and altered mental
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 status.
 Check if the patient can swallow saliva or is drooling
 Then open the airway using the jaw thrust maneuver (don’t use chin-lift maneuver)

Figure 70: Jaw thrust

 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).
 These are 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.
 Establish an airway surgically if intubation is contraindicated or cannot be
accomplished.While assessing and managing a patient’s airway, take great care to
prevent excessive movement of the cervical spine

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Figure 71: Cervical spine motion restriction technique

Breathing and Ventilation (B)

 Ventilation requires adequate function of the lungs, chest wall, and diaphragm; therefore,
clinicians must rapidly examine and evaluate each component.
 Evaluate the following during breathing assessment
 Look chest movement, listen to the breath sounds, and feel the airflow 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 in drawing/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
 Injuries that significantly impair ventilation in the short term include:
 tension pneumothorax,
 massive hemothorax,
 open pneumothorax, and
 tracheal or bronchial injuries
 If there is tension pneumothorax, perform needle decompression at the 5 thintercostals
space at the MAL line immediately and give IV fluids and oxygen. Then perform chest
tube insertion as fast as possible.

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  For patient with open pneumothorax /sucking 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 inserts chest tube as fast as possible.

Figure 72: Three-way valve dressing for sucking chest wound

 For patient with massive hemothorax give oxygen, secure Iv line and insert chest tube
then consider referral if thoracotomy is indicated.
 For patients with tracheobronchial injuries give oxygen and early surgical consultation
Circulation with Hemorrhage Control (C)
 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.
 Assess the following during circulation:
 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 tamponed.
Sources of bleeding during trauma
 Chest
 Abdomen
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  Pelvis
 Long bones.
 External
 Immediate management may include:
 Pressure dressing,
 Tourniquet application
 Application of a pelvic stabilizing device and/or extremity splints.
 Establish Vascular access
 Appropriate replacement of intravascular volume
 Vascular access typically two large-bore peripheral venous catheters should be placed to
administer fluid, blood, and plasma.
 When peripheral sites cannot be accessed, intraosseous infusion central venous access, or
venous cut down may be used depending on the patient’s injuries and the clinician’s skill
level.
 IV solutions crystalloid should be warmed either by storage in a warm environment (i.e.,
37°C to 40°C, or 98.6°F to 104°F) or administered through fluid-warming devices.
 The infusion of greater than 1.5 L of crystalloid has been shown to be associated with
increased mortality in trauma. For this reason, the early use of blood products is
advocated, and there is no place for the infusion of large volumes of crystalloid fluid in
trauma patients.
 Massive transfusion should be utilized if needed and is defined as the transfusion of more
than 10 units of blood in 24 hours, or more than four units of blood in one hour.
 Early resuscitation with blood and blood products in low ratios (1:1:1) is recommended
in patients with evidence of Class III and IV hemorrhage.
 Blood samples for baseline hematologic studies are obtained, including a pregnancy test
for all females of childbearing age and blood type and cross matching.
 Tranexamic acid can be administered within 3 hours of injury in severely injured patient
sat a loading dose of 1 g IV over 10 minutes, followed by 1 g infused over eight hours.
 Definitive management may require surgical or interventional radiologic treatment and
pelvic and long-bone stabilization. Initiate surgical consultation or transfer procedures
early in these patients.
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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 Glasgow Coma Scale /GCS/ is a quick, simple, and objective method of determining
the level of consciousness. Fig
 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.
Table 10: GCS components and scoring

 Primary brain injury results from the structural effect of the injury to the brain. This
includes contusion, axonal injury, intra-parenchymal hemorrhage
 Secondary brain injuries result from
 ischemia (insufficient blood flow);
 cerebral hypoxia (insufficient oxygen in the brain);
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  Hypotension (low blood pressure);
 cerebral edema (swelling of the brain);
 raised intracranial pressure (the pressure within the skull)
 Prevention of secondary brain injury by maintaining adequate oxygenation and perfusion
are the main goals of initial management
 If there are signs of increased ICP, early lowering of ICP is mandatory with head
elevation, and other medical measures.
 Patients with evidence of brain injury should be treated at a facility that has the personnel
and resources to anticipate and manage the needs of these patients. Consult a
neurosurgeon once a brain injury 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.

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.
 Also, 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
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 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 history and physical examination, including a 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

H. Definitive Care
Ultimate disposition is dictated by several 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.

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 5.2 Chest trauma

5.2.1 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.

5.2.2 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.
5.2.2.1 Tension Pneumothorax

A. Diagnosis

 Diagnosis 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 hypovolemic.
B. Treatment

 If a tension pneumothorax is suspected, immediate needle decompression is

indicated. This is done by introduce a 14-gauge IV needle and catheter into the pleural
space through the chest wall in the 5th ICS at mid axillary line.
 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

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 pneumothorax.
 Once the tension pneumothorax is decompressed the patient's perfusion often improves
immediately.
 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.
 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.

5.2.2.2 Massive Hemothorax

 Is defined in the adult as at least 1500 mL, or approximately two-thirds of the available
space in the hemithorax.
 Causes of massive hemothorax include injury to:
 lung parenchyma,
 intercostal artery, or
 Internal mammary artery.
 Each hemithorax can potentially hold approximately 40% of a patient's circulating blood
volume.

Figure 73: Massive Hemothorax

A. Diagnosis

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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.

B. Treatment

 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 is generally indications for operative management.
 Even in patients not meeting these criteria, evidence of ongoing hemorrhage or
rebleeding may warrant consideration of operative intervention.
Because massive hemothorax is, by definition, associated with the 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.

5.2.2.3 Open Pneumothorax

 Open pneumothorax is a communication between the pleural space and the 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 maybe due to small rents in the parietal pleura or
small air passages without penetrating injury
A. Clinical Finding

 Respiratory distress
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  Air entry and breath sounds are often diminished on the affected side, and
 Chest wall motion can be impaired.
B. Treatment

 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.
 Three-sided dressing is a temporary measure only and should be followed promptly by
the insertion of chest tube to areas other than the wound.

5.2.2.4 Flail Chest

 Is a Segmental fracture (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.
 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 hypoxemia is contusion to the underlying lung.
 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.
A. Treatment

 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 the relief of pain by analgesics or intercostal nerve block and
maintaining good ventilation and pulmonary toilet.
 If SPO2 remains <90% despite supplemental oxygen and adequate pain control
ventilatory support should be provided.
 Indications for early ventilatory support include:
 Shock, severe head injury, comorbid pulmonary disease, fracture of eight or more
ribs, other associated injuries, age >65 years
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Figure 74: Flail chest

Chest Tube (Tube Thoracostomy) insertion Technique

Tube thoracostomy for the 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.

A. Technique

 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 (Figure11.7).
 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

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Figure 75: Chest tube insertion, the 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.
 Then 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 does not adhere to the chest.
 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.
 Then 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

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hemothorax). However, in intubated patients, chest tubes should be maintained while mechanical
ventilation continues to prevent the sudden development of a new pneumothorax.

B. 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 patients the so-called “hidden
six”.

 Thoracic aorta disruption

 Tracheobronchial disruption
 Esophageal disruption
 Myocardial contusion
 Pulmonary contusion
 Diaphragmatic tear.

5.3 Abdominal and Pelvic Trauma

5.3.1 Abdominal Injuries

A. Introduction

 Abdominal trauma accounts for 15% to 20% of all trauma deaths.

 These deaths primarily occur soon after the 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.
B. Mechanism of Abdominal Injuries

1. 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 an injury to solid organs (e.g., liver or spleen) or hollow viscera
(e.g., the GI tract).
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  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.
 E.g.: - 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.
2. 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.

Figure 76: 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.

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 C. Clinical Features

 Abdominal injury often presents insidiously.

 Young patients may lose 50% to 60% of their blood volume and remain
asymptomatic. Besides, 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.

D. 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 (per umbilical and flank ecchymosis) generally
represent delayed findings of intraperitoneal bleeding.
 Following the 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 a 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
exams are later found to have a significant intra-abdominal injury

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 E. Diagnosis

Although multiple diagnostic modalities exist to detect intra-abdominal injuries, no study fails
proof.

Therefore, a combination of a careful physical exam, attention to the mechanisms and

circumstances of the injury, and judicious selection of diagnostic studies are used for diagnosis.

F. 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 intra-peritoneal fluid.
 The greatest benefit of FAST is the rapid identification of free intra-peritoneal
fluid in the hypotensive patient with blunt abdominal trauma.
 The 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 intra-peritoneal fluid.

Figure 77: Red arrow showing a thin stripe of fluid in Morison's pouch.

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 G. 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.

H. CT- Scan
 CT scanning has become the gold standard for the diagnosis of abdominal injury.
 CT scanning can make the diagnosis of organ-specific abdominal injury and images both
the abdomen and the retro peritoneum.
 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.

I. 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 retro peritoneum.
 All patients with hypotension, abdominal wall disruption, or peritonitis need
surgical exploration. In addition, the presence of extra luminal, intra-abdominal, or
retroperitoneal air on plain radiograph or CT should prompt surgical exploration.
Table 11: 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 radiograph High suspicion for trans abdominal
trajectory after gunshot wound
Positive FAST or DPL in thermodynamically unstable
patient
CT-diagnosed injury requiring surgery
CT-diagnosed injury requiring surgery (i.e., pancreatic

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 transection, duodenal rupture, diaphragm injury) (i.e., ureter or pancreas)
Relative Positive FAST or DPL in thermodynamically stable patient Positive local wound exploration after
Solid visceral injury in stable patient stab wound
Hemoperitoneum on CT without clear source

J. No operative Management of Blunt Trauma

The evolution of no operative 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.

5.3.2 Pelvic Injuries

A. Introduction

 Pelvic fractures and associated injuries are a cause of significant morbidity and mortality.
 The mortality rate from all pelvic fractures is approximately 5%. However, with complex
pelvic fractures, the mortality rate is 22%.
 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.

B. Clinical Features

1. History

 The possibility of pelvic fracture should be considered in every patient with serious blunt
trauma.
 Determine the mechanism of injury and the pre-hospital 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.

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 2. 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 greater trochanters and determine the range of motion of the hips.
 Pelvic stability 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).
 A 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.

C. 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.

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  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.

D. 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 a pelvic fracture 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.

1. Initial Management
 Follow principles of ATLS for hemodynamic resuscitation. (refer to ATLS section)
 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.
 Apply longitudinal traction (distal femur skeletal traction) for vertically unstable pelvis.
 Suprapubiccystostomy might be indicated if transurethral catheter could not be passed.
 When indicated, put it far away from area of symphysis pubis and pelvic injury side as
putting cystectomy with in close distance to the symphysis compromises future definitive
surgical intervention for the pelvic/acetabulum injury. (Insert it as close to the umbilicus
as possible)
 Appropriate antibiotic coverage for open wounds started as soon as possible. (Initiating
antibiotics within 3hours has been shown to significantly lower infection risk in open
fractures).
 If a patient with a pelvic fracture is hemodynamically unstable and other sources of
bleeding have been excluded: pre-peritoneal pelvic packing (or angio-embolization by
intervention radiologist if available) is indicated.
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  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.

Figure 78: Pelvic stabilization with bed sheet

5.4 Head trauma

A. Introduction

 Traumatic brain injury (TBI) is defined as an 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 are <20%, but long-term disability is as high as 50%.

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 In severe TBI mortality approaches 40%, with most deaths occurring within the first 48
hours.

B. 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):

CPP=MAP – ICP

 The local adjustment of cerebral blood flow within the brain microcirculation is termed
auto regulation.
 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).
 Auto regulation is impaired in many TBI patients.
 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).

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  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 auto-regulation, below which local control of cerebral blood
flow cannot be adjusted to maintain flow adequate for function.
 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.

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

1. 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 the patient outcome than treatments initiated later in
the process.

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 2. Airway and Breathing

 Hypoxia increases mortality, so aggressive airway and breathing 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%.

3. 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.
 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%.

D. Disability and the Neurologic Examination

 The neurologic vital sign is the GCS.

 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 the outcome almost as well as the
full GCS.
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  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
and
 Bilateral pinpoint pupils suggest either opiate use or a pontine lesion.

E. Glucose Control

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

F. Temperature Control

 Elevated temperature is associated with increased metabolic demand.

 Elevated temperature elevates ICP and worsens outcomes in many neurologic
critical care conditions including TBI.
 Treat fever with the goal of normothermia

G. Seizure Treatment and Prophylaxis

 Seizures after a head injury can change the neurologic examination, alter oxygen delivery
and cerebral blood flow, and increase ICP.
 Prolonged seizures can worsen the 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.

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 H. Increased Intracranial Pressure
 Patient’s 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 the head of the 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 the 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.

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Table 12: Clinical decision rule for head CT

5.5 Management of burn

Introduction
The commonest types of burns in our community are:
 Flame burns with associated burns caused by melted synthetics and
 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 the
water is usually below the 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 leads to
severe burns.
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Classification of Depth
1. Superficial burns:
C. Superficial epidermal burns
 To epidermis only
 Skin pink or red, painful, no blisters
 Not included in the evaluation of burn area
D. 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:
A. Deep dermal burn
 May have some blistering
 Base of the blister demonstrates the 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.
3. Full Thickness
 Injury to epidermis, dermis and extending into the 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 the face
 Signs of inhalation injury include:
 Carbonaceous sputum

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  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 an 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 the non-burnt area if possible
 Consider intraosseous route if above not possible
 Take blood concurrently for CBC, biochemistry, Group and Match, glucose.
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  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
It is determined by the severity, and extent of the burn.
Consider:
 Electrolytes, RFT, CO level if available
 CBC with Cross match, Urinalysis for hemoglobinuria/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

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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 the first 8 hours following the time of burn, the remainder in the next 16
hours. (Estimate time since burn and not since the arrival of patient)
 This is a guide only and should be monitored.
(2) Aim for a urine output of:
 Adult > 1ml/kg/hour
 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.

5.6 Summary
 Trauma is best managed by a systematic approach according to ATLS protocol.
 A thorough primary and secondary survey is key to identify life threatening injuries.
 Once a life threatening injury is discovered, intervention should not be delayed.
 Disposition is determined by the patient’s condition as well as available resources.

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 CHAPTER SIX: COMMON GYN/OBS EMERGENCIES
Duration: 3hrs
Chapter description

This chapter is designed to provide participants with the knowledge and skills and attitude
required to care competently for patients who have Obstetrics Emergencies. This chapter
includes hypertensive disorder of pregnancy, vaginal bleeding during pregnancy, post partial
hemorrhage and trauma in pregnancy.

Chapter objectives:
By the end of this chapter the participants will be able to:
 Describe systematic approach to hypertensive disorders of pregnancy, vaginal
bleeding during pregnancy and PPH
Enabling objectives:
By the end of this training session, the participants will be able to:
 Diagnose and manage preeclampsia & eclampsia
 List causes and management of vaginal bleeding during pregnancy
 Identify and manage PPH
 Perform systematic approach to trauma in pregnancy

Outline
6.1. Hypertensive disorders of Pregnancy
6.2.Vaginal bleeding during pregnancy
6.3. PPH
6.4. Trauma during pregnancy
6.5. Summary

Group Exercise:

Be in group of 4

Discuss common gynecologic and obstetric emergencies

160 |10
Time: P aMinutes
ge
 6.1. Hypertensive Disorder of Pregnancy

Hypertension which is induced by pregnancy and this disorder 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
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
 Past history of preeclampsia or family history of preeclampsia
 Preexisting medical condition(DM,HTN,CKD)
 Twin pregnancy
 First pregnancy
 advanced maternal age
 ART (Artificial Reproductive Technology)
Diagnostic evaluation
 The main goal of initial evaluation of newly developed hypertension is to differentiate
gestational hypertension from preeclampsia
 Measure protein excretion(to r/o proteinuria)
 Urine dipstick
 Protein to creatinine ratio
 Evaluate for feature of severe disease(to r/o end organ dysfunction)
 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
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  Outpatient management with weekly /2x ANC visit (for BP, urine protein check-up)
 Antihypertensive therapy is not recommended
 Timing of delivery: at term
 No need of intrapartal MgSo4
 BP ≥ 160/110 mmHg
 These patients have rates of pregnancy complication comparable with those with severe
preeclampsia
 Antihypertensive therapy to decrease risk of stroke with BP goal of 130-150 systolic and
80-100mmHg diastolic BP
 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
 MgSo4 is administer for seizure prophylaxis

6.1.1 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

 SBP>=160mmHgor DBP>=110mmHg and proteinuria (with or without significant end
organ dysfunction)
 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

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Clinical presentation
 On history –persistent and severe head ache, visual disturbance, epigastric and RUQ
pain, altered mentation dyspnea
 On physical exam-Elevated blood pressure
 Laboratory –CBC, RFT, LFT, urine protein, coagulation profile(not routinely done
unless complication occur Abruptio placentae, severe bleeding, severe liver dysfunction)
 Asses fetal status(for IUGR, oligohydraminos)
Case Scenario: Preeclamsia
19 years old primigravida comes in emergencyat 32 weeks of gestation. she is complaining of
blurring of vision and gross edema. upon examination her B.P is 152/95 mmHG.

What is the most likely diagnosis and how do you manage her?

Help syndrome
Definition: an acronym that refers to a syndrome characterized by hemolysis elevated liver
enzyme and low platelet
 Incidence: it occurs in 10-20 % 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
 Microangiopathic hemolytic anemia on blood smear
 PLT<100000
 Total bilirubin ≥1.2mg/dl
 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
 Disease severity
 Maternal and fetal condition
 Gestational hypertension

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Preeclampsia with feature of severe disease (formerly called severe preeclampsia)
 Severe preeclampsia is an indication for delivery
 Route of delivery is based on standard obstetrical indication
 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
 Previously called mild preeclampsia
 Delivery is recommended for Term pregnancy (>=37 week)
 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
 Fluid balance should be monitored
 Excessive fluid administration should be avoided preeclampsia mother are at risk of
pulmonary edema and third spacing
 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
 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
 Hydralazine
 begin with 5mg iv ifbp goal is not achieved within 20 min give 5-10mg IV max
dose 20mg if total dose of 30 mg doesn’t achieve BP control add another agent

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  Fall in BP begin within 10 to 30 min and lasts from 2 to 4 hours
 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
 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
 Esmolol or nicardipine by infusion pump
 Nitroprusside as last resort
 MgSO4 should not be substituted for antihypertensive therapy
 Target blood pressure
 130 to 150 mmHg systolic: 80 to 100mmHg diastolic
 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

 Severe preeclampsia during evaluation, labor and continued for 24-48 hrs after delivery
 Eclampsia immediately continue until 24 -48hr after delivery or last seizure
 Magnesium sulphate
 is drug of choice for prevention of eclampsia
 Timing-initiated at the onset of labor induction or cesarean delivery
 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%

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 solution) IV slowly until respiration begins.

6.1.2 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

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
 A rise of BP to the severe range or severe symptoms or resistant HTN
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 anti -seizure prophylaxis up to 0.6%fo mild preeclampsia

Management of eclampsia
 Initial stabilization
 Maintaining airway patency
 Adequate oxygenation
 Put the patient on supplemental oxygen 8-10 l/min via non rebreather mask to treat
hypoxia from hypoventilation during the seizure
 Protection from trauma
 Position the patient on lateral side
 Prevent aspiration
 Treatment of severe hypertension if present
 Prevention of recurrent seizure
 magnesium sulphate –drug of choice
 Persistent seizure despite MgSo4 use alternative drug diazepam or lorazepam
 Diazepam-5 to 10 mg iv every 5 to 10 min at rate <=5mg/min max dose 30 mg
 Evaluation for prompt delivery

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  Definitive management -delivery
 Eclampsia is an absolute contra indication for expectant management
6.2.Vaginal bleeding during pregnancy

Case Scenario: vaginal bleeding

A 28 years old G3 P2 lady has presented with complaints of brownish vaginal discharge ,
passage of vesicles and excessive vomiting . Ultrasound scan shows snowstorm appearance in
the uterus with no fetus.

What is the most likely diagnosis ?

Discuss the interventions needed for this patient?

Vaginal bleeding is common event at all stage of pregnancy

 This include:-
 1st trimester vaginal bleeding
 2nd trimester vaginal bleeding
 3rd trimester vaginal bleeding
 Postpartum hemorrhage

6.2.1 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

A) Ectopic pregnancy:
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%)

Clinical presentation
 The most common are 1st trimester vaginal bleeding- which is preceded by amenorrhea
and Abdominal pain

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  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

Diagnostic evaluation
 Do HCG and confirm pregnancy
 Evaluate for hemodynamic stability
 If unstable, patient should be transferred to resuscitation area
 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
 Stabilize with fluid and blood if needed
 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
 Unlikely if Intra uterine pregnancy on ultrasound

B) 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)
 Inevitable -bleeding with dilated cervix& open internal os but there is no passage of POC
 Incomplete -open os, there is passage of only parts of POC but it not fully expelled
 complete -closed os, fetus and placental materials fully expelled)
 Threatened - bleeding + closed internal osCx + US with IUP. Risk of abortion 35-50%.
 Septic abortion: fever, abdominal pain; can complicate any abortion.
 Missed abortion: Spontaneous abortion in a patient with or without symptoms and with
closed cervical os.

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Management of abortion

 Assess hemodynamic stability

 If unstable –give priority for resuscitation
 Based on the type of abortion
 Threatened – patient can be safely discharged with close follow up
 Inevitable /incomplete-
 Evacuation can be medically with Misoprostol PO 600microgram or surgically with
dilation and curettage
 Complete- do USG: if no RPC, discharge with close follow up

C) 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
 Vaginal bleeding
 Hyperemesis
 Pregnancy induced hypertension before 24 week
 On physical exam uterus larger than the gestational age

Diagnostic evaluation
 Lab- abnormally high HCG level
 Sonographer feature
 Snowstorm or Swiss chess pattern
 Large central fluid collection

Management
 Consult OB if no marked bleeding, Suction curettage if bleeding, ensure OB follow up
to trend HCG
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
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 E. 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

 Assess amount of visible bleeding.

 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

A) 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
 Severe abruption
 Heavy vaginal bleeding
 Severe frequent uterine contraction
 Fetal distress
 Coagulopathy
Vital sign derangement (hypotension, shock)
 Mild /moderate abruption
 mild/moderate of vaginal bleeding
 Mild /moderate abdominal pain
 Normal maternal vital sign

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  No fetal distress
Lab-CBC, blood group and Rh, fibrinogen level
 Imaging USG is specific but not sensitive it can’t rule out abruption
 Maternal Complications
 Hemorrhagic shock
 DIC
 Utero-placental insufficiency
 Fetal complication
 IUGR
 Fetal distress
 IUFD
Management option for APH

 Initial stabilization (ABC’s)

 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.
 Expectant management (admission, steroid administration)
 Indicated-for milder abruption or remote from term
 Aim of management- to prevent prematurity.
 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.

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 B. 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:
 Low lying placenta
 Marginal placenta previa
 Major placenta previa (may be partial or total)
Diagnosis
 Clinical presentation
 Painless vaginal bleeding
 Brisk, bright red bleeding
 Do not perform digital vaginal exam
 Lab-CBC, blood group and Rh, fibrinogen level
 Imaging USG- helps for confirmation
Treatment
 Initial stabilization(ABC’s)
 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.
 Mode of delivery: Cesarean section.
 Vaginal delivery may be considered if low lying placenta.

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.

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6.3 Post-Partum Hemorrhage (PPH)

Definition:-Vaginal bleeding > 500ml after singleton vaginal delivery of >28 weeks. (If
cesarean delivery or multiple vaginal birth, bleeding >1000ml)

Evaluation of PPH
• Vital signs, estimate the blood loss, uterine size and extent of contraction, completeness
of the placenta.

Causes of PPH
 Atonic Uterus (Uterus not contracted)
 The most common cause of primary PPH.
 Hypotonic uterus leads retention of the placenta and excessive bleeding.
 Diagnose if: soft, not contracted uterus with fundus above the umbilicus.
 Retained placenta
 The common cause of placental retention is poor uterine contraction.
 In retention of the placenta without bleeding, pathological adherence (accreta,
increta and percreta) should be considered.
 Manual removal of the placenta has to be done in the operating room with all the
preparation for laparotomy and possible hysterectomy.
 Traumatic causes
 Risk factors for tears of the birth canal (including uterine rupture) and PPH:
Fetopelvic disproportion (leading to obstructed labor), instrumental deliveries and
scarred uterus.
 Diagnosis: bright red (arterial) bleeding with a contracted uterus.
 Coagulation defects
 Risk factors: abruption placenta, intrauterine fetal death, infection etc.
 Physical examination: gross haemostatic failure is revealed.
 Bed side clotting tests and deranged laboratory coagulation profiles support the
diagnosis.
 Acute inversion of the uterus
 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
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 parasympathetic nerves.
 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:
 Retained placenta: PPH with undelivered placenta:
 Apply controlled cord traction (CCT)
 If CCT fails, manual removal of the placenta in operating room
 Consider laparotomy for possible pathological adherence if both fails.
 Atonic uterus: if PPH with delivered placenta and atonic uterus:
 Stimulate contraction by massaging the uterus.
 Start oxytocin 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.
 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 laparotomy is indicated.
 Clotting abnormality: Correct with fresh frozen plasma or whole blood.
 PPH after acute inversion of the uterus: under appropriate analgesia, apply:
 Immediate gentle upward transvaginal pressure.

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  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.

Case Scenario: PPH

Mrs. Bizunesh gave birth to a 3.9 kg male newborn at her home by a traditional birth
attendant 01 day back. It was her first pregnancy. The new born is okay but, the mother has
continuous vaginal bleeding. Her family brought her to GYN opd.

Upon physical examination,

Vitals revealed BP=80/50mmhg, PR= 126bpm, RR is 26 bpm and Sao2 is 89%.

She has pale conjunctiva , the uterus is relaxed and boggy. She has dark red bleeding.

A. What is your diagnosis ?

B. What is the cause of PPH in this particular women?

C. How can you measure the accurate blood loss.

D. How do you approach and manage her?

6.4 Trauma during Pregnancy

Trauma remains the leading cause of non-obstetric morbidity and mortality in pregnant women..
Trauma during pregnancy is common
 Motor vehicle crashes are the most common cause of blunt abdominal trauma,
accounting for up to 70% of acute injuries
 Trauma during pregnancy is associated with
 Increased risk of preterm labor
 Placental abruption
 Fetomaternal hemorrhage
 Pregnancy loss.
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Approach to trauma in pregnancy

Approach patient according to ATLS

A. Air way-
 Maintain airway patency and immobilize cervical spine if necessary
B. Breathing-
 If breathing inadequate, assist with bag-valve-mask ventilation with high flow
oxygen via mask with reservoir
C. Circulation:
 Put the patient on monitoring (both maternal and fetal) pulse, BP, capillary refill.
Secure double I/V line
 Sent sample for cross match resuscitate with two bags of NS
 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)
 Do bed side USG
 Test neurological disability
D. Disposition
 Up to 20 weeks - Routine trauma care with confirmation of FHTs
 After 20 weeks (including falls, whether abdomen was hit or not)
 Routine trauma care. Continuous fetal monitoring/tocograph for 4 hours after
trauma.
 Patient may be discharged after this time if above is reassuring.
 Patient should return if “tightening” or back pain.
 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)

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 6.5 Summary
 Definitive management for preeclampsia/ecclampsia is DELIVERY. Anti
hypertensive are recommended for severe and persistent hypertension. Magnesium
sulphate is the drug of choice for prevention of seizure
 PPH is a life threatening obstetric emergency. It should be prevented by active management of
third stage of labor
 Approach to pregnant with trauma should follow ATLS and team approach. Fluid
resuscitation should be twice that of the non-pregnant patients. Resuscitating the mother is
resuscitating the baby.

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 CHAPTER SEVEN: COMMON PEDIATRICS EMERGENCY
Duration:6.5 hrs

Chapter description

This chapter is designed to provide participants with the knowledge and skills and attitude
required to care competently for pediatric Emergencies. This chapter includes pediatric triage,
pediatric airway management and respiratory resuscitation, management of pediatric burn,
poisoning, seizure and snake bite.

Chapter objectives:
By the end of this chapter the participants will be able to:
 Describe systematic approach to pediatric triage, pediatric emergency case
identification and management
Enabling objectives:
By the end of this session, the participants will be able to:
 Demonstrate pediatric airway assessment and management
 Diagnose pediatric patient with respiratory problem
 Assess pediatric patient with circulatory problem
 Demonstrate CPR in pediatric patients
 Assess and manage pediatrics burn
 Diagnose childhood poisoning
 Manage childhood seizure disorder

Outline
7.1. Pediatric triage
7.2. Pediatrics Airway
7.3. Pediatric respiratory emergency
7.4. Childhood seizure management
7.5. Pediatric circulation
7.6. Basic Life Support
7.7. Management of pediatric burn
7.8. Pediatrics Snake bite and poisoning

178Newborn
7.9. | P a g e Resuscitation
7.10. Childhood Seizure Management
7.11. Summary
Group Exercise:

Be in group of 4

Discuss common pediatric emergencies

Time: 10 Minutes

7.1 Pediatric triage

Triage is the process of rapidly examining all sick children when they first arrive in health
facility in order to place them in one of the following categories:
E=Emergency
P= Priority and
Q=Queue (non-urgent)

7.1.2 The principle of pediatric triaging

For 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.

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7.1.3 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 in drawing 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:
 Assessing using AVPU:
 A - Alert
 V - Vice response
 P - Pain response
 U - Unresponsive
 If a patient is on the V level has to be taken us emergency

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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 eyeball
 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
Trauma
Pain
Poisoning
Pallor
Rest less 3R
Respiratory distress
Restless
Referral
Malnutrition/ marasmus M
Oedema O
Rest less
Burns B

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

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7.1.4 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 several signs 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.

7.2 Pediatrics Airway

7.2.1 Unique features of the pediatric airways:

 Tongue relatively large in proportion to oral cavity

 Infants <2 months of age are obligate nose breathers

 Trachea is smaller and shorter than that of adults

 Smallest diameter of trachea is at the cricoid ring, below the cords,

 Chest wall of infants relatively weak and unstable

 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.

 Immunologic immaturity leads to increased susceptibility to respiratory

infections

 Developmental immaturity leads to increased susceptibility to foreign body

aspiration.
7.2.2 Air way emergency:

 The patients tongue in a patient who is unconscious

 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

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  Insertion of oro-pharyngeal air in unconscious

 In conscious nasopharyngeal air

 Remove the foreign body if suspected

Figure 79: Head tilt chin lift

Figure 80: Open air way (Jaw thrust)

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7.2.3 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 Figure 81: Chest thrusts and back slap

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Figure 82: Abdominal thrusts

7.3 Pediatrics Respiratory Emergency

7.3.1Pediatrics respiratory emergencies
 Acute Severe Asthma
 Bronchiolitis
 Croup
 Epiglottis
5.5.1 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.

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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 Ivor po
 Adrenaline 0.01ml/kg 1:1000 SC in severe case
5.5.2 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 salinevia nebulizer.
 If no improvement with patient in moderate to severe distress:
 1ml of adrenalin in 5 ml of Normal saline via nebulizer May repeatx1.
 Maintain hydration status
5.5.3 Croup
A 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
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 respiratory distress, stridor, and barking cough.
 Symptoms often worse at night

Croup Management:
 Positioning
 Highflowo2
 Nebulizer 1ml of adrenaline 3ml ofN/S
 Dexamethasone 0.6 mg/kgIV
 Nebulization can be repeated every 30 to 1hour
 If no improvement intubation has to be considered
5.5.4 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 than12months.

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

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7.3.2 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.
3. 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.
7.4 Pediatrics Circulation

7.4.1 Assess the circulation

To assess if a child has a circulation problem or (compensated shock) you need to know:

 Does the child have warm hands

 Is the capillary refill time longer than 3seconds
 Is the pulse weak or fast

7.4.2 ARE THE CHILD’S HANDS WARM

 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.
7.4.3 IS THE CAPILLARY REFILL TIME LONGER THAN 3 SECONDS
 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

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 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.

7.4.4 IS THE PULSE WEAK AND FAST

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
7.4.5 The unavailability of BP cuff may delay in diagnosing uncompensated shock which
can be diagnosed without BP cuff.

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7.4.6 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 requires 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 over1hour

 Stay with the child and check the pulse and breathing rate every5-10minutes.

 Discontinue the intravenous infusion if either of these increase (pulse greater than15,

 Respiratory rate greater than5/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).

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  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

7.5 Basic life support

7.5.1 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

loudly. If the child is having gasping type of breath, we have to start CPR.

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 Chest compressions—Essential elements for effective chest compressions:
 Hard
 Fast chest compression
 With full chestrecoil
 Minima 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

7.5.2 Technique of cardiac compression

Infants Chest compressions for infants (<1 year) may be performed with either two fingers or
with the two thumb-encircling hands technique. Two figure techniques is recommended when
there is a single rescuer.

Figure 83: Two fingers chest compression

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 Two thumb encircle hands- the two thumb-encircling hands technique provides optimum
chest compressions when there are two redcuers.

Figure 84: Encircling chest compressions

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

7.5.3 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
compressions for single rescuer.
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 ventilation pression

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 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 85: Choosing appropriate size of mask

Figure 86: 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 lone rescuer 2 breaths per 15 chest
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 compressions for two rescuers.
7.6 Management of Pediatrics Burn

7.6.1 Introduction
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.

7.6.2 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.
7.6.3 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

7.6.4 Fluid resuscitation

 Assess burn size and depth

 Establish good intravenous access and give fluids
 Give analgesia
 Catheterize patient or establish fluid balance monitoring

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  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

 Total fluid requirement for first 24hours ;4 ml × ( total burn surface area)×(wt. in
kg)/24hours
 Half to be given in first 8 hours, half over the next16hours
 Subtract any fluid already received from amount required forfirst8hours
 Calculate hourly infusion rate for first8hours
 Calculate hourly infusion rate for next 16hours
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 bodyweight

End point
Urine output of 1.0-1.5 ml/kg/hour in children
7.6.5 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.
7.6.6 Investigations
The amount of investigations will vary with the type of burn Hematocrit /Hct/, Total Serum
Protein/TSP/

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7.6.7 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.
7.6.8 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.

7.7 Pediatrics Snake bite and poisoning

7.7.1 Introduction:

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.

7.7.2 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
 The only incisions to be made are extensions of not more than1cm long and
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 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 first band.
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.

7.8 Child hood poisoning

7.8.1 Introduction
A poison is any substance that causes harm if it gets into the body. Harm can be mild
(headache or nausea) or severe (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.

7.8.2 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

7.8.3 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
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 usually household agents, medicaments and plant material.
 Non-Accidental 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.

7.8.4 Consequences of Poisoning

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

 The amount of poisoning tested
 The nature of the substance
 The age of the child.
 The nutritional status of the child.
 The state of the stomach-whether empty or full of food.
7.8.4 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.

A. 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

B. 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.

7.8.5 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.
7.8.5.1 First aid at home
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 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.

7.8.5.2 Treatment in hospital

The clinician should take a brief history, examine the child thoroughly and rapidly and then do
the following:
 Ensure a clear airway and support respiration.

 Treat shock if present.

 Remove poison from the body before it is absorbed, by inducing vomiting or doing a
gastric lavage if victims come within one hour except when kerosene or a corrosive
has been ingested.
 Reduce absorption by administering activated charcoal which absorbs many toxins
and prevents subsequent absorption. ( 0.5-1gm/kg of activated charcoal)
 Anti-dotes should be used but these are available for very poisons.

 General supportive measures are important to ensure adequate hydration,

temperature control, fluid and electrolyte balance, nutrition intake and control of
convulsions

7.9 Newborn Resuscitation

7.9.1 Introduction

Resuscitation efforts should focus on improving respiratory status and maintaining body
temperature.

7.9.2 Evaluation and Treatment Priorities

 During delivery, suction mouth then noses before delivery of body.
 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
 If infant becomes bradycardic (<60), discontinue suctioning and provide ventilation
immediately.
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  Assess Breathing and adequacy of ventilation.
 Stimulate the infant by rubbing the back or flicking the soles of the feet.
 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 second 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.
7.9.3 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
7.10 Childhood seizure management

7.10.1 Introduction

Seizures, the most common pediatric neurological disorder, are a frequent presentation in the
ED. It is estimated that between 4% and 10% of children will have at least one seizure before

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age 16 years. The highest incidence of occurrence is seen in children younger than age 3 years;
this frequency decreases in older children.
Elements that are highly suggestive of true seizure activity include:
 Lateralized tongue-biting (high specificity)
 Flickering eye-lids
 Dilated pupils with blank stare
 Lip smacking
 Increased heart rate and blood pressure during event
 Post-ictal phase

7.10.2 Subtypes seizures:

Tonic-colonic, atonic, absence and myoclonic
Partial seizures can be subdivided into simple or complex, depending on whether consciousness
is impaired.
The most common causes of acute seizures are: A cause is identifiable in < 20% of children with
seizures includes.
 Metabolic Disorders (hypo or hyper Natremia, hypo Calcemia, hypomagnesaemia,
Hypoglycemia)
 Brain malformations
 Genetic disorders
 Traumatic or previous infectious injury of the brain
 Neoplasms
 Neuro-developmental abnormalities make it more likely a cause will be identified or
may already have been determined before seizure onset.
Initial Management
 As with critically ill patients, the first and most vital step in managing a seizing patient is
to assess:
 Airway, Breathing, Circulation
Medical management:
 Correct metabolic disorder: hypoglycemia, electrolyte disorder
 Diazepam 0.5mg/kg per rectum
 Phenobarbitone 20mg/kg loading then 5mg/kg maintenance

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7.10.3 Febrile Seizures
A seizure that occurs in association with a fever (temperature at or above 38°C by any method)
 Very common in children (3-4%)
 Age of onset age 6 months to 5 years (median age 18-22 months)
 No evidence of a CNS infection, or acute neurologic illness
 Usually occurs in an otherwise normal child
 There may/may not be a family history of febrile seizures/epilepsy Simple febrile
seizures are generalized tonic-clonic convulsions that last less than 15 minutes and do not
recur within 24 hours.
 Complex febrile seizures are less common and are focal or prolonged beyond 15 minutes
or recur within 24 hours. These account for about 25% of febrile seizures
Treatment:
 Treat the fever
 If it persists, start anticonvulsant
7.10.4 Pediatric Status Epilepticus Algorithm

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 7.11 Summary
 Triage is the sorting of patients according to their need . All children should
undergo triage.
 Look for any Priority signs ( 3TPR MOB) and place priority patients at the front of the
queue
 To assess pediatric airway and breathing you need to know: Is the airway
obstructed? Is the child breathing? Is the child cyanosed? Are there any signs of
respiratory distress?
 If the patient is not breathing you need to open the airway, remove any foreign
body and ventilate with bag and mask
 The major respiratory emergency in pediatrics includes: Upper airway, lower
airway, lung parenchymal problem and breathing control disorder
 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.
 It is estimated that between 4% and 10% of children will have at least one seizure
before age 16 years.

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CHAPTER EIGHT: DISASTER PREPAREDNESS AND
RESPONSE
Duration: 3 hrs

Chapter Description
This chapter is designed to provide participants with the knowledge and skills set required to
develop a disaster preparedness plan and address competently a coordinated disaster response
system. This chapter includes a common basic understanding of disaster, a disaster preparedness
plan, and disaster responses at site and facility levels.

Chapter Objectives
By the end of this chapter the participants will be able to:
• Describe systematic approach to disaster and develop a feasible on-site and facility
response plan
Enabling Objectives
By the end of this chapter the participants will be able to:
• Describe the different types of disasters
• Define and differentiate the key disaster-related terminologies
• Describe disaster preparedness and its aim
• Demonstrate comprehension of the key concepts and skills in disaster preparedness
and response at site and facility levels

Outline
8.1.Introduction to disaster
8.2.Disaster preparedness and response
8.3.Types of Disaster preparedness and response
8.4.Health facility disaster preparedness and response
8.5.Summary

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 Case discussions (Discussion on Case 1, 2 & 3)
Case1
A 7 years old son of our national celebrity brought to your ER being poisoned by
organophosphate, atropine is expired and not available all over the nation.
Questions
• Is it disaster or Mass Casualty Incident (MCI)
• Is it Static or dynamic
Case2
If FMOH informed about suspected Ebola case at one of the ports
Questions
• Is it disaster or MCI
• Is it Static or dynamic
Case 3
Assume you are working in non COVID 19 designated facility ER and found a patient
with typical COVID 19 symptoms
Questions
• Is it disaster or MCI
Time: 20 Minutes

7.2 Introduction to Disaster

7.2.1 Introduction
A disaster occurs quite often and no nation in history has been immune from its consequences.
From time to time risk of disasters is increasing and when the effect occurs in developing
countries is huge due to lack of preparedness and safety measures.

Possible reasons for the disaster incident increment includes

 Improved data collection

 Global warming
 Increased technology (especially in developing countries with immature safety systems)
 Rapid human population growth and urbanization
 Civil war and conflict with a potential for population displacement
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  Rise of terrorism
 Increased population density
When disaster happens both human and infrastructures are affected and usually response with
available local resources is difficult therefore, always is necessary to have National Health
Service response preparedness to a disaster.

Definition of key terms

Disaster WHO defines disaster as is a sudden ecologic phenomenon that results potential injury
creating effect with sufficient magnitude requires external assistance

Disaster Prevention refers to measures taken to eliminate the root causes that make people
vulnerable to disaster.

Disaster Mitigation is permanent reduction of the risk of a disaster. Primary mitigation refers to
reducing the resistance of the hazard and reducing vulnerability. Secondary mitigation refers to
reducing the effects of the hazard (preparedness).

Disaster Preparedness is building up of capacities before a disaster situation prevails in order to

reduce impacts.

Disaster Response is the set of activities implemented after the impact of a disaster in order to
assess the needs, reduce the suffering, and limit the spread and the consequences of the disaster.

Risk is the product of the probability of the occurrence of the hazard and its consequences. It is
the product of hazard and vulnerability.

Risk mapping is the process of establishing geographically where and to what extent particular
hazards are likely to pose a threat to people, property and the environment.

Relief is the provision of immediate shelter, life support including medical care and needs of
persons affected by a disaster.

Mass casualty incident: Any event resulting in a number of victims large enough to disrupt the
normal course of emergency and health care services.

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Table 13: Types of disaster

Disaster Type Definition Examples

Natural disaster Disaster caused by a Earthquakes, tsunamis, tornadoes,

naturally occurring event hurricanes/typhoons, volcanic-
eruption, pandemic influenza

Man-made disaster Non-natural events that Vehicle crashes (e.g., car, plane, bus),
are not purposefully mass casualty events, explosions, fires,
produced industrial accident/chemical release

Terrorist-related Events that are Events of September 11, 2001, as well

disaster purposefully produced in as intentional chemical, biological,
an effort to cause terror radiologic, or toxin releases

Internal disaster An event that occurs Hazardous materials spill in hospital

within the hospital laboratory, fire or explosion within
hospital, power failure

External disaster An event that occurs Transportation accident, industrial

external to the hospital accident

Acute disaster Disaster that occurs in a Explosion, industrial release,

narrow and well-defined earthquake
timeframe

Non-acute disaster Disaster with no well- Pandemic infectious disease,

defined start point or incremental release of a biological or
continuous production of toxin (e.g., anthrax sent through mail
casualties over a broad
timeframe

7.3 Disaster preparedness and response

7.3.1 Preparedness
Preparedness is the development of plans designed to save lives and to minimize damage when a
disaster occurs.

Disaster preparedness measures should be developed and put in place and tested long before a
disaster strike. Preparedness plans should be developed based on the identified potential disaster

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risks. When possible, this should include hazard mapping to specify locations at high risk for
specific disasters.

7.3.1.1 The preparedness plan aims are:

 Strengthening community based disaster preparedness
 Minimizing loss of life and disability
 Minimizing disruption of critical services
 Minimizing damage of infrastructures when the disaster occurs
 Increasing the efficiency, effectiveness and impact of disaster emergency response
mechanisms at different levels.
7.3.1.2 Preparedness plan should include:
 Effective warning systems
 Development of emergency preparedness plans
 Maintenance of inventories
 Training of manpower
 Financing
 Sectoral offices
 Partnerships to establish alliance
7.3.2 Disaster response
Disaster response is the set of activities implemented after the impact of a disaster.

7.3.2.1 Objectives of Disaster Response

 Providing immediate assistance to maintain life

 Improve health and support the affected population

 Rehabilitation until sustainable solutions

7.3.2.2 Factors that Determine the Nature of Disaster Response

 The type of disaster

 The ability to take pre-impact actions (EWS)

 The severity and magnitude of disaster determines the response required

 The capability of sustained operations (resource, management, assistance)

 Identification of likely response requirements (understanding the disaster threat is vital)

7.3.2.3 Requirements for effective disaster response
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  Information
 Coordination
 Communication
The group of Units, Organizations, and Sectors during a mass casualty event should work
jointly.

7.4 Types of Disaster Preparedness and Response

Disaster preparedness and response is divided into two levels.

 Pre-hospital (Field Response): Activities at the Scene and transportation

 Health facility level

7.4.1 Field Response in Disasters/Mass Causality Incident

Disaster response is based on:

 Pre-established procedures
 Maximization of use of existing resources
 Multi-sector preparation and response
 Strong pre-planned and tested coordination
7.4.1.1 Approaches of Field Response in MCIs/disasters
C. Scoop and Run
 Most common approach and does not require specific technical ability from rescuers. It
may be justified for small numbers occurring near a hospital the purpose may be just
transfer problem to the hospital

D. Classic approach
 First responders are trained (basic triage and field care). Since there is no communication
and coordination between field and health facility, it will quickly results chaos to health
facility
7.4.1.2 Mass Casualty Management Approach
 Most sophisticated approach includes pre-established procedures for resource
mobilization, field management and hospital reception
Steps in MCIs/Disaster response

Activation

• Notification and initial response by the affected community and community

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 administrators .Establish incident command Center (ICC): the affected area disaster
responders are responsible to establish the ICC. Members of the ICC includes but not
limited: local higher official, police, fire, rescue, search, health manager, official from the
pre hospital & ambulance services, transport authorities, representative of community 1st
responder, NGOs ….
• Scene assessment: establishing safety of the scene prior to the entrance of the aid
providers should be the 1st action to be done by the ICC. The scene should encircled by
security body in order to manage overcrowding and to facilitate the movement of
responders. Assessment of magnitude of the disaster: the local ICC should assess the
magnitude of the impact of the event in order to decide either assistance from outside is
required or not

Implementation

 Search and rescue

 Triage

 Treatment

 Transport/evacuation

Establish command system

 Senior member of first arriving unit becomes incident commander and should remain in
charge until relieved by a higher authority. Unified command should be established early
in the event. Establish communication is very important to notify all players who may be
involved in the response.

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Figure 87: Basic Command Structure Single Command

Scene management

Organizing the disaster site is very important and the disaster area can be organized in the
following way:

 Impact Zone

 Impact zone may be dangerous (e.g. Terrorist attack, active violence etc.) If you can
secure impact zone (both safety and security) than triage can be done in the impact zone.
If impact zone dangerous for responders than need to move patients to collecting area for
triage

 Command Post

 Collecting Area in Unstable Location

 Advance Medical Post (AMP) Area (3-T Principle)

 Triage

 Treatment

 Transport

 Evacuation Area

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  Press Area (Information Officer)

 Access Roads (geographical presentations if available)

 Check point for resources (Staging Area)

Figure 88: shows disaster organization site at scene

Traffic and crowd control

 Notify security and police early to assist in managing flow of people and resources which
will need a team to work closely with incident command to ensure safety of victims,
responders and bystanders. If possible best to have identified access and egress points

Search and rescue

 Determine most qualified individuals for search and rescue and assessment risks for
rescuers is very important and should address the following risks before the activities get
started

 Structural instability/ collapse

 Fire, carbon monoxide, cyanide

 Dirty, chemical (neurotoxic) bombs, radiation

 Blood exposure

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Goal of Search and Rescue

 Locate victims and

 Assess victim’s status (on-site triage) – START triage

 Remove victims from unsafe locations – collecting area

 Transfer victims to AMP thru entry triage (medical triage)

 Goal is to get the most patients to advanced medical care in the “golden hour”

Victim Management: Advanced Medical Post (AMP)

 Provide “entry” medical triage, effective stabilization for victims of a MCI/Situation

like, intubation, tracheostomy, chest drainage, shock mgt , analgesia , fracture
immobilization, fasciotomy, control external bleed & dressing . It can be done by ER
(A&ED), physicians/ nurses (trained & skilled), Anesthetists / Surgeons / EMT’s /
Nurses / Aiders, etc.

Figure 89: Activities by AMP

Goals of MCIs triage are to establish treatment priority, determine evacuation priority and
ongoing reassessment.

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Figure 90: Triage

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Figure 91: Victims flow from entry to AMP to evacuation to hospital
Transfer organization: Evacuation Procedures: Regulation Rules:

 Victims should be in most possible stable condition an adequately equipped for transfer.
Receiving facility correctly informed and ready and the best possible vehicle and escort–
available

7.5 Health facility disaster preparedness and response

7.5.1 Hospital-based disaster Response

 Every hospital department must participate in the disaster planning process. After plan
activation, the primary role of the emergency department is to assess and treat individuals

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 with illness or injury

 At minimum the disaster plan should have:

 Clearly delineate the circumstances in which the plan is activated

 Identify the command structure with defined lines of authority and responsibility

 Describe a response strategy for each anticipated incident

 Estimate an incident’s impact on safety and hospital function, providing for evacuation if
necessary

 List essential information, such as critical telephone numbers (e.g., elevators, key
personnel

 The hospital emergency operations plan provides for an organized response of the
hospital from the time of notification of a disaster until the situation normalizes.

7.5.1.1 Components of Hospital/health facility emergency operation plan

 Activation of the emergency operations plan

 Establishment of an emergency operations center

 Assessment of hospital capacity

 Surge capacity planning

 Communications

 Supply and resupply

 Triage and treatment of casualties

 Establishment of support areas

 Termination of the disaster state to allow for recovery and the return to normal activities.

A. Activate the Emergency Operations Plan

 The roles and responsibilities of all employees in the ED Or Any employees who may
respond to the ED must be clearly delineated in the planning process. Those roles must
be clearly listed and easily accessed in the event of a disaster
B. Establish Emergency Operations Center

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  Incident management system is now a standard component of emergency command and
controlling mechanism. It provides a flexible management structure on which to
organize a response. By principle, It works for both hospital and field disaster response.

Figure 92: Organizational structure of the incident command system

7.5.2 Assess health facility Capacity

 Before the hospital can receive casualties, it must be determined if the hospital itself has
sustained any structural damage or loss of use as a result of a disaster. These include
blocked passageways or inoperable elevators; potential for fire, explosion, or building
collapse; failure of utilities; loss of equipment or supplies; contamination of water; and
outside access problems.
 Once it is determined that the hospital/health facility itself is safe, the hospital should
determine how many casualties from the disaster site it can safely manage

7.5.3 Create Surge Capacity

 Surge capacity is the ability to increase hospital bed capacity over normal limits. Intra
hospital surge may include doubling patients in rooms, converting an acute care ward to
an intensive care level unit, opening previously closed wards, or caring for patients in
typically nonclinical locations, such as the cafeteria.

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  Inter hospital or regional surge may include discharging hospitalized patients to an
external low acuity unit, either mobile or fixed, and altering standards of care for nurse:
patient ratios (typically a role of the state governor and legislature and only during
governor-declared disasters

7.5.4 Establish Communication Systems

 Establishment of good communications is critical in any disaster or mass casualty

situation. Without a clear method of communication, the best disaster plans fail. Cellular
telephones, in particular, are often overwhelmed in disasters. Disaster planning must
include a multi-tiered plan for intra hospital (blackboard, two-way radios, and
messengers/couriers) and inter hospital (citizen band groups, cellular telephones, satellite
telephones, two-way radios) communication.

7.5.5 Establish Support Areas

 Family Information Center

 A separate area should be pre designated for family members seeking information.

 Volunteer Coordination Center

 In major disasters, the potential for large numbers of volunteers including those wishing
to donate blood. A separate place should be identified to handle these volunteers

 Media Center
 Members of the media should be directed to a room or office of the hospital away from
the ED
 Closely supervised by a hospital administrator or public information officer
 Responsible person may give press release

7.5.6 Decontamination, Triage and Treatment

Certain areas of the hospital must be designated for specific functions, including
decontamination, triage, care of major and minor casualties, pre surgical holding and surgical
triage, psychiatric care, and morgue facilities. The plan should be quite specific as to the
function of these areas, staffing requirements, and basic supplies to be used.

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Decontamination

Decontamination is performed in an area that is outside of the clinical care area of the
ED.Typically, this area is located external to the ED but may be in internal locations. The
decontamination facility should allow for the removal of clothing and cleansing of the skin and
hair of patients exposed to a chemical

Triage

Patient entry should be restricted to only one location, the triage area. The primary functions of a
disaster triage area are rapid assessment of all incoming casualties or ill patients, patient
registration and identification, the assignment of priorities for management, and distribution of
patients to appropriate treatment areas in the ED and hospital.

Figure 93: Simple Triage and Rapid Treatment (START).

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Figure 94: Jump START for pediatrics MCI triage

Figure 95: Triage tag

Treatment
Patient care in disasters requires alteration of scale and sometimes location of clinical care, but
staff should perform the clinical roles that are familiar to them. Several exceptions to this rule

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may exist (decontamination); however, in general, staff are more efficient at performing typical
tasks quickly than learning new tasks in real-time.

It is suggested that treatment are may divide in to

 Resuscitation area

 Minor case treatment area

 Pre surgical Holding Area and Surgical Triage

Morgue Facilities

 Many disasters can result in a large number of fatalities. This may require that present
morgue capacities be expanded to other areas of the hospital. I.e@AA.( medical school,
auditorium etc.). Viewing of expired patients should take place here, not in treatment
areas.

7.5.7 Terminating Disaster Response (Recovery)

 Efforts should be directed toward returning the hospital to normal operations.

 Restocking and cleaning

 consideration should be given to the emotional stress experienced by both

hospital staff

 The Critical Incident stress debriefing (CISD) offers immediate emotional support
to health care workers.
Practical session
Experience sharing of participant in their facility on
• Any encountered disaster/MCI, plan, triage treatment, patient disposition
• Any challenges faced and way forward

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 8.5 Summary
 A disaster occurs quite often and no nation in history has been immune from its
consequences. From time to time risk of disasters is increasing and when the
effect occurs in developing countries is huge due to lack of preparedness and
safety measures.
 Disaster preparedness measures should be developed and put in place and
tested long before a disaster strike. Preparedness plans should be developed
based on the identified potential disaster risks. When possible, this should
include hazard mapping to specify locations at high risk for specific disasters.

 Surge capacity is the ability to increase hospital bed capacity over normal limits.
Intra hospital surge may include doubling patients in rooms, converting an acute
care ward to an intensive care level unit, opening previously closed wards, or
caring for patients in typically nonclinical locations, such as the cafeteria.

 Certain areas of the hospital must be designated for specific functions, including
decontamination, triage, care of major and minor casualties, pre surgical holding
and surgical triage, psychiatric care, and morgue facilities.

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 8. REFERENCES
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